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Pen and paper game to explain the theory of evolution
Sometimes when explaining the theory of evolution one sees a glazed-over look on the persons face. To this person the theory seems completely incomprehensible no matter which avenue one takes to explain it. This leads me to think that a game might be a fun alternative. In the process of playing, I suspect that the player might pick up a stronger intuition of how and why it works which would eventually lead to understanding the basics as a whole.
It is easy enough to dream up any number of problems that can be presented as a genetic algorithm with pen and paper, the challenge however is to make it easy to understand and fun to play.
Does anyone know of such a game or able to construct such a game?

I'm voting to close this question as off-topic because it is asking whether people know of, or know how to create, a game and not about biology.

I think this question can be carried forward in the chat?

The theory of evolution is a big umbrella term for a whole lot of concepts and evidences. What exactly are you trying to explain (genetic drift, natural selection, sexual selection, common descent and the logic of phylogenies, coevolution, ...)?

If you are having a hard time to explain it, maybe you don't understand much of it (no offense, I have no idea about your level of knowledge). You might want to follow an intro course such as understanding evolution for example Sometimes, the resistance of some people to understand anything is a failure to understand the basics of philosophy of knowledge as well (such as the fight between a whole bunch of evidence and a naive intuition shaped by a cultural environment).

@Remi.b, by explaining evolution, we should probably start with the basics. So, optimisation using mutation, selection and reproduction. As for the possibility that I do not understand evolution. I am pretty sure that I do, I use it often in Computer Science in the form of genetic algorithms to a good degree of success. Furthermore, I do quite a bit of reading on the topic as well, so it seems unlikely to me that I don't understand it.

@terdon, If you insist that we close it as off topic then it is fine. I would however like to know under which topic you would group it if not biology?

Game design, I guess. You're not actually asking any biological question here. You're asking if i) anyone knows of such a game (which is off topic anywhere on the SE network since we don't do such open-ended questions) and ii) can anyone make such a game or, presumably, how to do so. The latter might be on topic on [gamedev.se], but I don't know their scope well. I'd check before posting there.

@terdon, I was thinking more along the lines of education in biology, since the main idea is to educate and it is about evolution. But I suppose game design might fit as well.

http://www.abandonia.com/en/games/4996/simlife.html

Related question in Meta Bio-SE: Questions about teaching biology: off limits?. Personal, I think your question could be on-topic, but it is currently a bit broad and vague.

Not sure if this qualifies as pen-and-paper, but one game I am familiar with to highlight natural selection goes something like this:
Materials:
Creatures - Small paper pieces of different colors from construction paper - hole-punch remnants work great, or you could cut squares
"Habitats" - Large, colorful surfaces. Whimsical maps work well for this, maybe certain posters, the important thing is to have some diversity.
Gameplay:
This is ideally done in multiple groups, each group should start with an equal ratio of creatures of at least two different colors.
One or more people spread the Creatures around the Habitat.
Another student (or multiple) act as the "predators". They sit/stand above the board and close their eyes; then they open their eyes, and harvest the first Creature they see. Close eyes again, and repeat until 1/2 of the Creatures have been eaten.
Count up the paper pieces and note the number of each remaining; for the next Generation, the Creature makeup should be 2X the number of remaining pieces: so if there are 30 Blue and 20 Red remaining, the new generation is 60 Blue and 40 Red.
Repeat over a few generations - the result should be that different habitats lead to different proportions. You can also change things up by suddenly shifting the habitat!
You could possibly include genotypes and recessive traits for an older group (the version I suggested is effectively haploid parthenogenesis), these might be harder to keep track of.
(I don't have a citation for this game but if anyone knows it, please provide in the comments!)

You could adapt this into a battleships-like game, where the predators choose squares at random, based on dice rolls, and the prey (of different sizes) occupy spaces on grids. If each prey is "killed" when any part of it is selected by a dice roll then, over time, you'd expect the smaller prey to outlive the larger ones (demonstrating natural selection due to a selection pressure). You could also show that predators that are allowed more dice rolls stack up more "kills" and maybe incorporate some kind of resource that's gained from a successful kill.

@Jam Yes I am sure there could be many variations. One that is nice about the variant I suggested (and that pairs well with your suggestion on the other question about moth coloration) is that it is very straightforward to change the environment and see the results. If you start with a map/"habitat" that has a lot of red on it, the red creatures are likely to survive preferentially, and then you move to a map with mostly green and suddenly red isn't such a good color any more. It's also fun in groups because different groups will get different answers depending on their "habitat."


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Terrarium Compatibility: Millipedes with Carnivorous Plants?
I have a child that loves his large millipedes (Desert Millipedes) and Venus Fly Traps.  He's also been wanting to get some Sundew Savages.  Given this little collection and his real enjoyment of terrariums, we're curious if we could consolidate his millipedes into a terrarium with these carnivorous plants without causing harm to either of them.
We keep the millipedes fed well with decomposing plant material, but weren't sure if they'd go wild after the fresh plants... and then of course if they would try to do that, could these plants harm the millipedes?
In the end I fear there will be some problems here and wanted to check to see if anyone knows about this compatibility before we dive in and have our hopes dashed.

Millipedes eat decomposing material, not fresh. Carnivorous plants eat very small things like flies, not millipedes. They digest their food using enzymes, just like you and I do - they're not poisonous. You're fine.

source: Stack Exchange

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How to distinguish between a genetic bottleneck and directional selection?
Genetic bottlenecks and directional selection should have relatively similar genetic signals: reduced heterozygosity and greater genetic divergence (Fst?) in contemporary populations compared to the past
How would one be able to distinguish between these two evolutionary forces if their signals are so similar?

Distinguishing between selection and specific demographic events can be quite complex and there exist a large set of tools to investigate such things. You might want to have a look at How to determine whether changes of an allele's frequency are due to genetic drift or selection?

I'm asking how one would be able to distinguish whether a population had undergone a bottleneck OR if directional selection had occurred given the high frequency/fixation of a specific allele(s) and reduction in expected heterozygotes in a population

I read "local selection" instead of "directional selection" for my first comment. Sorry! I removed my comment and my close vote and answered the question!

