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GWAS terminology "Tag" vs "Lead" vs "Index" SNP
I'm trying to get my head round the correct GWAS terminology. I keep seeing the terms like "tag", "lead" and "index" SNP to be used almost interchangeably and I would like to get a clarification from someone inside the field.
My (limited) understanding is as follows:
Tag SNP - the SNP included on the genotyping microarray. Once we have a compendium of SNPs for a given sample we can use reference haplotypes to impute the rest of the SNPs.
Lead SNP = Index SNP - the SNP assigned the highest association significance after we've run association analysis for all the imputed SNP. The other SNPs in high LD with the lead SNP will form the associated locus.
Am I correct in my understanding? Any other / better terms I should be aware of?
Many thanks!

Hi. One question for clarification: have you read the wikipedia article on "Tag SNP"?

I did. It explains "Tag SNP" quite clearly, but it doesn't really touch on "downstream" terminology, even in the GWAS section. Thanks for bringing it up though - it's a useful link to have in this question.

I found a review paper that addresses your questions, see
Schaid, Chen, Larson (2018): From genome-wide associations to candidate causal variants by statistical fine-mapping
Tag SNP. You correctly identified tag SNPs. From the paper:

[T]he SNPs on microarrays, called tag SNPs...

Lead and index SNP. These are apparantly synonyms. From the paper:

This allows one to focus on the SNPs with the smallest
  (that is, most significant) P values in distinct regions,
  sometimes called the lead or index SNPs.


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Please help me to identify this creature, is it harmful and possible solution of how to get rid of these in my house
Please help me to identify this creature, is it harmful and possible solution of how to get rid of these in my house.
Please forgive me for bad image quality, some of these have white dot at the back(I guess male/female identification mark).
I am from north India, Punjab region
Please help me to get rid of these.
min size found: 3mm
max size found: 6-7mm

These look like mealybugs (Hemiptera: Sternorrhyncha: Coccoidea: Pseudococcidae); if so, then you have an infested houseplant (you're implying they're indoors).  Step one is to identify the houseplant that is harboring the animals; after that, I don't have much to tell you (I'm not an economic entomologist).

they are both indoor and outdoor, first these were out of my house, then I found these inside too. I don't have plants inside house but I do have flowering plants in my gallary, inside house but outside our living areas. I am not sure if they are really mealybugs, as they don't look much like them and I could not find any plant with these. these are mostly on wall and floor

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/

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How to characterize stability of a protein from Trp fluorescence vs [denaturant] curves?
A colleague of mine has taken Trp fluorescence measurements from a dimer in combination with various ligands, over a range of denaturant concentrations.
The idea is that ligands which bind more tightly to the dimer will stabilize it and delay changes in fluorescence. This is what our data look like:

Total fluorescence decreases, probably due to quenching from the denaturant. Papers I've seen using this method show it's possible to calculate the fraction of denatured protein by analyzing displacement in peak emission wavelength. However, they use monomeric proteins with few Trp, whereas I have a dimer with several Trp plus some additional variability introduced by the different ligands.
Additionally, we have data from a scintillation proximity assay that indicates ligand affinity is ordered as 1<...<5 and 6<...<11. Ideally, we would like to replicate this same ordering through the analysis conducted on the data above. I would appreciate any suggestions of methods that will allow us to carry out such comparisons.

Papers I've seen using this method show it's possible to calculate the fraction of denatured protein by analyzing displacement in peak emission wavelength.

Have you tried doing that with your data? What do you get if you plot peak emission wavelength as a function of denaturing agent concentration? If these look like sigmoidal curves (you might need a log scale on the X axis) with a clear upper plateau, then you can apply the method mentioned by these papers because the signal you observe is correlated to the fraction of denatured protein and saturates (this part is important: the signal must saturate past a certain concentration of denaturing agent, because all protein molecules are fully denatured and therefore adding more denaturing agent won't give further signal change; if your signal doesn't saturate, something is wrong).

However, they use monomeric proteins with few Trp, whereas I have a dimer with several Trp

Oligomeric state and number of Trp residues should not matter, because peak emission wavelength is only correlated to the fraction of denatured protein. Total intensity will increase with more Trp residues, but you're not using intensity as a measure of the fraction of denatured protein (and if anything, it's good to have more intensity to begin with given the quenching effect you observe with increasing denaturing agent concentration).

plus some additional variability introduced by the different ligands.

To take care of this concern, you need two controls that:

prove that none of the ligands alters the fluorescence of your protein,
prove that none of the ligands emits fluorescence between 300 and 450 nm, or if they do then you need to measure it to be able to subtract it from your total spectra, in order to recover the protein contribution to the total fluorescence.

For 1, record fluorescence emission spectra of the protein without denaturing agent but as a function of ligand concentration (span a few orders of magnitude) and see if the peak emission wavelength changes with ligand binding (it might change, which means the same assay can yield binding curves and Kd values for your ligands, which could also be useful!). Full ligand titration curves would be the most robust control, but you can simply use the same ligand concentrations as used in the denaturation experiments.
For 2, the simplest case would be that your ligands are not fluorescent, but you cannot simply assume that. Therefore, an important control you also need is to record emission spectra for each of your ligands at the concentrations used in the denaturation experiments, and this at each concentration of denaturing agent (or simply at 0 and max concentration: if there's no difference between these two spectra, you don't need to record one at every concentration in between). If the ligands emit fluorescence between 300 and 450 nm, you need to subtract that from your total spectra to recover the fluorescence arising from the protein only.

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Measure Water-Use Efficiency without using carbon isotope fractionation?
I read "Measurements of delta (C-13) in C3 species may usefully contribute to the selection for transpiration efficiency." I think the device to measure carbon isotope fractionation is very expensive. Are there some easier ways to measure the water-use efficiency of plants, please? Thank you.


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How to solve these kinds of problems?
16% of people in a population can not roll their tongue .what is the frequency of people which are heterozygous of this character? Please ,any one help and guide me to solve these kind of problems.
 I tried to solve it using punnet square but i failed .
So i tried my best please help me to solve this.

Homework questions are off-topic on Biology unless you have shown your attempt at an answer. For more information see our homework policy.

@David  He show some attempt.

Possible duplicate of Solving Hardy Weinberg problems

Hint: The very first step is to define which genotype can not roll their tongue. Then, you know that 16% of the population have these genotypes. From this, you can find out the frequency of heterozygote in the population thanks to Hardy-Weinberg. For more information, please look at the post marked as duplicate.

I definitely recommend looking at your calculations. The "unable to roll tongue" trait is recessive, not dominant. Look at the Hardy-Weinberg equation $p^2 + 2pq + q^2 = 1$. Try to extract the root of $q^2$ and you will get the right solution.

https://www.nature.com/scitable/definition/hardy-weinberg-equation-299 this might help you too.


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Rubisco and Nitrogen Shortage Condition
Suppose a plant sprouted when $t=0$ and died when $t=T$. Let $t_*$ be the time when the plant shifts the resources usage to maximize its reproductive organ. In the case of nitrogen shortage during plant growth, it is known that $t_*$ becomes earlier. Would someone please explain this phenomenon by relating to Rubisco?
Here are some of my findings:

It was shown that the decrease in the amount of Rubisco during leaf
senescence is higher compared to plants grown under suboptimal
N‐feeding conditions (Tercé‐Laforgue et al., 2004).
Rubisco is also considered as one of the most important Nitrogen
source that can potentially be remobilized and translocated to growing
or storage organs.

Currently, I understand how the nitrogen shortage is related to Rubisco, but I still do not how to relate this to the prioritization of reproductive organ. This might be a mere uneducated guess, but does this have something to do with survival of the plant? Say, it senses that Rubisco itself cannot replace the needed amount of nitrogen, then it is wiser for the plant to reproduce rather than growing.


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What type of insect in this?

Can anyone tell what of kind of insect is in this image ? They have been showing up in my room for the past month; never happened before that. The room is generally hot during daytime.
Thanks

Wow i saw same bug hour ago!

Where was it found and when? That is basic info for species identification questions.

This question has previously been asked/answered here: Identification of an insect from midwest US. A post about their smell can be found here: The smell of the shield bug (aka stink bug).

Brown marmorated stink bug (Halyomorpha halys):

Source: Brown marmorated stink bug (wikipedia)

That is a "shield bug" in the order Hemiptera. They're often called stink bugs because they release noxious chemicals for defense. I agree that it does look like the brown marmorated stink bug, but there are several species that look similar. Depending on where you live, the brown marmorated stink bug may be an invasive species. The links below show how to distinguish them, and give info about the invasive species. They're showing up in your room because they over-winter in houses, and become active at warmer temperatures. They can become a serious problem due to forming large colonies, so you may want to look for obvious places they could be getting in, and seal up the entries. Once they start hanging out in your house, they attract others with scents. The Farm and Dairy article has a simple, inexpensive cleaner recipe to remove the chemicals they release to attract more stink bugs.
Identifying stink bug species, including marmorated stink bug: http://www.stopbmsb.org/stink-bug-basics/look-alike-insects/
The brown marmorated stink bug as an invasive species: https://hort.uwex.edu/articles/brown-marmorated-stink-bug/
How and why stink bugs get into your house, and how to keep them out: https://www.farmanddairy.com/top-stories/simplest-way-to-eliminate-stink-bugs-indoors/373786.html


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What is this insect I found in northern Europe?
Found this one in my bed in Northern Europe.

Around 6 mm long (5 mm body + 1 mm nozzle). Seems to have 6 legs. The back looks a bit like black-brown camouflage, the legs are red-brown, the nozzle is black.
Could this be some kind of bed bug?

Possible duplicate of Small black slow-moving insect showing up in the home

The nose is a dead giveaway: it's a weevil. See this post for identificaron and info on bed bugs.

Definitely not a bedbug. It is a weevil, family Curculionidae. A beetle, and not normally found indoors. It looks a bit like Baris, but I cannot tell from the picture. https://en.wikipedia.org/wiki/Baris_(weevil)

great, thanks! The Weevil type looks definitely right. Not sure about Baris though, it looked a bit more like one of these Lixus Junci https://en.wikipedia.org/wiki/Weevil#/media/File:Lixusjunci.png (the picture i provided doesn't really give a lot detail, sorry)


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How compelling is the hypothesis that dinosaurs were killed by toxic plants?
A friend of mine has recently told me that dinosaurs were "killed by flowers". I was a bit surprised and so I googled. And I did find a lot of recent articles in popular media on this topic, probably based on this. To me it doesn't sound convincing at all, but I'm an outsider. Does anyone think that there's more to that than just a usual journalistic overhype?

Things in the paper that strike me as suspicious
Associating toxic plant defenses with the Cretaceous

Although there continues to be uncertainty about precisely when plants
first evolved toxic defenses, this period of angiosperm proliferation
would seem to be a strong candidate case. (pg 50)

Against this Gleadow and Moller (2014) discuss Cyanogenic glycosides (CNglcs), a class of organic compounds that can kill overgrazing herbivores from cyanide poisoning,

CNglcs are unusually widespread in the plant kingdom. They are found
in the oldest of terrestrial plants (the ferns) and in gymnosperms and
angiosperms.

Similarly, poisonous terpanoids are found in the Ginkgo; Proanthocyanidins, of which oak or wine tannins are a member, is found also in maritime pines; etc. There doesn't appear to be a strong link between angiosperms and chemical defenses against herbivory in plants.
Claiming that the angiosperm proliferations and extinction of dinosaurs are linked in time

The relative co-occurrence of angiosperm proliferation and the
disappearance of the dinosaurs has not gone completely unnoticed.(pg 50)

The diversification of angiosperms occurred starting about 112 MYa for the Monocots, and 100 MYa for the Eudicots, according to De Bodt, et all (2005). From Figure 1 of that linked paper, we can see that both branches of the Angiosperms were approaching their modern diversity by 90 MYa; a time still 25 million years before the extinction of the dinosaurs. 25 million years ago, our nearest ancestor hadn't diverged from the line that would lead to Old World Monkeys, and was probably arboreal. Evolution can do a lot in such a time. Calling these two events linked in time is suspicious, at best.
Using crocodilians as a test case for taste aversion

Since crocodilians are descendent from the same creatures that gave
rise to dinosaurs, this creates the opportunity to evaluate the
tenability of the proposition that dinosaurs went extinct due to an
inherent inability to learn to avoid eating toxic plants.

Reptilian cladistics are far from settled, but I would suggest that crocodilians diverged from dinosaurs by at least the early Triassic. They are almost certainly more divergent from all dinosaurs than birds. Here is what the authors have to say about birds.

However, in contrast to caimans, birds are in fact capable of forming
learned food aversions. (pg 51)

That seems to really undermine the argument here.

Learned taste aversions does exist in crocodilians, if caimans do lack it (unlikely) it is secondary event. http://sydney.edu.au/science/biology/shine/publications/reprints_legal/712hatchling.pdf

Rather than talk to the specifics of this idea, which others have already done well, I'll contextualise it as one anti-consensus view among many. Many. Many.
The extinction of non-avian dinosaurs is the most publicly well-known part of a much larger systemic event at that time, one of the largest extinction events in the last 500 million years. The Cretaceous-Palaeogene extinction event killed something like 70% of Earth's species, and unless the large clade that is the dinosaurs suffered an extinction (excepting some birds) at the same time a lot of other life, both on the land and (which is arguably even better understood from the fossil record) in the oceans, suffered one coincidentally for a different reason, we need an explanation of the pattern.
This was not initially recognised. After dinosaur fossils were discovered, there was a period of about 100 years when scientists didn't think much about why it happened, because "life progresses up a ladder" was a popular idea in biology until surprisingly recently. (Bear in mind that Charles Darwin only lived to see evolution become uncontroversial among biologists, not his model of how it happens.)
Then, from c. 1920-1980, a zillion in-hindsight-stupid ideas were proposed; see here for details, including the toxic plants idea dating to 1976. It's not even the only "something went wrong with the plants they ate" idea. The consensus view (the Chicxulub impact) explains a food chain collapse, which explains why all animals over 25 kg became extinct except for ectothermic marine reptiles (crocodiles and leatherback turtles), whose different metabolism and diet explain why they could get away with being larger. Other plant ideas included "geologic uplift reduced plant supplies on the uplifted terrain" and my personal favourite (among all hypotheses, not just plant ones), "caterpillars ate the plants". Pointing out the fact that butterflies evolved 10 million years too late for that to work, making this more scientifically feasible, feels like taking a sledgehammer to a nut.
In the end, we have to look at "maybe miscellaneous heterodox idea #23 is the real answer" the same way we do when people deny contemporary anthropogenic GHG-driven climate change. The point often missed in both cases is that the consensus view explains an enormous pattern of pieces of evidence, while the rival ideas each contradict something observed, requiring a detractor from the consensus to assert inconsistent ideas to explain it all.

IOW, the culprit was Astrophysics, in the Caribbean. with a great big meteor :-)

No, it's not convincing; angiosperms evolved in the middle part of the dinosaurs' reign, not the end, and toxins evolve slowly which gives herbivores a chance to compensate, also conifers can be riddled with toxins just as easily.
Lastly, the idea that dinosaurs could not learn taste aversion is ludicrous; it is one of the simplest neurological feats, anything with even the simplest brain can accomplish it. Claiming dinosaurs would not be able to do so would require extraordinary evidence and the article provides nothing even slightly convincing.

The "evidence" is supposedly (I didn't check if its true or not) is crocodiles don't have taste aversion now.

@Joshua Which is pretty weak evidence, considering the fact that crocodiles don't usually eat plants anyway, so they don't speak to the neurology of any herbivorous dinosaur.

@Joshua its also wrong, crocodiles have and learn taste aversion, http://sydney.edu.au/science/biology/shine/publications/reprints_legal/712hatchling.pdf


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Pictures of trigger point muscle fascia
Are there any pictures of an actual trigger point looks like? All I am able to find online are animations.

I found plenty of pictures of therapists conducting trigger point therapy on their patients. Are you looking for a picture of the actual trigger point picture underneath the skin?

Yes, exactly...

You can use @TheLastWord in your comment such that your comment will be seen in the inbox of the tagged user.

@TheLastWord Yes, exactly.

You could have easily find these using a simple google search, however I will point several out:

See figure 1 of this article for an ultrasound image of a trigger point. Really interesting!
See figure 1 of this article for a schematic representation, and figure 2 for a real image. Although you did not ask for a deeper understanding of this topic, if you want to read more about it I would recommend reading this paper as it covers a lot of aspects (such as pain signals to the brain).
This article covers different imaging techniques and facilitates interpretation by using arrows to point out the trigger points.

If this is not what you are looking for please specify what you mean with "pictures"? (vibration sonoelastography, schematic, ultrasound, etc.) I cannot point you in a direction for real life images (if these even exist).

This is so insightful. Thanks for aggregating all of the info in this answer.


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Do individual mammal hairs absorb water?
In my look into the world of shaving I've seen claims that it is better to shave after a shower because the hairs will absorb water and soften, making the shave easier. Likewise, I've seen it claimed that natural hair brushes (i.e. boar and badger hair brushes) should be soaked before use. My question is: do the hair fibers actually absorb water, presumably thickening in the process, or does the water just adsorb onto the surface (maybe lifting the scales in the cuticle) meaning you can wet hair in aggregate, but it doesn't soften when soaked? Especially, is there a side-by-side comparison of a single hair under a microscope before and after soaking showing what happens?

Researching this answer took me to some strange literature, but it appears to suggest a little bit of both (at least for human hair, which is porous, implying that some water can suffuse through the cuticle into the cortex). For example this paper looks at the impact of this effect on drug testing.
There's also a few papers in cosmetics science journals describing various elements and effects of increased hair porosity, but I was unable to find one primary citation which characterised the trait.


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Calculation of extinction coeffcient of GFP
I want to convert the absorption of a protein into concentration. Hence ı need to calculate the extinction coefficient of the protein (GFP). ı found the formula (nTrp)5500+(nTyr)1490 on the internet but not able to use it since ı dont understand what n in front of the amino acids stand for and how ı reach to the n value

Only the number ("n") of the aromatic amino acids Tryptophan (Trp) and Tyrosin (Tyr) in your protein contribute significantly to its absorption at 280 nm (and Cystein (Cys), albeit to a lesser extend), see also here.
You could retrieve the protein's amino acid sequence from uniprot (see GFP here). Looking through the GFP sequence, one can identify n=11 (4.6%) Tyr and n=1 (0.4%) Trp. Now you can insert those in your formula and end up with an extinction coeffient of 21'890 M^-1 * cm^-1. This formula is only valid if all Cys are reduced (GFP has n=2 Cys that could form a disulfide bridge).
If you want to avoid all the formulas I suggest you copy the sequence of GFP and paste it into ExPASy ProtParam. This way you get a nice overview of the amino acid distribution of your protein and also retrieve the extinction coefficient under oxidizing conditions, which BTW is 22'015 M^-1 * cm^-1.


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Insect identification - pantry moth vs clothes moth
Are the following insects a pantry moth or a clothes moth? I live in Europe, if geographical location is of importance in this case.

The insects are about 7 - 10 mm in length.
For several months I have been fighting with recurring invasion of pantry moths and those were caught in pantry moth pheromone trap. However, the specimens seem  to be smaller than the pantry moths that I have been fighting a couple of months before (I have read that clothes moths are smaller) and I have seen some flying near the wardrobes. I couldn't find traces of infestation in the food as well. Is it possible for clothes moth to be attracted by pantry moth pheromones?

Although the images are very grainy and oddly lit, the second two images look a lot like a pantry moth. Specifically, it reminds me of a very common pantry pest:
Plodia interpunctella (Indian-meal moth).