Population bottleneck will have genome-wide effect while directional selection will affect only the locus (and closely linked loci via a selective sweep).
You can typically screen through the genome and calculate Tajima's D. Under a bottleneck scenario, Tajima's D will be expected to be negative everywhere. Under a directional selection scenario, Tajima's D would be negative only at the locus (and closely linked loci) to the one that is under selection.
There are of course a whole lot series of technics but the above is probably the simplest and most straight-forward (it probably lacks in power though).

Makes sense: a population bottle neck will affect all loci the same way, while directional selection will only affect the loci under positive selection (and other linked loci due to selective sweep)

Some species are regarded as having a very wide genetic base and some less so, which commensurately signals that a bottleneck has taken place, and that diversity takes a while to be amended. You can make some measurements on when the species population may have been small in the past, although some of those kinds of study have been found to be very misleading, because populations can interbreed cross species, like neanderthal, which brings up a much more complicated picture to the genetic bottleneck model, and makes some research results seem over stated. In otherwords, recent studies in that field by trained scientists have found errors.
here are some measures of recent or distant small populations: http://www.tiem.utk.edu/~gross/bioed/bealsmodules/bottlenecks.html
Directional selection generally is related to a considerable force on the population which changes is population dynamics and can therefore amount to a bottleneck, or which selects only one type of adaptations from a population in a region, which is then transferred to the rest of the population by a less sudden kind of evolution, which amounts to a semi bottleneck with a wider base. different branches can converge from 40,000 generations distance in speciation, or in 50, which means that it's difficult to gauge a bottleneck without very complete studies.
Take for example moths at the beginning of industrialization when coal was used in large amounts. They noted that the same species of moth could change from light to dark to blend in with the background, and that the white moths dissapeared.
That illustrates a kind of bottleneck as a result of directional pressure, although the species may have been far from failing, it just underwent a bottleneck to some degree.
Bottleneck genetics is very complicated and difficult to understand, because they have quite a strong effect on the genetic base of the animal and it variability. and because low genetic variation implies a range of mutations which can be fitness or protein malfunctions or dynamic changes depending on the kind of bottleneck.

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Can certain jellyfish photosynthesize in the medusa stage?
Can jellyfish (at least some of them) do photosynthesis in the symbiosis with zooxanthellae in their medusa form as well? I've heard that only Cassiopea andromeda can but I wasn't able to find a credible source upholding such claim. (Wikipedia would be enough)

''Can jellyfish photosynthesize when mature?''
or
''Can jellyfish (at least some of them) in their medusa do photosynthesis? ''
Which one is your primary question?

I'd like to know about the photosynthesis in the medusa form

Then please change the title accordingly. However I think it would get closed as an under researched homework question . I did a simple google search and found numerous websites and a few books claiming that they cannot but their symbiont zooxanthallae can.Take a look at this wikipedia article.I learned something new, so thank you.

@SanjuktaGhosh Of course, I did mean their symbiant

@SanjuktaGhosh The title has no problems. It's common and acceptable to have a broader title with more specific details in the body of the question. Don't be so picky

According to Wikipedia; Zooxanthellae are not bacteria but are dinoflagellates, a sort of protist. That means they are Eukaryotic.


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Do human populations differ in core body temperature?
Human body temperature is a very complex and tightly regulated system. Hypothermia or fever of only 1-2K (i.e. changes of about 5%) already cause major symptoms and changes of 3-4K (i.e. about 10%) are life threatening. Many humans live under relatively cold outside temperature conditions and maintaining an inside 36-37 degree C in these conditions is very energy consuming (most probably a reason why the body temperature in the periphery is several degrees lower), indicating very strong evolutionary constraints on not changing the core temperature too much (I remember a professor in biology classes in university saying that most fungi have a growth minimum around 37 degree C). However, other mammals have higher or lower body temperatures than humans which suggests that the 36-37 degree C of humans are not a universal gold standard (in mammals).
Probably, for a long time in hominin evolution maintaining the core body temperature was not extremely energy consuming due to tropical conditions. This could have changed during the out-of-Africa migration some 100-60 thousand years ago. Of course this is somewhat difficult assess because early modern humans started to wear protective clothing. In fact, wearing clothes is a most probably adaptive trait to save energy while maintaining core body temperature. Still, it is unclear to me whether physiological adaptations took place as well. Furthermore, there is considerable variation between individuals and also within individuals, the latter in response to environmental conditions and/or behaviour (e.g. exercise), which in principle allows natural selection to change the trait and also shows that slight shifts in body temperature are not harmful individuals.
My question is: Are there significant differences in core body temperature between human populations? Please note that my questions is not why the (average?) human core body temperature has this particular value or why it is different from other mammals or birds.
There is a somewhat related question (also on Skeptics.SE) about lower core body temperature in Japanese people. As far as I know, this difference is rather a measurement thing than a real biological difference, so my question remains unanswered.

Related: http://health.stackexchange.com/questions/9981/fever-lower-limit-99-0-f-37-2-c-at-armpit-is-it-universal