 Source: Urban & Structural Entomology, Texas A&M University, USA
Range: [source]
The Indian-meal moth can be found on all inhabited continents. Although it is primarily tropical, it can live in a range of habitats and is a very common nuisance pest in food storage facilities and people's pantries worldwide.
Description: [source]

7-10 mm long (wing span ~ 1-1.5 cm)
Wing color:
-Posterior 1/2 of wing red/brown/bronze
-Anterior 1/3 of wing is white/light gray / ochre-yellow

Separated by dark band

Body color: reddish-brown

Pest Info: [source]

Adults live 5-7 days
Females lay 60-300 eggs
Eggs hatch in 2 - 14 days
Larvae do all of the destruction

Can even eat through plastic to get to food! [source]
Common Foods: Cornmeal, flour, dried fruits, nuts, seeds, health foods, pet foods.

The first picture is of a Clothes Moth (Tineola bisselliella). The uniform gold colour of the wings (with shiny dust that easily comes off) is diagnostic.
The second and third pictures appear to be Pantry moths.
I could not find a scientific reference, so I describe my own observations below. Happy to delete this if it is not appropriate.
Both species mostly are caught in the trap with the matching pheromone. A few are caught in the "wrong" trap, and both are caught on a trap with no pheromone at all (a control).
In this case it looks like the moths pretty much are attracted to their own pheromone trap, and only caught in the wrong trap by accident.

Clothes moth trap (with pheromone bait above it)

Pantry moth trap above

Control trap above - no pheromone


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Does trapper/hunter harvest reflect abundance or community composition?
I'm working on a study where a single professional trapper removes furbearers and corvids (who the trapper is changes annually). I would suspect that the composition of the harvest would be strongly influenced by the individual's trapping style, ie. how and where they choose to set their choice of traps, as none of this is regulated. However, others argue that the harvest is reflective of species abundance and community composition. I'm having difficulty finding sources for either argument that aren't fisheries-centric. Can anyone suggest any?

It would be more reflective of relative abundance, rather than actual abundance unless you have 100% catchability.  Comparatively these concepts for furbearer traps should be similar those in fisheries related to catchability and selectivity.  This is my opinion  as a  hobbyist trapper and professional fisheries biologist.


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Comparison between Transmission Electron Microscope (TEM) to Scanning Electron Microscope (SEM)
Can someone state the advantages of Transmission Electron Microscope (TEM) over Scanning Electron Microscope (SEM) and vice versa?

Well, the main difference between them is that with SEM you get information about the surface using scattered electrons whereas with TEM you get information about the inner structure with transmitted electrons. TEM has higher resolution, but SEM is simpler because you do not need a thin sample.
I recommend these videos about SEM and TEM. Short description of both can be also found at this webpage and in the material for students by ThermoFisher Scientific.


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(Reference request) Formal abstract theory of evolution?
EDIT: please feel free to suggest books that are the closest you can come up with to what I'm looking for, even if it doesn't exactly overlap!
I am very well acquainted with the theory of evolution as informally taught. E.g. I don’t need a book that explains the theory, or refutes popular misconceptions.
Instead, I am looking for a formal theory of evolution as a process, and I am not specifically interested in the biological aspect of evolution, but in evolution as a more generally occuring process.

How do we formally state the different assumptions of Darwinian evolution? (Random change, heritability, natural selection).
What happens if we change these different assumptions? (Non-random mutation? Maybe, selection criteria that are influenced by the mutations, rather than independent of it)
Are there quantitatively different results of evolution based on these assumptions?
Something I find very interesting: What kind of non-biological evolutionary processes can we describe formally? E.g. evolution based on some form of non-random mutation, or based on different types of heritability. What are the different implications of different formal assumptions. How do these differences apply to different evolutionary systems? (E.g. evolution of ideas, cultures, computer viruses, evolutionary algorithms).

In summary, I am looking for a book that introduces in a very abstract way the properties of evolutionary systems (does not have to be focused on biological evolution. I’m interested in the formal properties of such systems).
NOTE: I am NOT asking about a book on modelling highly specific processes that apply to specific biological systems, such as population dynamics of preditor-prey relations. I’m interested in general, abstract theoretical analysis of the notion of an evolutionary process in general.

This question is quite wide i hope you will get answer.

@L.Diago, but someone could give me SOME suggestion, without necessarily giving me everything I’m interested in, right?

[Thomas Cavier-Smith] (https://en.wikipedia.org/wiki/Thomas_Cavalier-Smith) had interesting idea about inheritance in clay. But this theory have never been proved/ disproved (some guy tried to do something like that but not with clay). I am not quite sure how the influence selection would look like.  But if non-random mutation exist i thing the specious wont  be able to adapt to their

enviroment effectlivly on the other hand you technicly can be a X-man in world of non random mutation. So in our world all mutation is random but there is some region which can be more mutated then others part of DNA. Others non biological evolution system is for example you languages systems. I hope i tell you something what do you really want to.

@L.diago, note that non-random mutation doesnt mean NO mutation. It just means that there is some directionality to the mutation. For example, I've heard it argued that businesses evolve according to a kind of non-random mutation. But yes language evolution s another example! I would like a book on the formal properties of such evolutionary systems. If there is no such book, any book that is somewhat like it would be welcome as well!

I didnt say no mutation, but mutation which wont be random..  The randomness is what life makes soo well adapt on diffrents enviroment..

If you are interested in non-biological evolution then you may be interested in artificial evolution and simulated evolution. .

Each of your bullet points could be a full question in and of themselves, as it is this makes the question way to board. You  will be better off asking separate questions, especially since several points are unclear or erroneous. .

@John, but I am not asking for answers to those questions... I am asking for a book on the topic that encompasses these questions. Also, what is erroneous?

You will not find a single book covering such a broad range of topics, Again you would be better off asking the questions separately, especially given how vague your criteria are.

@John, I'm pretty sure that given the responses, the think I'm looking for either doesnt exist or is not well-known. I think this question should be closed

neither is the case you are simply asking for too much from a single source. Each bulleted point would come with recommendations for several books or hundreds of papers. Or you could simply ask the questions you really want and let the answers lead you to sources.

@John, perhaps it is better if I first try to get an overview of which sub-fields in evolutionary theory there are, and what they study, then I might be able to ask a more pointed question.

Perhaps this would be a good way of stating it: I am interested in a rigorous mathematical introduction to generalized Darwinian mechanisms

@Programmer2134 then you will (mostly) find it in the books that have already been mentioned. Although I should note that the generalization of population genetic principles to macroevolution is still contentious and an area of active research.

@NatWH, I'm not sure why you mention macroevolution?

Because not all of evolution has been satisfactorily mathematically formalised :P

you may want to look at the field of "adaptive dynamics" for a more abstract look, the most detailed mathematical explorations will be tied directly to genetics.

@John yes that is closer to what I want. The more abstract the better. I don’t want details.

The theoretical framework that best fits the kinds of questions you have in mind is evolutionary game theory.
The foundational text is perhaps Maynard Smith's Evolution and the Theory of Games, but I'd recommend one of the standard textbooks instead, say Gintis (2000), Game Theory Evolving or the more advanced Hofbauer and Sigmund (1998), Evolutionary Games and Population Dynamics.

Summarizing evolutionary processes to game theory is, IMO, border-line  ridicule. Of course evolution of social behaviour do matter but in no way can evolutionary game theory be seen as the core principle of any thin one would want to call evolution. Typically, I don't think game theory is being used in evolutionary algorithm at all.

Evolutionary game theory applies to any and all evolutionary processes. It is not tied to social behavior in any interesting sense.

From wikipedia : Game theory is "the study of mathematical models of conflict and cooperation between intelligent rational decision-makers". Its application to evolutionary processes as well as Hamilton's extension by including a relatedness term are fundamentally limited to the study of the evolution of interactions (conflict, cooperation, etc..) among agents (aka. social evolution).

Evolutionary game theory precisely forgoes the assumption of rationality in favor of evolutionary regimes. The interactions and conflicts in EGT usually just codify differences in fitness between, e.g., a base phenotype and a mutant.

Difficulties in your question
It is a little hard to know exactly what you're after because 1) the question is broad 2) some concepts you talk about are a bit unclear.
For example, by 'random change' I suppose you mean genetic drift but I am not sure. The term 'random mutation' is a little undefined (see this post). You list 'Random change, heritability, natural selection' as a list of assumptions (at least I think you mean those are assumptions) but those are typically not common assumptions of evolutionary models. Also, the list is not in any way intuitive, so it is unclear what you mean by it. The phrasing "selection criteria that are influenced by the mutations" is also very unclear. Of course, selection, by definition, is dependent upon the genetic variance.
From our discussion in the comments, I think you are attempting to group different fields under a single concept just because they have the same name. But it is not because they have the same name that they are governed by the same basic principles. For example, it is not because the concept of plasticity exists in both biology and physics that these concepts are in any way related and that there is a general theory of plasticity that encompass both fields.
Evolutionary genetics
That being said, you could gain from any good intro textbook to evolutionary genetics. I especially recommend Population genetics, a concise guide. You will find more such recommendation in the post Books on population or evolutionary genetics?.
Evolution of ideas, cultures, computer viruses, evolutionary algorithms
In your last question you mention 'evolution of ideas, cultures, computer viruses, evolutionary algorithms'. I think you are referring to these concepts so as to clarify that you are not so much interested in the biology of specific organisms but really into the process of evolution. I do not recommend starting reading about these concepts before having a background in evolutionary genetics. You might otherwise make the mistake to over stretch an analogy.
Note also that the field of memetics (evolution of ideas, cultures) is a young field in which very little empirical testing is possible. So, I don't think it is wise to start there if your goal is to increase your understanding of evolutionary biology.
In any case, I am not able to suggest a good book in any of these fields (Evolution of ideas, cultures, computer viruses, evolutionary algorithms).

see my answer, I'm guessing those parts that are less clear come from fusing ideas on natural selection, Hardy-Weinberg population stuff, and neutral theory. In which case I think the related monographs should clear it up. Just throw up your favourite evolution books! I would love to hear them as well.

"by 'random change' I suppose you mean genetic drift but I am not sure." No I simply mean mutation of individual genes. "In your last question you mention 'evolution of ideas, cultures, computer viruses, evolutionary algorithms'. I think you are referring to these concepts so as to clarify that you are not so much interested in the biology of specific organisms but really into the process of evolution." No that is not the reason why I mention it. I mention it because I am specifically interested in the process of evolution in general, not just to organisms.