Yes there are different physiological temperatures in different ethnicities. To know which temperature range differences are inherited and which are learnt by living in different climates requires surveys of people who are from the same region.
This study states a 0.35 degrees difference between a japanese and a malaysian, 36.95 and 37.3, it's alot.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3929238/
The following study states states a 0.15 degree difference measured with similar precision,
https://www.ncbi.nlm.nih.gov/pubmed/20824480
This graph shows that the human body temperature is 36.2 at rest, at night/morning and 37.5 in the middle of the day. :
http://millar.bio.ed.ac.uk/andrewM/WE%20book99/Part2-examples.html#tth_sEc8.3.4.2
That may account for the 1 degrees difference in Japanese studies, they measure first thing in the morning/ at rest/at night, and japanese body temperature of 0.15-0.35 lower that some other ethnic groups.
There are geographic differences if you test the homeostasis response of different populations, the inner body temperature responses, the temperature of the extremities, sweating responses, the physiological responses and the blood cell characteristics.
Mitochondria has also been shown to be selected by climate type. Populations living in colder environments have lower mitochondrial diversity and that the genetic differentiation between pairs of populations correlates with difference in temperature, and they have found certain genes mutations in the ND3 and ATP6 that seem to be independantly implicated in similar climate adaptations.
The temperature is measured in lots of zones of the body and of the extremeties and the capillary flow. That doesn't account for habituation and acclimatization to tropical or northern climates.
The tropical population was found to have different thirst and sweating efficiency, and to change temperature at different rates to compensate for the same ambient conditions and exercise.
Some schools in China enforce that children run around in shorts in the snow in the winter and at playtime so that they regualte their body in the cold. Some northern people are apparently able to override the unconcsious response of the physiology that can raise body tempereture very effectively, and be able to hold in cold tanks for surprisingly long times.
Cold and hot weather are a strong force on natural selection, as illustrated by mitochondrial adaptations, because an advantageous in temperature regulation brings about a global performance advantage. The physiology of temperature regulation has been subject to many theories and studies, and they have found physiological conditionings can be honed by genetic adaptations in different populations.
Even chimpanzees have similar temperatures:
The cycles of increasing and decreasing body temperature of chimps
are exponential and symmetrical, with an amplitude of 2.6-2.9?F
(2-3 AM - 2-3 PM) and a 24-hour mean of 99.0?F, or 98.7?F. The S.D. of the 17 daily means was 0.53?F; and
of the values at any single hour, 0.63'F....Thus, in the bulk of the species the temperature ranges daily from
37.5- to 39+?C whereas the ordinary range in man is 36.5 to 37.5?C. Low
values are similarly reported for several primitive primates.
some references: http://rspb.royalsocietypublishing.org/content/276/1672/3447 https://www.jstor.org/stable/1377087
Actually this study states a 0.35 degrees difference between a japanese and a malaysian, 36.95 and 37.3, and study referenced afterwards states states a 0.15 degree difference,
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3929238/
https://www.ncbi.nlm.nih.gov/pubmed/20824480

That is very interesting! Can you provide references for your claims, though?

Hi, it's an interesting quesiton and it gives me a subject upon which to educate myself. I read through 4 papers and 10-20 graphs to get the figures, and saw also a dozen other related research papers. for example http://rspb.royalsocietypublishing.org/content/276/1672/3447  https://www.jstor.org/stable/1377087  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3929238/  especially the ncbi page study which answers your quesiton with a high degree of certainty. ill add them to the text. thanks.

Hi, I hadn't seen the above study, which measures a difference of 0.35 between malay and japanese, it's considerable, i had seen the following study from the same researchers states a 0.15 degree difference is similar conditions: https://www.ncbi.nlm.nih.gov/pubmed/20824480


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Is the information in the brain stored in the connections rather than neurons?
Can I imagine the difference between the model of the grandma neuron and the model of interconnected neuron network so that the information isn't primarily stored in the neurons (respectively in their states) but in the connections between them.

Also in discussions of neural networks we don't use the term "parent" or "child" when describing a network. So your term "grandma neuron" is not something that is commonly used. Instead use terms like "sender" and "receiver".

Would the connections be the same as the axons? Since an axon is either charged or discharged, the information (1 for charged, 0 for discharged)  could be said to be stored in the axion which is a part of a neuron.

@GabrielFair The question asker is probably referring to the "grandmother neuron" in the context of the famous papers by Quiroga et al or more generally, rather than in terms of hierarchy. "Sender" and "receiver" are also not terms typically used in neuroscience, instead words like "afferent" and "efferent" or "presynaptic" and "postsynaptic."

As I understand memory... The connections help you recall them. Short term memory is consolidated into long term memory in the hippocampus. However, if you want to aid in recalling memory, you can store the memory by using different parts of your brain, to attach to the memory. Example visual, sound, emotion... This is basically why the "mind palace" works. You bind connections to a memory and the connections aid you in retrieving it. this is pure thought, don't take it as fact

This article says that memories are not stored in synapses: https://www.scientificamerican.com/article/memories-may-not-live-in-neurons-synapses/

Is the information in the Brain stored in the connections rather than
  in the neurons ?

It depends on what information you are referring to.
The brain does not just store one type of information,the model of a grandmother cell and the model of an interconnected neuron network are 2 subsystems of a greater system working together perhaps in a competitive or complementary arrangement. The purpose of this system is to extract information from the environment and identify it again for the organisms benefit. 1.
So let's say we see something that will benefit us in the future or that we might want to avoid. This is a simplification, but as you see that something, neurons in your neocortex light up specifically in region V1 in the back of your head, they arrive there after a lot of computations along the way from your retina, but also project to other parts of your brain where they are perhaps processed consciously,they fire in an orderly fashion, in a map, this bouncing around of electrical signals represents your conscious, and unconscious processing of the image, so the information exists as a network of electrical signals. 2.
During recollection, ( there are different types of memories so the structure in charge could be the neocortex,basal ganglia, hippocampus or even a muscle)3. this same map ( or a smaller subset ) gets replayed. The mechanism(s) by which this information is first encoded and later retrieved is still not entirely understood, but it involves a map and a getaway or switchboard.4. This switchboard ties together different percepts ( a smaller network of electrical signals), so in a way the information is represented at the switchboard level, if you disable this switchboard, you can't make new memories or lose previous ones.
A grandmother cell in the scheme of what I just explained, is the result of another subsystem that helps recognize something. Once you successfully encode a percept ( thing we want to remember seeing) you might want to associate it with something ( good,bad,delicious,etc), at the top of a series of associations lies a grandmother cell, which in turn is a handy evolutionary way of signaling back to other systems when some previous information has been experienced. So in this way the information of whether a subset of relationships in between networks of electrical signals has been experienced and encoded lies here.
References/Sources:

The idea of grandmother cells and object recognition in general is summarized in the Object Recognition chapter of ( Cognitive Neuroscience,Gazzinga-3rd ed 222-225) along with the problems a grandmother cell introduces in object recognition (ie if you lose the grandmother cell you would lose all the information about your grandmother)
Koch( Quest for Consciousness-2004) chapters on vision provide a very readable account of how the information goes from retina to v1. Vision Science (Palmer) is a more thorough account.
The chapter on learning and memory (Cognitive Neuroscience) gives an overview.
(Gluck -2001-Gateway to memory) presents different models of this arrangement.