By "evolution" I mean the general process that occurs roughly whereby (1) there is a sequence of "samples" from a space of possible elements (e.g. a sample from the space of possible DNA sequences, where each such sample is a "generation" of individuals), and where each sample is determined as a random deviation from the previous sample (previous generation).

@NatWH I've listed books I like in the linked post Books on population or evolutionary genetics?. My worry with suggesting a book like The Neutral Theory of Molecular Evolution is that it is not introductory and the OP might have a hard time reading it. I have never read Gould and Lewontin so I can't comment on these books.

By "random", in this case, I roughly mean: "independent from the other factors in the model". Though I didn't intend to specify randomness very precisely, as my goal is not to get a specific answer to these points, but to get a general introductory book about these topics

@Remi.b that is very fair. That's why I put Futuyma in as the start of my suggestions.

@Programmer2134 Such concept of evolution encompass many different processes. One should not make wrong analogies from one field to the other. You won't find a good book that talk about all these very different types of evolution. Note that you will need to understand the existing models before trying to investigate violation of their assumptions.

I think population genetics is not exactly what I'm looking for, as it seems to be quite specifically biological (in the sense that it goes into the specifics of the biological mechanisms behind the relation between genetic an phenotpyic traits for example), and therefore not very applicable to say, evolutionary algorithms in intelligent computing.

@Remi.b, I'm not sure what "wrong analogy" you're talking about, but ok....

Again, I'm looking for a formal theory of these different processes. it is possible that this simply doesn't exist yet. (I am not interested in empirical testing, or in understanding how biological evolution happens in the real world).

Of course, they exist. The book I suggested (as well as Kimura's book NatWH suggested) are all about modelling. There is no mention of specific species. It will teach you how to compute expected heterozygosity after n generations of drift and selection and other stuff of the kind. Generally speaking, there is a lot of math in evolutionary biology, more than in most other fields of biology.

@Remi.b you clearly don't understand that I am not interested in specifically biological evolution, despite me repeating this a few times now. That is, I'm not interested in specifically genetic/biological factors such as heterozygosity, etc. I'm interested in the more general process of evolution, e.g. as applied in evolutionary algorithms for computer programs, etc.

@Programmer2134 most evolutionary algorithms will be founded in at least some way in fundamental evolutionary math. However, I suggest that biology.SE might not be the best place to ask if you're looking for things that veer into algorithms in machine learning...

@NatWH, It seems I'm in the wrong forum, yes... (though I'm interested in theory, not specific algorithms. But nevermind) I'll wait for some more responses, but otherwise I think this question should be closed

@Programmer2134 I think you are attempting to group different fields under a single concept just because thy have the same name. For example, it is not because the concept of plasticity exists in both biology and physics that these concepts are in any way related and that there is a general theory of plasticity that encompass both fields.

@Remi.b, let's just agree to disagree. This is not going anywhere

@Programmer2134 I can agree with that :D Good luck!

As a body of literature, that covers quite a broad range of topics that have been discussed at length in many, many papers. Of course, you might find something out of a broad-level textbook (I suggest Futuyma's Evolution). You might also enjoy Kimura's The Neutral Theory of Molecular Evolution (although be aware of its follow ups and critics), and its (somewhat) ecological counterpart, Hubbell's The Unified Neutral Theory of Biodiversity and Biogeography. There are loads more, but this might be a good starting point.
EDIT: also Gould's The Structure of Evolutionary Theory, and Lewontin's The Genetic Basis of Evolutionary Change.
EDIT: also, not directly but since I have just finished reading it: Simpson's Tempo and Mode in Evolution. This is mostly from a palaeontology perspective, but it brilliantly preempts several arguments about rates of phenotypic evolution, individual vs population processes, and the asymmetry between mutation and substitution and what that means for evolutionary biology.

Add in several of Dawkins books (selfish gene, extended phenotype, and climbing mount improbable) which will dive into basic assumptions, artificial evolution and provide a counterpoint to Gould.

@John I would classify most of those under things OP would already have read, given the intro to his question. Dawkins is one of the most well-known popular science authors after all. Also bringing in some Dawkins necessitates bringing in some E. O. Wilson...

I make no assumptions about what the OP has read since they seem unclear about some of the basic tenets of evolution. And of course asking about non-biological evolution always makes me think of dawkins work on virtual/simulated evolution and ideas about memetics.

Eh, I've voted it be closed, anyway. You're right that it is far too vague, and appears to be more about machine learning.

@John, purely out of curiosity: what basic tenets do I seem unclear about?

random mutations are an assumption of evolution, that mutations are statistically random is an independent conclusion and not necessary for evolution, mutation is not even really necessary for evolution it just will not occur for very long without it.

@John, lol ok. I didn’t say any of those things, but let’s just stop this discussion, because this isn’t going anywhere.


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Is this plant Yucca filamentosa color?
I am trying to find the name of this plant for a while. The closest I got is Yucca filamentosa color. The leaf blades are near 4-5 inches and are almost thin(without pulp). Please help me in identifying it.

Location: Hyderabad, India.

Yucca mostly has smooth leaf  and this has spine shaiped leaf.  Yucca ussaly dont have so wide leaf. (https://www.swcoloradowildflowers.com/White%20Enlarged%20Photo%20Pages/yucca%20baccata.htm) here is some pictures of semi desert yuccas

No, not the Yucca baccata . I was thinking Yucca filamentosa color guard(http://www.missouribotanicalgarden.org/PlantFinder/PlantFinderDetails.aspx?kempercode=d184). As per the wide part, the leaf blades in my picture are around 4 inches wide.

You know i am not professional botanic so i hope you will get proper answer for this question.  But i think that yucca has smooth leaf without pulp(mostly), but agave has spike shaiped leaf with pulp.

Thanks for mentioning the pulp part. The plant that I uploaded has almost no pulp in it's leaves.

I found out the picture that I posted belongs to  Furcraea foetida 'Mediopicta'. It belongs to "Agave" family like L.Diago suggested in comments.


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what is the name of this small plant with yellow flower?
Can someone please help me find the name of this flower. The close I got to is maybe some kind of diasy?.

Location: Hyderabad, India

This looks like Sphagneticola trilobata also known as Singapore daisy, creeping-oxeye, trailing daisy, and wedelia.  It is now found throughout the Neotropics but is native to Mexico, Central America, and the Carribean.  It is a weed that is classified in the top 100 worst invasive species in the world.

Source: Sphagneticola trilobata (ePlants)

Thank you very much Kurt for your answer. It's funny though, how Mexican native species got the name of Singapore daisy.


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Were there any marine/aquatic dinosaurs?
Most dinosaurs were terrestrial, but there were a couple of groups of arboreal and flying dinosaurs (microraptors, birds etc).
I have read that the theory that Brachiosaurids were aquatic has been largely discredited1, but that Spinosaurids were probably semi-aquatic2.
Excluding modern marine birds (e.g. penguins etc.), were there any other marine/aquatic dinosaurs?

Note: I am aware that the marine reptiles mesosaurs, phytosaurs, mosasaurs, dolichosaurs, Icthyosaurs, thalattosaurs, Sauropterygia (placodonts, nososaurs, plesiosaurs etc), Choristodera were not part of Dinosauria.

References:

Three new sauropod dinosaurs from the Upper Jurassic of Colorado, Great Basin Naturalist.
The Physiology of Dinosaurs: Circulatory and Respiratory Function in the Largest Animals Ever to Walk the Earth, Respiratory Care
A note on the habits of sauropods, Annals and Magazine of Natural History
Tipsy punters: sauropod dinosaur pneumaticity, buoyancy and aquatic habits, Proceedings of the Royal Society of London

Oxygen isotope evidence for semi-aquatic habits among spinosaurid theropods, Geology
Semiaquatic adaptations in a giant predatory dinosaur, Science
Convergent evolution of jaws between spinosaurid dinosaurs and pike conger eels, Acta Palaeontologica Polonica
Functional Morphology of Spinosaur 'crocodile-Mimic' Dinosaurs, Journal of Vertebrate Paleontology

How about the mosasaurs for example?

@Remi.b mosasaurs were squamates, not dinosaurs: Mosasauroid phylogeny under multiple phylogenetic methods provides new insights on the evolution of aquatic adaptations in the group, PLOS ONE

Fair point! I am wondering why this post has been down voted.

Hesperornithes could be a good example but they are Aves (a "basal branch") if I am not mistaken. They are not modern birds though. Would you accept it as an answer?

@Remi.b ah, thanks! I was thinking of pre K-T extinction dinosaurs when I posted the question, which this is, so yes I would - unless someone responds with a larger list of examples :)

There are a couple of specimens of a dinosaur species named Liaoningosaurus paradoxus that have been found with fish in their stomachs and skeletal features suggesting it was at least semi-aquatic.  It is a member of the ankylosaurian dinosaurs from the early Cretaceous period of China.
From Fish Hunting Ankylosaurs( Dinosauria,Ornithischia) from the Cretaceous of China:

With elongate and fork-like denticles of cheek tooth crowns,L.
  paradoxus has a dentition capable of penetrating into animals like
  small fishes. The carnivorous adaptation of the dinosaur is also
  supported by the ungual modification to a sharp claw in both the
  fore-and hind-limbs. The evolution of a shield-like ventral armor
  plate and the loose sacrum-pelvic connection suggest that L. paradoxus
  may have adopted an aquatic way of life,using the ventral armor plate
  to protect the body from underwater attacks; as such,the open suture
  between the neural arch and centrum of the vertebrae cannot be used to
  indicate the juvenile nature of the type specimen. L. paradoxus is the
  first carnivorous ornithischian dinosaur since dinosaur was first
  known in the 18th century and represents not only the first aquatic or
  semi aquatic example of armored dinosaurs but also the smallest
  species of ornithischian dinosaur so far known.