The physiology of memory is still poorly understood, but there are some generalizations we can work with:
There are four "types" of memory which the human brain works with.
Sensory memory is very short-term (milliseconds), cannot be consciously accessed (it's used by the sensory processing centers of the brain for things like tracking moving objects), and is stored in the activation state of neurons (ie. which neurons are firing at any given time).
Working memory is short-term (it lasts up to 30 minutes), and stores "what you're thinking about now". It is not yet fully understood exactly how it works. However, we know that drugs which interrupt neuron state can "delete" working memory to some degree; this suggests that working memory is stored at least partially in the activation state of neurons.
Long-term memory is persistent and lasts, in theory, until the end of a person's life. It has been well established that long-term memory is stored in the connections between neurons.
Intermediate memory is a relatively new theory of memory which operates somewhere between working memory and long-term memory. As far as I'm aware, we don't yet understand many of the mechanisms behind it.

I don't see where you have tried to answer the question

Grandmother Cells vs Distributed Representations
The idea of a "grandmother cell" is effectively the ultimate in sparse representations: that there is one, single neuron in your brain that represents your grandmother, and that everything you know about your grandmother is associated with that cell through connections.
At the other end of the spectrum is a "distributed representation," where a network of simultaneously active cells represents a concept, and that these cells are connected to each other and to related concepts (see here, here, and here). These networks could be highly overlapping, and could potentially overlap more when you are talking about related concepts: i.e., "dog" and "cat" might overlap more than "fish" and "squirrel" because the former are both 4-legged animals that live on land and are kept as pets - lots of similarity.
Realistically, no one in modern neuroscience is truly arguing for the existence of "grandmother cells" but there are certainly arguments about sparse vs. distributed representations, and now large or small the cell assemblies or networks are that reflect particular concepts, and what the importance of context is. The main arguments you will see today concern the extent of distribution across brain areas: that is, are there brain areas that contain somewhat-distributed representations of abstract concepts, or are those concepts distributed across modalities (where your concept of 'baseball' includes a synthesized visual representation in visual cortex, the texture of the seams in somatosensory cortex, the sound of ball-on-bat in auditory cortex, the motor plan for throwing the ball in motor cortex, etc).
Evidence for Grandmother cells?
Despite what I just said, there were some interesting papers from human subjects published several years ago, especially this one. These papers showed neurons in a particular area of the brain that had invariant responses to particular concepts, perhaps most famously "Jennifer Aniston" cells and "Halle Berry" cells that responded not only to various pictures of each actress but also to other more abstract representations such as their written name. Clearly, these are not the cells typically described in the primary visual cortex that respond to stimuli like bars and edges.
These papers were reported in the lay science and general press as evidence or proof of the "grandmother cell" theory. Some were more responsible and included some of the authors own words (see also here): essentially, what the authors are arguing is that cell assemblies might be pretty small (but not too small - the authors only recorded from a few cells yet found dozens that responded to Jennifer Aniston, not just one, for example).
Information in cells or connections
To get back to your original question: you asked about whether the difference between a grandmother cell and a neuronal network is whether the information is stored in the cells vs. the connections. I would argue that, although in the "grandmother cell" model there is a lot of importance placed on individual cells, in both cases the information is stored in the connections.
Even if you assume the extreme case of the "grandmother cell", where one cell is the hub that alone represents your grandmother, the information isn't stored as "grandma", it's stored as the associations you have with her: maybe smells of cookies, the shape of her face, her name signed on a birthday card. If you pulled someone's grandmother cell out of their brain network and interrogated it, you wouldn't be able to learn anything at all about their grandmother.
The difference between the "grandmother cell" and a more distributed network is that in the "grandmother cell" case, we would expect to find another cell that represented specifically the cookie smell, yet another that represented the shape of her face (and only her face), and so on. In a more distributed network, each of those related concepts would be encoded by their own network, and those networks might overlap somewhat where the concepts are closely related: that is, part of your representation of "grandmother" is the smell of her cookies.

I would love an explanation for the downvote - I am happy to update my answer if it would help in any way.

I think you went for the tree while ignoring the forest :) , I upvoted though.

@Keno Ironic, because that's sort of what a "grandmother cell" theory does ;)

From what I can gather, the short answer is that we don't have the full picture of how biological neural networks store information.
If you are willing to relax the constraints of your question to extent to artificial neural networks, then your answer becomes significantly easier to answer in part because we understand them much better. Artificial neural networks do store information as synaptic weights which is the only part that changes during the training of a network. The rest of the network such as the topology and the activation function remains unchanged.
Image classifiers are a convenient example of information as synaptic weights since we can see what the neural network 'sees' by maximal activation of neurons. It is immediately obvious that there is a lot of information stored in the weights of a network. The image below is taken from Understanding Neural Networks Through Deep Visualization

Some feedback as to why this is being down-voted would be nice.


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Calculation of NADPH molecules number needed to reduce a substrate in enzymatic reaction
I am inquiring if it is just simply possible - as it seems to be - to calculate the number of NADPH molecules needed by an enzyme (let say for example Dihydrofolate Reductase DHFR) to reduce the substrate (FH2 or BH2 for DHFR) to (FH4 or BH4) directly from the apparent enzyme reaction?
In DHFR case, can I simply figure it out that I need two NADPH molecules to reduce (FH2) to (FH4)?
Here is the reaction of reducing FH2 to FH4:
https://upload.wikimedia.org/wikipedia/commons/2/29/DHFRmechanism.png
Or is there anything else to keep in mind?
In the figure in the link, the NADPH transferd Hydride, but where did the positive hydrogen come from?

But then where does the other hydrogen come from? one of them comes from NADP(H), which is in hydride form, but what about the second one? it comes in proton form (H+), but from where?


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Do DNA viruses have their own DNA dependant DNA polymerase?
There's an exception to the rule that all DNA viruses need to get to the nucleus in order to replicate. Poxviruses do not require to get into the nucleus because they can make protein from their very own DNA-dependant-RNA-polymerase.
That is fine. But then, how do they make new DNA (for daughter virions)? Do they also have their own DNA-dependant-DNA-polymerase?
So here are my questions -

Does the pox virus also have its own DNA-dependant-DNA-polymerase? If yes, is it unique in having so?
How about other DNA viruses? The rule that they need to get into the host nucleus - is it for making protein using the host DNA-dependant-RNA-polymerase or for replication using the host DNA-dependant-DNA-polymerase? Or for both?
Do all other DNA viruses need to get integrated into the genome to be able to replicate, and do so along with the cell? Are there instances where the host DNA-dependant-DNA-polymerase is expressed at times other than the cell's S-phase?
Are there viruses that replicate inside the cell's nucleus without being integrated into the genome?