Image Source: [Paleontology • 2016] Liaoningosaurus paradoxus • Fish Hunting Ankylosaurs (Dinosauria, Ornithischia) from the Cretaceous of China

I found this wikipedia page which lists a few more examples:

Only a few nonavian dinosaurs are thought to have been semiaquatic. The combination of being oviparous and endothermic seems to have prevented the evolution of fully aquatic dinosaurs.

Theropoda
Paraves

Avialae

†Ichthyornis - a toothed ornithuran analog of modern seabirds such as gulls and petrels
†Hesperornithes - a mostly flightless group of diving bird-like ornithurans

†Dromaeosauridae

†Halszkaraptor - a mallard-sized basal dromaeosaurid from Mongolia with flipper-like forelimbs

†Megalosauria

†Spinosauridae - thought to be piscivores, the group had crocodile-like skulls and includes some of the largest known carnivorous dinosaurs

†Ornithischia
†Ornithopoda

†Hadrosauriformes

†Lurdusaurus - an unusually heavy-bodied and short-limbed iguanodont conjectured to have been similar in lifestyle to the modern hippopotamus

List of semi-aquatic tetrapods: Non-avian dinosaurs

Chapter 23 of New Perspectives on Horned Dinosaurs: The Royal Tyrrell Museum Ceratopsian Symposium, "A Semi-Aquatic Life Habit for Psittacosaurus, describes the evidence suggesting Psittacosaurus was semi-aquatic.
P57-59 of Discovering Dinosaurs: Evolution, Extinction, and the Lessons of Prehistory suggests some hadrosaurs may have been semi-aquatic:

Dinosaur
Illustration

Icthyornis

Hesperornithes

Halszkaraptor

Spinosaurus

Lurdusaurus

Psittacosaurus

The only example I could find for the moment are Hesperornithes. Hesperornithes are actually part of the Aves clade (see here on tolweb.org) but they are not modern bird species as they existed during the Cretaceaus.

Note that there are examples of aquatic species in Squamata (Squamata are not Dinosauria) though such as the mosasaurs for example.

According to the latest discovery, Nature (Published: 29 April 2020), Tail-propelled aquatic locomotion in a theropod dinosaur, Spinosaurus was probably aquatic or at least semi-aquatic. See also this video.


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What is the name of this plant with leaves having two different shades of green?
I am trying to find the name of this plant. I am attaching the relevant images. Thank you for your help.

Location: Hyderabad, India

They just look like juvenile leaves...

I have been looking at this plant for a while now and the colour has been consistent with leaves. It might be possible that they are juvenile leaves and are taking their time. Any ideas with what the name of this plant is?

Do you have any images of the flowers of this plant, or if not, would you know how the flowers might look like? This will help, thanks.

With the Help from Taimur in above answer, I was able to deduce that the picture that I posted belongs to Ficus Benjamina.

So after searching a bit, I think this plant is of the genus Ficus:

I am still unaware of the species but the nearest I could find was Ficus retusa. I hope I have been of help.

Yes, Thank you Taimur for your help. You have narrowed my search area.

Hi, I found that the pictures that I attached might belong to Ficus Benjamina. It is grown as ornamental plant where I live.

@vamsidharmuthireddy great, if you are certain of it, you can answer your own question then. I am glad I was of help.


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What is the Darwinian explanation for hallucinogenic plants?
What advantage is there to being hallucinogenic when eaten by some or most species for survival? I can only think that perhaps it stops the organism from eating the rest of you as they are confused? Perhaps some animals seek out hallucinations thereby increasing the amount you are eaten so you can spread seeds?
I am not a biologist by any means but can understand basic biology any information would be gladly appreciated

Related: Why are there so many medicinal plants?

Is the hallucinogen properties of plants something that's useful to the plant, or did the particular chemicals evolve to do something else, and it's only an accident that they have that effect on human nervous systems?  It seems unlikely that they would have evolved as a deterrent, since a reasonably large critter could eat a whole bunch of plants before the onset of hallucinations.

In hallucinagenic mushrooms there is psilocybin, which I can't find a reason for being created for the mushroom on an evolutionary or a reason to do with growth for the mushroom, and it has been created in mushrooms several times (in multiple different evolution chains I believe). Are all hallucinogens not understood yet like this one?


text:
Antibiotic resistance
I have a biological puzzle that's been perplexing me for years.  Can you review my logic and tell me where I'm wrong or if I'm on to something.
As I understand it, most, if not all genetic engineering uses a marker gene to identify transformed bacteria.  This marker gene was/is usually an antibiotic resistance gene so the transformed bacteria will be the only ones that can grow on an antibiotic laced culture medium.
So, every (most) GMO will contain a copy of a bacterial antibiotic resistance gene.
Also, I believe that bacteria are able to spontaneously aquire DNA from their environment and / or other bacteria.
So, is it a fair question to ask if the unnatural proliferation of antibiotic resistance genes in the wild due to the commercial propagation of GMOs might be at least partially responsible for the increase in multiply resistant organisms that we are seeing?
Has anyone, for example, mashed up GMO matter, added non antibiotic resistant bacteria, grown the mix up overnight, added the antibiotic used as a marker in the GMO, incubated for a few days and then seen if any bacteria survived?

As I understand it, most, if not all genetic engineering uses a marker
  gene to identify transformed bacteria. This marker gene was/is usually
  an antibiotic resistance gene so the transformed bacteria will be the
  only ones that can grow on an antibiotic laced culture medium

Most but color markers (which gives the host cell a color that can be used for selection) are also used. More complicated selectable-counter selectable markers are also used (ie  HyTK gene). A counter selectable marker is a marker that kills a cells when it is present. A selectable-counter selectable marker is a hybrid marker that allows you to both select for cells with the marker using one selection agent and kill the same cell with a second selection agent.

So, every (most) GMO will contain a copy of a bacterial antibiotic
  resistance gene.

Well not quite. GMO ie Genetic modified organism, includes both prokaryotes (bacteria) and eukaryotes (plants, animals, and yeast). The promoters which drives gene activity in prokaryotes and eukaryotes are different. So a eukaryote markers do not work in prokaryotes and vise versa.
Furthermore, genetic modification of eukaryotes is difficult. Hence modified viruses are often used. These viruses are made in such a way that their genome has been replace by desired DNA playload. And as the payload size is limited, often time any unnecessary DNA is also removed, like prokaryotic markers which have no function in a eukaryotic host.
Lastly due to public pressure, there has been a push towards cleaning up after genetic engineering work in GMOs that are to be marketed to the public (GMO crops). So things such a selection markers are removed (either by use of counter selectable markers followed homologous recombination or site specific recombinases).

So, is it a fair question to ask if the unnatural proliferation of
  antibiotic resistance genes in the wild due to the commercial
  propagation of GMOs might be at least partially responsible for the
  increase in multiply resistant organisms that we are seeing?

Given the wide spread use of antibiotic in animal husbandry and by the public general, and move toward removing selection markers in commercial GMOs, I do not think GMOs are the cause of the increase in MR bacteria.
A more likely cause would simply be because we are using so much antibiotics and thus there is a selection pressure to aquire multiple resistance. Remember all our antibiotics resistance genes and most of our antibiotics were acquired from nature.

Has anyone, for example, mashed up GMO matter, added non antibiotic
  resistant bacteria, grown the mix up overnight, added the antibiotic
  used as a marker in the GMO, incubated for a few days and then seen if
  any bacteria survived?

Yes, lots of times around the world to varying degrees of sucess. I have personally spent time doing this and so have my labmates. It will work if you prepare good quality DNA that has not been degraded by endonucleases, the bacteria are very transformable (ie the bacteria has been treated to take up DNA easily), electroporation is use (to force the DNA into the cell) and you have prokaryotic marker. A eukaryotic marker, is a marker that works in an animal cells will not work in bacteria. So you have to engineer your GMO animal to carry both a eukaryotic and prokaryotic marker.


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mRNA and Protein relation
A and B are two different proteins:
1- can they have same mrna
2- is it possible that the gene types which encoding the synthase are same ?
my answer is yes to both .
because after protein synthased cell can remove aminoacids with  post-transcriptional modification etc.

It also depends on what you mean by the same mRNA? Same mature mRNA? The same transcript can be differently alternatively spliced, leading to different proteins.

What on earth is meant by "the synthase"? No synthase has been mentioned. And what is meant by "gene types". Please clarify the question, i.e. give it in full. And provide a better explanation of your reasoning for each part.

1) Can two different proteins have the same mRNA?
This isn't clear enough to give you an answer:

Can two different proteins be made from the same mRNA molecule?

Yes, polycistronic mRNAs can encode several proteins which are translated separately (we can engineer this using internal ribosome entry sites, IRES).
Yes, different proteins can be translated from one open reading frame by failure of peptide bonding between two amino acids (we can engineer this using 2A peptide sites).
Yes, identical proteins can be translated from one mRNA and then modified differently after translation to yield different "final" proteins.
Yes, identical polypeptides can be translated from one mRNA and then incorporated in different protein complexes.

Can two different proteins be made from the same mRNA code?

No, not made in the sense of translated.
Yes, as above, identical proteins/polypeptides can be made and treated differently after translation.

2) Is it possible that the gene types which encode the synthase are the same?
Gene types? Do you mean genotype, i.e. allele? What synthase? Sounds like a homework question to me.

I don't understand what you mean by failure of peptide bonding between two amino acids. Do you mean post-translational cleavage into two chains like insulin? And if you want to ask a new question of whether two proteins can be translated from the same eukaryotic mRNA without any post translational modification of any sort, I can give you some examples that might surprise you. (This question has already got 4 close votes, so I imagine it will be closed soon.)

2A peptides don't cleave in the sense of proteolysis, rather, the ribosome "skips" peptide bonding and releases the current polypeptide while continuing translation of the ORF into a second polypeptide. So it's not strictly a post-translational modification. E.g. https://www.ncbi.nlm.nih.gov/pubmed/11297676 and more recently https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5438344/. (Note this doesn't always work, the ribosome will sometimes cancel and not translate the second polypeptide, and sometimes it won't skip and make one long fusion polypeptide)

My guess is there are also miRNAs that can modify what polypeptides an mRNA molecule produces; but sure, shoot :)

Answer is yes, by a logical approach, in superior organism where alternative splicing and post-transcriptional modification alter the protein structure.
In bacteria, this thing is not allowed. This scenario isn't common in functional protein, and start occurring by some alteration in the splicing process.
In real life, this is nearly impossible. A protein domain could be conserved, and so different protein can share parts of the amminoacidic sequence and, by that, the mRNA. But, as far as I know, there's no study confirming the evidence of same transcript and different proteins.