I know that's a lot of questions! Hope someone does help.
Note: Discussion limited to those viruses infecting eukaryotic cells. Also excluding Hep B (hepadna virus).

My guesses 1. yes. meaybe not unique. 2. for both transcripton and DNA synthesis. 4. Adenoviruses

Please avoid asking multiple questions in a single post.

Probably I won't be able to answer all of your questions satisfactorily, but let's begin one by one.

Does the pox virus also have its own DNA-dependant-DNA-polymerase?

Yes. See this article from Wikipedia:

The replication of poxvirus is unusual for a virus with double-stranded DNA genome (dsDNA) because it occurs in the cytoplasm, although this is typical of other large DNA viruses. Poxvirus encodes its own machinery for genome transcription, a DNA dependent RNA polymerase, which makes replication in the cytoplasm possible. Most dsDNA viruses require the host cell's DNA-dependent RNA polymerase to perform transcription. These host DNA are found in the nucleus, and therefore most dsDNA viruses carry out a part of their infection cycle within the host cell's nucleus.

If yes, is it unique in having so?

Actually no. Hepatitis B virus also has its own DNA polymerase. And there's also the classic example of retroviruses: they have an RNA-dependent-DNA-polymerase (but yes, you can't consider it since it isn't a DNA-dependent-DNA-polymerase). See this wikipedia article:

Some viruses also encode special DNA polymerases, such as Hepatitis B virus DNA polymerase. These may selectively replicate viral DNA through a variety of mechanisms. Retroviruses encode an unusual DNA polymerase called reverse transcriptase, which is an RNA-dependent DNA polymerase (RdDp). It polymerizes DNA from a template of RNA.

Another example, as mentioned by @David in comments, is the Herpes simmplex virus (HSV) which contains a bunch of its own enzymes for DNA replication on its own. See this article:

Herpes simplex virus (HSV) encodes seven proteins necessary for viral DNA synthesis—UL9 (origin-binding protein), ICP8 (single-strand DNA [ssDNA]-binding protein), UL30/UL42 (polymerase), and UL5/UL8/UL52 (helicase/primase).

The rule that they need to get into the host nucleus - is it for making protein using the host DNA-dependant-RNA-polymerase or for replication using the host DNA-dependant-DNA-polymerase? Or for both?

Umm, both. Viruses (generally; there might be exceptions) need to reach to the nucleus of host to replicate as well as transcribe their DNA. See this article (emphasis mine):

Most DNA viruses replicate in the cell nucleus, which is where cellular replication and transcription proteins are localized. After infection, the nucleocapsid of DNA viruses is therefore usually delivered to the nucleus where uncoating occurs. An exception is poxviruses, which replicate in the cytoplasm of infected cells.
The first stage in the viral replication cycle is expression of the viral early genes. Transcription of these genes occurs using cellular RNA polymerase II and cellular transcription factors. These proteins bind to the viral DNA in regions called early promoters/enhancers, and promote synthesis of the early pre-mRNAs.
Once the viral early genes have been expressed, and the cells have been induced to enter S phase, viral DNA is replicated. This occurs in the nucleus of infected cells, and gives rise to new viral genomes. Many hundreds or thousands of new viral genomes can be produced in the nucleus of a lytically infected cell.

Are there instances where the host DNA-dependant-DNA-polymerase is expressed at times other than the cell's S-phase?

I think it has already been answered in your 2nd question. No, and the exception is the poxvirus itself. Again see the same article (emphasis mine):

Most DNA viruses replicate in the cell nucleus, which is where cellular replication and transcription proteins are localized. An exception is poxviruses, which replicate in the cytoplasm of infected cells.

Are there viruses that replicate inside the cell's nucleus without being integrated into the genome?

Wait! There's a difference between being inside the host cell's nucleus and being integrated into the host genome. Integration of the viral genome into the host genome requires a special enzyme called integrase and, you know, DNA viruses don't have integrase because they don't need it. So your question can be changed a bit to Are there viruses which replicate inside the cell's nucleus by getting integrated into the genome? Now, I could find only one such example i.e. Ectocarpus siliculosus Virus (EsV).

Ectocarpus siliculosus virus-1 (EsV-1) is a lysogenic dsDNA virus belonging to the super family of nucleocytoplasmic large DNA viruses (NCLDV) that infect Ectocarpus siliculosus, a marine filamentous brown alga...the EsV-1 and FirrV-1 genomes encode a large putative integrase/recombinase for which no counterpart exists in current protein databases. Only the Tyr-recombinase domain at the carboxy terminus of this enzyme is similar to phage integrases. Therefore, this enzyme might be involved in the integration and/or recombination of the integrated viral fragments.

References:

Pox virus

Hepatitis B virus DNA polymerase

Herpes simplex virus

Herpes Simplex Viruses: Mechanisms of DNA Replication

Wikigenes: UL9, ICP8, UL30, UL42, UL5, UL8, UL52

Reverse transcriptase

Viral Life Cycles in Cells

Integrase

Ectocarpus siliculosus Virus-I

You may wish to add Herpes viruses to your answer. There is a good open-access review considering all the viral-coded proteins involved in DNA replication at http://cshperspectives.cshlp.org/content/4/9/a013011.full. There is also an extensive review of polymerases and viral replication at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4711277/

@david surely I can add many more examples (obviously we don't even know all yet) but thr pirpose was just to tell OP why the answer is yes or no, so just 1 or 2 examples should be appropriate. Anyways, I'll add them too, thanks :)

Hepatitis B virus is a bad example, it is very close to retroviruses in its replication strategy (except that reverse transcription occurs before the virion egresses), its so-called DNA polymerase is essentially a reverse transcriptase.


text:
Does genetic morbid obesity exist?
With the acceptance of being a little overweight
I hear of people saying they were born morbidly obese and it was genetically passed on. I'm aware being so obese leads to countless health issues, yet we have people defending fat shaming and the likes. Is the excuse of having 'obese' genetics scientifically justified? Do people have genetics that make them ridiculously fat? Alongside, would this simply be down to the diet of the person from a young age?
Thanks.

To understand ny answer, you will probably have to make sure you understand the concept of heritability first by reading Why is a heritability coefficient not an index of how “genetic” something is? for example

It's a myth that obesity is mostly caused by genes. Yes, there are many genes that predetermine your apetite but when a baby is born obese, it's not a matter of genes but a matter of the mother's health and diet. And because till the birth, the fetus shares a single bloodflow with the mother, it gets everything the mother has in her blood. Thus, some babies are born obese, some are born addict.
Indeed, there are papers showing that there's a higher chance for the newborn to die during birth, even though you can't always say what was the main cause of death (also it depends on what you connect with obesity).

It'd be great if you could link to a peer-reviewed paper instead of livescience.com small article

Down voted this answer due to poor sources. Also the point regarding newborn obesity is certainly true, but the strong dismissal of the influence of genetics on obesity is not scientifically correct! I have provided a more balanced and better documented answer, that also focuses on the effect of lifestyle on obesity.

It is certainly a very difficult question to answer.
There are some genetic disorders that can predispose individuals for becoming obese: https://www.ncbi.nlm.nih.gov/pubmed/18230893
There are also evidence of epigenetic influences on obesity: http://www.nature.com/nrendo/journal/v12/n3/full/nrendo.2016.18.html
Typically each case of obesity is caused a combination of both genetics, epigenetics and lifestyle: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3873060/
However also keep in mind that obesity is a fairly recent problem and as such the genetic changes are likely minimal between the 1980 and 2008 populations sampled by WHO: http://www.who.int/gho/ncd/risk_factors/obesity_text/en/
A doubling in the prevalence of obesity in the two populations are most likely caused by changes in lifestyle and the availability of food, rather than genetic changes as the time frame is so short.
So to sum up: Morbid obesity caused by currently unfavorable genetics exists but is very rare. People can be genetically and epigenetically predisposed for developing obesity, which when combined with certain lifestyles can further increase the risk of becoming obese.

Genetics is not a yes or no question, every gene is affected by its environment and often the environment is influenced by other genes as well.
Are their genes that can make you more likely to be obese, Yes. There are also genes in our gut flora that influence it as well. How these genes are expressed may or may not be influenced by environmental factors. It likely varies by the gene. And of course no gene will make you obese in a absence of calories, but they can greatly change the number of calories you need to become obese.
Morbidly obese is a tricky phrase, since the BMI is not actually based on scientific measure of health. Many athletes score very high on the BMI. So you may want a more concrete definition to work from.

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


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All neuromodulators (dopamine, serotonin, acetylcholine, histamine, and norepinephrine) act only on metabotropic receptors?
All neuromodulators like dopamine, serotonin, acetylcholine, histamine, and norepinephrine act only on metabotropic receptors?

What research have you done to answer this on your own? The Biology.SE community has agreed that questions that show little or no prior research effort are off-topic on this site unless you have shown your attempt at an answer. Please [edit] your question and tell us where you've looked, what you do know about the topic, and where exactly you still have questions. Unresearched questions may be subject to down-voting and closure.

I have already search about this and I found that the receptors for neuromodulators are typically metabotropic receptors, what I want to know is if this is always the case, or there are cases where neuromodulators like dopamine act directly on ionotropic receptors. Any help will be appreciated

No, they don't act only on metabotropic receptors - please look into each of them if you can't find the information with broad search terms.

Also, do you consider neuropeptides such as endorphins, enkephalins, etc. (opiod peptides), oxytocin, and Substance P as neuromodulators? What about GABA? Are you just wondering about internally-synthesized molecules, or do you include pharmaceuticals and "natural products" like SSRIs, psilocybin, phencyclidine (PCP), opiates (natural and synthetic), etc.? This question can get too broad very quickly...

Not all neuromodulators act only on metabotropic receptors. However, you are correct to observe that this is a general rule of thumb.
Of the substances you have listed:

Acetylcholine is not primarily a neuromodulator, but rather a "normal" neurotransmitter. As such it acts on both ionotropic and metabotropic receptors.
Serotonin - the one exception among the neuromodulators you have listed - acts on numerous classes of metabotropic receptors, but also on the 5-HT3 receptor, which is ionotropic.
All other neuromodulators you have listed act on metabotropic receptors only.

This tendency of neuromodulation to be metabotropically mediated is possibly a consequence of the nature of the neuronal function itself. Neuromodulatory systems do not per se relay information, but change how other information relays work. As such there is no need for the most rapid, temporal, coding (best achieved via the more rapid ionotropic signal transduction), and a slower coding may even be more efficient.


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The concept of backpropagation in neural networks actually occurs in the brain?
I am aware the Human brain has many functionally distinct components, but let us specifically consider the Human visual cortex: could Artificial Neural Networks (ANNs) be "trained" (through, e.g. backpropagation) in an analogous way to how the visual cortex "learns"?
Is the concept of backpropagation in ANNs a phenomena actually observed in the Human brain?
Related

Books on machine learning applications in Biology

Is this a homework question? Have you done any research about it before asking it here?

No, its not a homework question, I'm just an amateur in neuroscience and I have this doubt. I thought some here could help me with the answer instead of having to read a book to find out.

I recommend Yoshua Bengio's recent works. E.g.: https://arxiv.org/abs/1502.04156 and his slides from the NIPS 2016 Brains and Bits workshop.
Also, Timothy Lillicrap's work: http://www.nature.com/articles/ncomms13276
This is still a big open question. In short, we (the neuroscience community) have little idea on how the brain learns at a circuit/systems level in general. We know a thing or two about how individual synapse changes under specific experimental protocols, but those are phenomenological models (e.g. STDP; there has been many many normative models of learning that concludes their learning rule is STDP-like). (Some systems such as cerebellum, we know relatively more, but the learning seems to be more specific to motor timing.)
The main technique we use in machine learning and artificial neural network are mostly gradient descent (or some sort of stochastic optimization algorithm), and people have been trying to find if the biological neural network learns in a similar way. There are several issues:

There's no error gradient being propagating according to chain rule. Information gets mushed together within a neuron, so there's no plausible way to trace exactly the forward-path during an backpropagation.
There's a lot of recurrent connections but they are not symmetrical.
Temporally, it is implausible that there's a clocked signal to backpropagate after a each forward path. Neuronal network doesn't seem to operate with clocks (some thing there are precise clocks, but I think there's little evidence).