Alternative splicing produces different mRNAs, so the first part of your answer is incorrect. You echo the poster's incorrect "post-transcriptional modification". It should be "post-translational modification", and it hardly counts as a separate protein anyway.

He's not arguing about "after" or "before" splicing.
So, starting from the same template, you could get different mRNA. For the 2nd sentence, you're right.

And, just for completeness, you're saying that post-translational modification doesn't change protein structure at all. Here, you're wrong.

Don't put words into my mouth. I know perfectly well what effects post-translational modification can have on proteins. I don't answer unclear homework questions because questions of that type should be unambiguous, and the answers often depend on the teaching context. In this case, unless it was specifically mentioned in class I would assume the reference was to a different amino acid sequence.


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Why is it beneficial for bacteria to conjugate? (Horisontal gene transfer)
Why is it beneficial for bacteria to conjugate? I would think it's more beneficial to take a plasmid from another cell, than to give yours away or "share". Not homework, I'm just curious.

I am going to try answer it. Bacteria in general has different survival tactics. In general for bacteria the best way how to surviva is as much copies as it cans. So imagine situation, when bacteria is surround with others bacteria. Then the race will bega. All bacteria wants to survive with same tactic as i mentioned. Thats mean the best way how to archived this goal is make your replication fast.
So when you take plasmid with resitantion to antibiotics its advantige to have those, but when you actually is not exhibit to that antibiotic it slow down your chance to survive (because it slows down your replication, cell division)

This article might be helpfull too here

So, it's to gain genetic variability? Because if they didn't have the ability to do HGT, the only mechanism to get genetic variability would be spontaneous mutation, which is way to slow, I guess.

@ThaleMathiassen Mutation rate is not too slow. Actually bacteria has mechanism to incries the rate. With the genetic variability you are right, HGT gets to bacteria something more, something new, what might be helpfull to survive. Good example is transduction in Griffith´s experiment.


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Identify this vertebra
I was walking on the beach in New Jersey (U.S.), at about 40 degrees longitude, and found this bone. It's not a fish. The long process in the front is interesting. It is likely a C2 vertebra. I looked on the web, but could not find anything aquatic that it might match. Certainly not a dolphin. It is 2 inches long (50 mm), and 2.5 inches high and wide (64 mm). I guess it need not be aquatic, and New York City (20 miles North of here) used to dump garbage in the ocean. It looks old. Can you help me identify it?

Looks very much like an axis (C2) vertebra. The give away is the odontoid process (aka "dens") clearly visible on the bottom of each photo. Spinous process looks uniquely shaped (keel like) which might help your search. Size sounds too large for dog/cat, but who knows. Definitely not human.

www.boneid.net provides a great searchable database of identified bones

I found a picture with various cow vertebrae here: https://www.chichesterinc.com/Images2012/1172-40-V1-Lg.jpg Not sure your's is there.

Still disappointed that I can't figure out what this is. Is it pretty difficult to identify a single vertebra?

By the size you said and using the bonid site mentioned, it can looks also like a wild boar C2. But do you have wild boar in NJ?

Looks like Lumbar Vertebrae or Sacral Vertebrae of a Cow like @Brian Hanson Said above.
Studying closely in laboratory can elaborate more secrets about the bones.

This is not a lumbar or sacral vertebra. It doesn't even look like it's from a cow: http://www.boneid.net/product/lateral-view-cattle-c2-vertebrae/


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How do drugs tests check so many substances?
There are about 170 drugs banned for sports and many other drugs that can be used in crimes.
How can blood tests practically detect so many different substances? Do they divide the sample into 170 different micro samples? How are sports and criminal blood tests arranged to be comprehensive?

There are a lot of different methods to test samples for drugs. The most common for a "screening" test, like one might encounter before being hired for a job, are based on immunoassays. These use antibodies to detect certain substances in the sample. These are good for testing for a few drugs or categories of drugs (like THC, benzodiazepines, opiates, amphetamines, etc.), however they can't test for a large number of drugs at once, and often won't tell you the specific drug (e.g. it'll say "positive for benzodiazepines", not "positive for alprazolam"). If someone tests positive on one of these screening tests, then the samples can be re-submitted for further testing to clarify what is causing the positive result.
Drug testing for elite athletes is a whole different story. The World Anti-Doping Agency has established protocols for the Athlete Biological Passport, which uses standard methods to test samples and record various biological parameters over time, to ensure that athletes aren't manipulating their bodies artificially.
The exact details of how this is done is pretty complex, but they don't need to divide samples into a bunch of separate samples and test each one for a single drug. These standardized kits are able to be run on one urine sample (divided in two) and a couple of tubes of blood, the same size you'd get drawn at a doctor (just 3-5 mL each).
One way they test for many different substances using a single tube is through gas-chromatography mass-spectoscopy (GC-MS), which is a combined method to separate apart substances in the blood and identify them by their molecular weight. By comparing athlete's blood and urine samples to known patterns produced by banned substances, they're able to test for many different compounds using a single sample.


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Inverse Agonist vs Neutral Antagonist
Could somebody explain in simplest terms the difference between inverse agonist and neutral antagonist?
Which one is more well natural and less likely to cause pathways to rebound?
Does neutral mean less effect such that stepping from an inverse agonist to neutral is the best idea to avoid withdrawal?
Edit: I am trying to determine how quickly the pathways rebound when stopped during withdrawal.  I would assume this might vary between inverse agonist and neutral antagonist.  I am not asking about actual withdrawal symptoms.

Where did you find these terms?

To those that are reading there are similar questions on this site https://biology.stackexchange.com/questions/6972/do-serotonergic-5-ht2a-mediated-psychedelics-elicit-stimulant-effects  https://biology.stackexchange.com/questions/66394/do-enzyme-inhibitors-change-equilibrium?s=2|40.7686

I will assume you are referring to these terms as used in molecular biology and pharmacology then. Have you looked at the wikipedia pages inverse agonist and receptor antagonist?

Many receptors have a natural constitutive, or "baseline", amount of response that they generate, they're not just an on-off switch. At baseline, many receptors will generate a partial response, which means that certain things binding to them can either increase or decrease their response.
A neutral antagonist is one that causes no change in the signaling response of the thing that it's binding to. It simply stays the same. Note that this can still be important, because a neutral antagonist can block the binding of other agonists, ones that would have generated a change in response, even if the antagonist itself doesn't cause a response.
An inverse agonist is something that decreases the response of the receptor from its baseline all by itself. Often, this is caused by stabilizing the receptor in it's "off" state. If the receptor has some degree of constitutive activity, an inverse agonist will decrease its activity.
See this graph from this wikipedia page for a good explanation:

@William Please stop using the term "brain shock" - if you mean "withdrawal" then use the term others use: withdrawal. Knowing whether a something is an inverse agonist or an antagonist is not sufficient information to predict the extent of withdrawal symptoms.

@Bryan to repeat my question which one is "more natural?"

@William That term doesn't have any meaning outside of pseudoscience unless you give it a particular definition.

@BryanKrause I am trying to understand the long term impact and withdrawal effects of inverse agonists and neutral antagonists.  I can ask another question if mine isn't clear.  You are correct my question is not strictly using scientific terminology because I have found little information understanding differentiating the 2's impact.  What in my question isn't clear?  How quickly do pathways rebound?

@William I thought I already made clear in my comment: Knowing whether a something is an inverse agonist or an antagonist is not sufficient information to predict the extent of withdrawal symptoms.

@BryanKrause Are pathways ability to rebound not independent of their use case?  When I am implying rebound I am implying the restoration of the pathways not the actual withdrawal symptoms.

@William Binding affinity is probably closer to what you are looking for.

What is the horizontal drug column mean?

Why are antagonist listed if they don't do anything?

@William the horizontal axis is drug concentration. This is a particular type of receptor, that does something whether or not a drug or endogenous (thing the body produces) compound is bound to the receptor. Like the answer says, antagonists definitely do something. They compete with other compounds at the binding site. The change in activity of the receptor is only seen when you have two  compounds present. This is not shown in the figure.

@William think about what would happen if you had a neutral antagonist bound to a receptor and you added a full agonist. How would this be different from just adding a full agonist with no antagonist?  Then think about what would happen if you had a neutral antagonist bound to a receptor and you added an inverse agonist. How would this be different from just adding an inverse agonist?


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Does natural selection apply to entire populations as it does to individual organisms?
The context: the other day I was reading an article about a peculiar species of ant that when threatened by a predator would “explode” in order to help protect the rest of the colony, although it kills the individual ant. I was wondering how this kind of behavior could evolve via natural selection if it only picks out the individual organisms best suited for the environment - because it seems like a self-destruct type of behavior wouldn’t be helpful to the ants that are trying to survive and reproduce. Though it would make sense if natural selection also applies to entire populations as it does to individual organisms - picking out entire populations that are best suited for the environment. It would make sense because populations that have individuals willing to explode to help protect the other individuals would have an advantage over the ones that don’t.
The question: does natural selection apply to entire populations as it does to individual organisms or have I made a mistake somewhere in my logic - and if so, where?

I’ll leave a proper answer to someone more qualified than myself, but in the meantime you could lookup kin and group selection.

In an evolutionary sense, you can't really think of worker ants as individuals, since they can't reproduce.  The "individual" is really the entire hill.  See "Aunt Hillary" in Hofstadter's " Godel, Escher, Bach".

Don't feel bad for feeling confused about this subject. The problem of the "unit of selection" has long been a philosophical and empirical discussion among biologists.
For example, Richard Dawkins has strongly argued that even the 'organism' as the unit of selection can be misleading. He argues that the unit is even deeper, the "replicator" (gene). He argues this in his books The Selfish Gene and The Extended Phenotype.