Recent efforts have made some progress with random backprojection, decoupled updates using synthetic gradients, target prop, autoencoder, weight/signal quantization, deep belief networks, etc. But there seems to be several more jumps needed to make it biologically plausible such that it agrees with the neural architecture and information flow. Even then, there's no guarantee that neocortex is learning with a similar principle.

See also: https://cogsci.stackexchange.com/questions/16269/is-back-prop-biologically-plausible

Not in the same sense as in artificial neural networks. Importantly, there is no biological mechanism for errors to be back-propagated further than a single cell/synapse.
You can look into spike timing dependent plasticity which uses a back-propagating signal within a single neuron, but this is not a back-propagation of an error so it does not accomplish the same thing.
I found this answer on another site had some useful references for further reading, as well.

I don't know much about backpropagation, but I'd have thought the only way to know if "learning" in an ANN is analogous to learning in the visual cortex would be long term comparisons to a developing neural cortex. Possibly having a microelectrode array in the VC of a test-subject throughout development (30 odd days for a mouse) and I'm not sure if they've done this kind of long term study. This paper looks like it might be interesting in terms of changes to the VC after motor task learning, but doesn't seem to have looked at backpropagation.
So I guess my answer is maybe ANN's can learn analogously to brain structures, but we don't know enough about how the brain learns yet to be able to know if the learning observed in an ANN is comparable to a brain.


text:
At which point does a cell switch its function?
In a multi cellular organisms there are many cells of different functions. How / when does a cell change its function compared to its parent?
Is it done by influence of other cells after its has been created?

Yes, as opposed to what? Cells respond to signals, both within themselves and from other cells/tissues/organs, to differentiate. Sometimes a parent cells differentiates, then divides, and other times a parent (stem) cell divides and one of its daughter cells differentiates. Since the mechanisms and reasons are as varied as there are types of cells, I'm voting to close this question as too broad.

Ok so the cell changes after mitosis not during mitosis. There is no mechanism during mitosis to change the function of a cell. Its all done by influences after the cell has been created.

That is not necessarily the case, as although it's rather unlikely that differentiation would begin during mitosis, there's no rule that says it can't. Like I said, this is a very broad question, as each differentiation event is slightly different.

As MattDMo suggested there are so much possibilities. I would recommend to take a look at this information:

Cellular differentiation wiki
The Cell: A Molecular Approach. 2nd edition (NCBI)

I will summarize some points, however note that this will not include every aspect.
Every cell contains the same genome (same DNA), so what can make these cells to differ so much form each other (e.g. neurons vs muscle cells). As noted in the Wikipedia article:

Since each cell, regardless of cell type, possesses the same genome,
  determination of cell type must occur at the level of gene expression

I added this figure just to give a representation of the hierarchy.
However probably you already knew this because you were asking about the mechanism of how these cells can become different from their parent cells.
I will provide two important examples (again notice that this is just a simple summary):

first let's talk about Cytoplasmic determinants

Cytoplasmic determinants are special molecules which play a very
  important role during oocyte maturation, in the female's ovary (wiki)

the cytoplasmic determinants are molecules such as mRNA or proteins which are e.g. unequally distributed in the egg cell, which means that if this cell devides one half will get other proteins(e.g. transcription factors(TF)) and mRNA than the other half. Different TFs --> different gene expression --> different proteins --> different cells.
Secondly we have induction which is really important in cell differentiation:

frequently we find that cells become different from one another as a
  result of inductive signals coming either from other cells or from
  their external environment (source)

These two (induction and Cytoplasmic determinants) are important to determine the fates of cells(we also have gastrulation, HOX genes, etc). But how does the induction and the cytoplasmic determinants cause a change in gene expression? The same is true for this, there are a lot of different ways how this can happen (see gene silencing):

Genomic Imprinting
Paramutation
Transposon silencing (or Histone Modifications)
Transgene silencing
Position effect
RNA-directed DNA methylation

I can write pages of Cellular differentiation because this question is really broad. So I will advice you to read the following articles:

Differential gene expression and development
The process of differentiation
Cellular differentiation


text:
Cousin Marriage from genetics point of view
In most societies marriages between cousin are viewed negatively, due to a fear of "bad genes".
But lets say I am a girl and I marry the son of my mother's brother (i.e. my uncle), than there is no gene similarity.
Then I have two X-chromosomes, where one came from my father and the other one from my mother. My cousin (the son of my uncle) will have one Y-chromosome from his father and one X-chromosome from his mother (wh o is unrelated to me). My mother will also not be a carrier of my cousins Y-chromosome (since she is a female).
Does this all mean that this particular cousin marriage is unproblematic, and no different than a marriage between completely unrelated people?

I tried to clarify your question, so that there are no confusion. If I have misunderstood you, please feel free to roll-back the edit. Your question is however based on a misunderstanding of human genetics (autosomal vs sex chromosomes), which @mattDMo has explained clearly.

I think I am confused with X and Y chromosome and how gene overlap happen, according to my understanding X and Y has completely different genes , which is wrong

It depends on the physical fitness of the parents. A village in italy has been studied because all 400 of its inhabitants descend from the same two people, and it has very low disease results and high longevity, whereas on average, places like SA and Pakistan have above median levels of club foot and genetic disorders from cousin marriage. pak has 55 percent marriage between cousins and 10-15 percent genetic recessive disorders more than non cousin marraiges. 4.4 percent higher mortality rates also from cousin marriages, which is on par with mothers over the age of 40.

The problem is that humans have 22 other pairs of chromosomes than just the sex chromosomes X and Y. Reproducing with your cousin (the son of your mother's brother is the son of your uncle which means your cousin) is generally looked down upon because of inbreeding.
Here's how it breaks down. Your mother and her brother (your uncle) each received 50% of their genes from your grandmother, and 50% from your grandfather. You received 50% of your genes from your mother and the other 50% from your father, who presumably is unrelated to the family. Therefore, you received 25% (50% of 50%) of your genes from your grandmother, and 25% from your grandfather. The same is true of your cousin - 25% from grandmother, and 25% from grandfather. The chances of some of your 25% and his 25% overlapping are rather high (for any one allele of a gene, it has a 1 in 4 chance of being the same as the cousin's). Combine that with 19-20,000-something genes, and that's a lot of overlap.
The problem with overlap/inbreeding is that any "hidden" (recessive) alleles may become homozygous. This may not be a problem for some genes, but a rather big problem for others (see my previous answer about Hunter Syndrome for an example.) There is a real potential of serious genetic diseases in any children resulting from such a relationship, which of course isn't fair to them.