Unit of selection
Your question is about the concept of unit of selection. Selection acts on any populations of things that have heritable features which explain at least part of the fitness variance in this population. The "things" can be genes, cells, organisms, groups of organisms, species, lineages, etc...
The standard is to view selection acting on population of individuals. But of course, selection can also act on populations of groups of individuals (or populations of populations if you prefer) or populations of species. When talking about selection on a population of groups of individuals, we talk about group selection (a concept very related to kin selection) When talk about selection on a population of species, we talk about species selection (or lineage selection).
Social evolution and altruism
An altruistic phenotype is defined as being a phenotype that is causing a decrease in the fitness of the carrier of the phenotype coupled with an increase in the fitness of one or more recipient individuals. Altruism can evolve at a level, only by selection applying at levels above it.
Imagine for example a population of individuals. If one individual mutates and as a result display a behaviour of donating food to the others. The cost for this individual is -0.5 and the benefit for the recipient is say 0.7. In absence of reciprocity, this mutation will not be passed on on future generations because  this individual carrying it have lower fitness. Therefore altruism should not evolve in this population. Imagine however if there are many populations and that some populations are altruistic and other aren't. Then, the altruistic population will likely outcompete the non-altruistic populations and therefore over time only the altruistic populations will remain.
It is by the way the existence of an altruistic behaviour that brought to wonder about the level at which selection can act.
The field that studies the evolution of such social phenotypes is called social evolution


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Can a creature fly and also walk?
These creatures, fly and walk, and have perfect eyesight and follow me everywhere I go.  They have many legs, they are about 1 inch and their color is almost translucent, but a very light shade of brown.  They smell me at all times and bit me like a mosquito.  I have used 2 pesticide companies to exterminate, but no one is able to identify the critter so I can't kill them.  They also have a very strong heartbeat. I know because they like to be under me.  They move so quickly that I haven't been able to catch a picture.  Please help me to identify these nasty things, so they can be destroyed.

Sounds like a puzzle! It is going to be impossible to ID this species without more info and probably without a picture. Where do you live? How come you know they have a strong heartbeat but did not manage to take a picture?!


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Why are humans only so tall/large?
In biology I've learned that cells rapidly divide and can grow and split undefintely, and that certain parts of the body have to grow and evolve before growing, but I am tied up on the fact that the body produces hormones to have only grow up to a few feet tall and stops growing at a certain age.
Why does it stop in terms of height or physical mass when it can still keep on growing? Why do the hormones tell the body to stop growing when it can continue?

Welcome to Biology.SE. Can you please clarify certain parts of the body have to grow and evolve before growing

Is there any reason you phrased your question as being specific to humans? You seem to assume "bigger is better" for humans. Would you assume the same for other species as well?

“Can grow and split [indefinitely]”, this is incorrect for normal cells due to something called the Hayflick limit. This statement isn’t essential to your question, but I felt like it needed to be clarified.

The question is a bit vague but I will take it to mean the following

Why does it (the body) stop in terms of height or physical mass when it can still keep on growing?

The answer is physics, specifically the ability for a body of a specific shape and structure to support itself and move itself, followed by the energy requirement to feed all those cells.
Strength of a bone scales with its cross sectional area, similar to muscle. Mean while mass scales with its volume. As a result, mass increases faster than bone strength. So the bigger your are, the weaker your bones become if all proportions are maintained. As a result for a certain design of animal there is an upper limit of how big it can become before it unable to support its own weight or able to move.
Next comes energy requirement. In general the more living bio mass you have, the more energy you require to keep it alive. The scaling isn't proportional but there is a general trend. And the more energy required the more food is needed, and given the habitat an animal lives in, there is only so much food around. And this places a limit on how big an animal can grow. An animal living in its niche has an energy budget.
Associated with energy budget, we meet biology and natural selection. Energy placed into growing, isn't energy placed into reproducing. All animals eventually die, either by predator or bad climate (winter, drought, even bad luck) . So it becomes a balance, given the amount of energy available, how much energy should be put into growth to give a more robust structure to survive vs how much energy should be put into reproduction so that the organism can multiply.
Put too much energy into growing bigger, your probability of dying before reproducing increases as you take too much time growing before becoming sexually mature. Put too much energy into reproducing, upon sexual maturity your body is small and weak and your die before you spend much time reproducing.
The ultimate right answer is dependent on the animal's niche, the physical environment around it, its biology, and the predators around it.

Your third reason seems to me more relevant. Arguably we should look for the first clue in reproductive success. After all we grow until... maturity. Bones could grow stronger, larger bodies can gather more food.
Contra, we could carry on growing stronger to protect our progeny. Socially though, we reach maximum power when we have to pay for the tuition fees.

I'm not sure this answers what the OP is asking.  Granted that the question is far from clear, but I took it to be asking what mechanism the body uses to control size. For instance, in Africa we can find ethnic groups with an average (male) height of 1.45 m ("pygmys"), other groups, other groups that average 1.9 m.  And of course we can breed dogs from chihuahua to Irish wolfhound, horses from minis to drafts, & likewise for most domesticated animals (and plants, e.g. miniature roses).  So what are the biological pathways that regulate size?

Thank you for the answer, it's answered and clarified my question; but, going along the thought of limited resources/energy, say that someone lives in some sort of "utopia" where resources are abundant, there are no environmental threats, no need for sexual reproduction, and some sort of evolutionary design that can support the body regardless of how large it is. Although this thought may be very abstract and impossible to happen, if such could, should a person be able to grow "indefinitely" (or very large)?

I would expect that organism to become very large and very old. I have listed two real world examples. These is a honey fungus colony that spanning 8.9 square km with an estimated weight of 605 tons, and about 2400 years old. There is also Pando a clonal colony of an individual male quaking aspen, about 6600 tons in mass and 10,000 year old, although some sections may be 1 million years old.  https://en.wikipedia.org/wiki/Largest_organisms>


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Can anyone tell me what this is?
On my one plants, this green worm is all over it, with white and yellow cocoons on the Leaves.

Where is the worm again? Do you have any pictures?

looks like a cocoon. Without the location and a picture of the actual worm, this is like searching for a needle in a haystack.

Please add your location, size of the white and yellow masses in your picture, and info about the green worm (size, pictures would be very helpful). Thanks

The green worm is inside the cocoon, I'll see if I can find one.  Leduc, Alberta, Canada

There is the worm, can't post anymore of them cause of size limit

You should keep the first picture of the worm and the old picture of the cocoon! as @theforestecologist said, we could need the size of the worm and cocoon.

Would it help to have a ruler in the picture so u can see wat the size of it is?


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Hormonal terms Somatotrophin or somatotropin?
Are Somatotropin and Somatotrophin hormones the same? It's confusing because when you type in Somatotrophin in google, it says, "a growth hormone secreted by the anterior pituitary gland.", but there's no Wikipedia about it. But when you type in Somatotropin, there's whole Wikipedia for this stating that it's a growth hormone. I am 100 % sure that there is a difference between these two terms: tropin and trophin because Wikipedia itself says not to be confused with these terms and has articles separately for these two terms. So, Can anyone help me be clear about these two terms?

Yes
They are the same thing, and both are old-fashioned terms for what is now termed specifically growth hormone (i.e. not generically as in "a growth hormone"). It is clear from the Wikipedia entry for growth hormone that this is equivalent to somatotropin.
I could not find a specific scientific reference that states that the two are the same, but I present a line of reasoning based on a search for mention of the terms in books using the Google ngram.

The initial similarity in the curves in the left-hand frame reflects, I think the competing use of the terms when the hormone activity was first discovered. Eventually somatotropin won, although the use of growth hormone is much more common now (right-hand frame).
If you look at the books cited by the ngram in which somatotrophin is used, you will find that many are in the field of animal science, especially dairy science in relation to the lactogenic effect of the hormone. Years ago I worked in this area, and remember that growth hormone had such lactogenic effects.  Presumably somatotrophin stuck in this area, whereas somatotropin was more generally used, especially in human endocrinology.
General Dictionaries and possible reasons for variation
I am hesitant to quote non-scientific dictionaries on scientific topics, but in this case it is probably justified, and it also addresses the difference in meaning of ‘tropin’ and ‘trophin’, referred to in the question.
The Merriam-Webster online definition of somatotrophin redirects to:

somatotropin
  variants: or less commonly somatotrophin

Chambers on-line only has somatotrophin, But my own 1994 printed edition has:

somatotropin or somatotrophin a polypeptide growth hormone

My Chambers Dictionary iPhone app also has both.
And Saunders Comprehensive Veterinary Dictionary, 3rd ed. (2007), according to a citation in the Free Medical Dictionary, has:

somatotropin, somatotrophin
  growth hormone

If you check the meanings of the two suffixes in Merriam-Webster:

-trophic
  of, relating to, or characterized by (such) nutrition

Whereas

-tropic
  1 : turning, changing, or tending to turn or change in a (specified) manner or in response to a (specified) stimulus
  2 : attracted to or acting upon (something specified)

It seems probable, therefore, that the original form was somatotrophin, but, either by confusion with the second definition of -tropic or a North American chemical aversion to ‘ph’ (as in sulphur/sulfur), somatotropin became dominant, except in the field of animal science. Perhaps that is why the Oxford Dictionary, both online and in my printed edition of 1991, ignores somatotropin completely. However you would have difficulty ordering somatotrophin from the chemical supplier, Sigma-Aldrich/Merck, whereas somatotropin is available.


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Phospholipid membrane fluidity if phospholipid had one type of fatty acid
How would membrane fluidity change if the phospholipid membrane had only one fatty acid?

Cell membrane doesn't have just phospholipid inside.
Components who influence fluidity in cell membrane are:
1) Fatty acids length
2) The grade of unsaturation of these fatty acids
3) Presence of cholesterol

So, if composed of just fatty acids, excluding every other component (carbohydrates, channels proteins and, mainly, cholesterol), the answer would be yes, its fluidity will change drastically.

Will it become more fluid of less?

Considering only saturated fatty acids and the total lack of cholesterol, answer would be less.

This depends entirely on the fatty acid and the reference membrane.
Amphipathic membrane fluidity is based on the intermolecular forces between the hydrophobic parts of the membrane. Like olive oil vs. butter or margarine, the specific type of lipid determines the fluidity and the temperature at which a phase change occurs.

You can construct a synthetic lipid bilayer with several different kinds of saturated fatty acids (think butter) that would have a phase change at a higher temperature and be less fluid than one with only one unsaturated fatty acid (think an extract of a single type of fatty acid from olive oil) .
In fact, with regard to cholesterol (from the same reference):

cholesterol tends to make lipid bilayers less fluid, at the high concentrations found in most eucaryotic plasma membranes

The point here is that fluidity is not specifically about whether you have all fatty acids, one kind of fatty acid, some fatty acids and some cholesterol, or any proteins. You have to look at the type of each of these things, and, in particular, the intermolecular forces between the hydrophobic parts of your amphipathic molecules.


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Antibody staining
I am staining tissue sections and I did a mistake, I was supposed to have mixed 3 primary antibodies but I stained only with one of them. After the 1h incubation I washed 10 min with PBS and then I did another hour incubation with the 2 antibodies I forgot to add before. Can that affect my staining? I am afraid I wanted to test different dilution of the first antibody I added alone, and then I added another hour incubation with 2 more antibodies.

Generally for IHC/ICC staining separately with the antibodies is not a problem. Staining with separate primary antibody steps is often done when the antibodies are from incompatible species and so might cross-react with each-other giving non-specific staining.
However, the 10 min wash and 1 hour incubation with the other antibodies may wash off some of first antibody, leaving you with weaker signal than expected. This may affect how "bright" your stain appears after the secondary antibody step.

Is this an ELISA? In that case, I suggest you doing this experiment again because now you are incubating for an extra hour. Incubation time is set at fixed range because increasing it may also increase the background noise of your assay.

Incubation times - sensitivity may be increased with a longer incubation time at room temperature. Be aware that the top of the curve may flatten out and become unusable, limiting the assay range. Additionally, background may increase

Resources:
https://resources.rndsystems.com/pdfs/datasheets/edbapril02.pdf

This is not an ELISA it is immunohistochemistry or immunocytochemistry.


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Heart rate vs body size
It is known that large animals have lower heart rates (beats per minute) than small animals. Is it the same situation in humans?
That is: if we have a group women, about the same age and fitness, and if we record for each women her body size (relevant indicators of body size are height, weight, BMI, body surface area) and her heart rate, will we see a trend that the heart rate decreases as size increases?
References to paper and studies about this issue are also welcomed.

See this paper which briefly states that it found no correlation but said it is not conclusive and should be further examined and studied.

The paper you link finds that there is not a significant correlation between body mass and resting heart rate in humans. While there is a well known negative correlation across mammals:

This is the ever-popular mouse-to-elephant curve that is found in one form or another for lots of physiological measurements.
I'll suggest, but have no evidence, that the lack of a significant correlation in humans is simply a result of there not being enough range in body mass among humans to allow finding a significant result. When the range of one variable is small, the association between that and another variable necessarily lessens. For example:

Although the linear relationship between the two variables is largely similar, when the range of x is truncated, the coefficient of determination, $R^2$, decreases. The correlation goes from 0.97 to 0.7. In this case, that might still be "significant", but I suspect that in humans that variation is much greater in resting heart rate.
It would have been nice if that paper included the actual data on HR, but they act like it doesn't exist just because it was not significant.


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What effect does taking antibiotics unnecessarily have on future bacterial infections?
I have been told by my biology teacher that you shouldn't take antibiotics unnecessarily because "the body gets used to them" and it reduces the effectiveness of antibiotics against future bacterial infections, which can be dangerous.
I can't understand how the body could "get used to" antibiotics. How does prior use of antibiotics affect their effectiveness against future infections?

Umm, you mean antibiotics, not antibodies.  Eating antibodies won't do anything, for the same reason eating insulin doesn't do anything.

As @swbarnes says:

Every time you expose a population of bacteria to an antibiotic, you
  select for organisms with resistance-granting genes.

But you're asking about the situation where you're not 'sick' when you're taking them, and how it affects future infections.
To understand why that's a bad thing, you need to understand a couple more things. Firstly, your body contains a massive number of harmless bacteria. Some of those are the same species as harmful bacteria - for example, your gut contains harmless Escherichia coli, even though some strains are highly pathogenic. Secondly, bacteria exchange genetic information.
When you take antibiotics, the harmless bacteria in your gut are put under enormous selection pressure for resistance. This will increase the frequency of any resistance alleles present in the population. If you then catch food poisoning, the 'bad' E. coli will exchange genetic material with the harmless ones, and some of that may include the genes conferring increased resistance.
So if you take antibiotics for no reason (or give them to animals as a growth promoter, for example) you're putting bacterial populations under selective pressure to develop resistance, which can spread to other strains or even other species, and means more bacteria that are antibiotic resistant.

Every time you expose a population of bacteria to an antibiotic, you select for organisms with resistance-granting genes.
Bacteria can pass plasmids full of genes back and forth.  So if you get a nasty E.coli infection, do you really want one of your usual bacteria with a resistance-granting gene sitting right next to it?
Let's say you are so sick you go to the hospital.  Do you think the hospital wants your antibiotic-resistant E-coli around?


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Is this an Eastern Banjo Frog?
[

I found this little guy in my orchid on the upstairs balcony. I live at Sanctuary Point which is on the south coast NSW

You should probably add more precise size indications, as well as the country and the meaning of "NSW" (my first guess would have been "North-South-West", but it doesn't really make sense...).

Funny, after some guessing work, it seems that you are in New South Wales, a region of Australia. I first assumed that people forgetting to indicate their country were from the United States...

Ok....a few more details. I live in Australia, in the state of New South Wales on the east coast. The climate is warm temperate, the area is semi rural and my house is built on a 100 year flood plain. The frog was about 60 mm long and 45 mm wide with darker brown markings down it's back. Hope this info helps!

I've just added a photo which shows the frog's back.


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How can I differentiate between polysaccharide bands and protein bands on SDS-PAGE?
I tried to extract bacterial polysaccharide but after running a SDS-PAGE I couldn't differentiate between the polysaccharide band and protein ones. I face a problem of moving up of the samples from the will and no clear bands. Any suggestions?


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Research papers that demonstrate work done on other species with honey bee pheromones
I found research where Queen mandibular pheromones (QMP) emitted by queen bees were used to find their affects on Drosophila melanogaster. However, I am curious to see if the QMP from bees have been used in other social insects like wasps or termites. Can you please guide me to any research papers on the same?
Since the eusocial queen pheromones among different species are more or less composed of the same hydrocarbons, treating wasp workers with honey bee QMP should have the same effect on worker wasps as it would have had on honey bee workers.


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What's the evolutionary reason behind feeling 'sorrow'?
As it's established that life's design is a product of evolution, what advantage does emotions like sadness play in the life of an individual/species ?

Do you really think you there is a concrete evolutionary advantage to every human emotion? And if you do, do you think that anyone knows for certain what it is. All you will get is subjective speculation. This is a question and answer site, not a discussion site. I have voted this off topic.

@david yes every emotion had better have an evolutionary advantage otherwise it is is really difficult to explain why humans have it.

@John — So there is no such thing as a neutral mutation being propagated? Yes the things that make us human attract us to others and we mate with them. Is that anything more than common sense. Except in Sparta or in Gengis Khan's army...

Won't answer your question, but if your name is an indication of another problem I may be able to help you there.

Basic emotions like sadness are wide spread basic behavior in multiple species, with strong  effects on behavior, they are not neutral effects, drift will not explain them.

I‘ll answer from a perspective I‘ve been studying in Psychology, but can‘t provide sources. If this is not within the scope of this SE, I‘d kindly ask to either add appropriate sources to my answer or close it.
Sorrow is an emotion that has specific cues and expressions like tears, distinct micro-facial cues (which are stable over practically all cultures according to studies of Paul Ekman et al.), a general tendency to withdraw from social settings.
This can be understood as communicating to other members of your group the need for consolation and social closeness, which would count as an evolutional gain.
Update:
I found an extensive article on the subject: http://www-personal.umich.edu/~nesse/Articles/Nesse-EvolutionBereavement-2005.pdf

First sadness and sorrow are not necessarily the same thing. Many consider them quite distinct and thus have different functions.
In the case of sadness it is currently believed that sadness functions to drive you to change disadvantageous behavior. Example 1. Bob insults Betty, Betty will not talk to Bob, Bob feels sad and depressed about this and learns to stop alienating potential mates and allies. Example 2. Lela the wolf takes too long to in sneaking up on what would be easy prey and the prey wanders off Lela feels sadness, a negative stimulation, at the loss and the behavior leading up to it and quickly learns to sneak faster. Source
Sorrow on the other hand is a bit more difficult because it is not clear what you mean by sorrow. Separation sorrow may function to maintain connection in anticipation of the return of a partner or ally. Source Michi's anwer explores some other possible advantages in more intelligent social species. This a a far more tentative explanation than sadness which is not surprising as we see signs that sorrow exists in far fewer organisms and thus is far more difficult to define or study.

This is just a thought......... overtime the animal brain has developed and became more sophisticated. Included in this process has been the development of emotions, such as love, need to perpetuate the genetic line, ability to feel a sense of loss and hence, sorrow and the need to belong. This emotional growth has contributed in no small way to the ongoing perpetuation of the species.  The ability to experience a variety of emotions enables us to feel both wonderful highs but also mind numbing lows. If we were incapable of feeling emotions and never knew was it was like to be happy or sad our subconscious yearning to perpetuate the species might not be so strong. In other words, I think there is a direct link between our capacity to feel and the innate need to perpetuate the species. If animals, including humans, didn't experience a range of emotions why bother to perpetuate the species?

We represent a science stack and thoughts or opinions are not really what we're after - we ask answers to be properly founded and backed up by references.