Simply put, if first cousins have children, there is an increased risk of birth defects in those children (as compared to children of unrelated couples).  This has been shown by studies such as this one reported in a major medical journal.
There is a genetic basis for this, which is known as inbreeding depression. Basically, everybody has some genetic defects, but they generally occur in different places among the genes.  However, in two closely related people, such as cousins, the defects are more likely to fall in the same genes because those people share some genes from the same source (e.g. the common grandparents).
It's true that certain kinds of cousins do not share either X or Y genes from a recent ancestor, but that has only a small impact.  That's because almost all genes are on chromosomes other than X or Y, and are inherited by all descendents regardless of the sexes of the people involved.  Therefore, the problem of birth defects (and miscarriages) occur for all kinds of first cousins.

Welcome to Biology.SE!

In most of society cousins marriage [..]

Who cares about marriage in biology? We only care about reproduction. Marriage is a social construct that is mainly irrelevant here.

[..] is seen bad due to fear of bad genes

The term "bad" is poorly used for 2 reasons. 1. There are no bad genes but only a selective differential between two alleles of this gene (or at any other sequence for that matter). 2. It relationship of dominance and epistasis that causes inbreeding depression and not bad alleles.

I have "X" and "X" chromosome, X came from my father and X from mother son of my mothers brother will have Y chromosome and X from his mother which is not family and since my mother has nothing to do with "Y" chromosome.

That's one long sentence :) Who is "mother son of my mothers brother"? You might have a typo here.
Why do you talk only about "X | Y" chromosomes? "X | Y" is one of the 23 pairs of chromosomes we have (not mentioning mtDNA).

Does this all mean that this marriage is as good as between unrelated people?

Yes.
The whole question is to know whether the two parents are related (in biological terms). What I mean by related is not is they know each or if their respective siblings got a baby together but if they share a common grandmother for example. If you draw the genealogical tree of each parent and you see a recent shared ancestor between the two parents, then inbreeding depression can be an issue. Otherwise, it is fine. The reproduction events occurring between their respective siblings is irrelevant.
However, be careful if you intend to jump into societal consequence. Science will not tell you what is acceptable or not in a society. It won't tell you what is good and what is bad. Knowing that a couple have no risk of inbreeding depression may affect your view about this couple but it does not mean that science has demonstrated that the marriage should or should not be allowed (assuming the society has anything to say on that matter).

The OP seems to be asking if a marriage between cousins (or rather, reproduction) could be problematic from a genetic point of view (restated: what if I would marry the son of by mother's brother? see: "...marry son of my mother's brother...[...] Does this all mean that this marriage is as good as between unrelated people?"). Therefore, your second to last paragraph is misleading or can cause confusion.

@fileunderwater i think you got my question, but answer I am not clear?

@fileunderwater Can you please expand to why it is unclear. I edited it but I don't quite understand what may have been unclear to the OP. Feel free to edit yourself as well. Thanks

@remi.b The question is asking whether reproduction between cousins (the "this marriage" part you are quoting refers to a cousin marriage), and the two persons are therefore definitely biologically related. Your initial answer was saying that this wasn't a problem - probably due to misunderstandings caused by unclear language in the question - which is incorrect.


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Evolutionary elimination of recessive gene
As recessive gene is suppressed, why over millions of year of evolution have not wiped them away completely, why don't they just go extinct, as people with those genes go extinct?

Possible duplicate of http://biology.stackexchange.com/q/35532/3340

Simply put, there may not be enough selective pressure to force those alleles out of the population. For example, take a hypothetical gene for eye color. The dominant allele gives brown eyes, the recessive blue, due to the lack of expression of a certain pigment-processing enzyme. So, two heterozygous (brown-eyed) organisms are crossed:
   |  A |  a |
--------------
 A | AA | Aa |
--------------
 a | Aa | aa |
--------------

which results in 75% brown-eyed offspring, and 25% blue-eyed offspring. Unless there is some very strong factor in the environment that has a negative selective pressure on blue eyes, the recessive allele will remain in the population.
OK, that's for an allele with no negative pressure acting on it. What about a disease allele, for example one that has a point or other mutation inactivating an essential enzyme, such as iduronate-2-sulfatase (I2S), a key enzyme involved in the breakdown of waste in the lysosome. It is part of a group of diseases known as lysosomal storage disorders, and is the causative agent of Hunter Syndrome.
People who have the so-called "wild-type" allele(s) of I2S have normal function, even if they are heterozygous. However, if two heterozygotes produce offspring (or if a heterozygote produces offspring with a homozygous recessive individual), then there is a chance of a child with two recessive or defective forms of the enzyme, and they are much more likely to develop Hunter Syndrome (almost no genetic disease is 100% penetrant). If untreated, this disease can have many quite horrible effects (especially given that it usually appears in childhood). The disease is also progressive (it gets worse the older you get), and while it in itself does not typically cause death, patients have (sometimes severely) limited lifetimes.
So why haven't the mutant, disease-causing forms of I2S been "weeded out" by natural selection? In a single word: heterozygosity. Studies (I don't have a reference, unfortunately) have shown that supplying a Hunter patient with as little as 10% of the typical amount of active enzyme in an unaffected person is enough to resolve the acute symptoms of the disease, and begin reversing many of the long-term effects. All things being equal, one would expect that a heterozygote carrying one functioning allele of I2S and one mutant allele would express about 50% of the amount of enzyme that a completely unaffected individual does, and this is more than enough to prevent the onset of disease. There are likely other molecular mechanisms involved to express the functional version even more, so their levels may be even higher than 50%.
So, while there is certainly a strong negative selection pressure on people carrying two copies of a mutated allele (or two different mutations, there are actually many of them) that prevent most or all expression of active protein, that same selection pressure does not apply to heterozygotes, and so the mutant alleles remain present in the population.
I strongly recommend reading through the fairly short but definitely thorough course Understanding Evolution from the University of California, Berkeley. It may explain some of the concepts I've mentioned more clearly.
Note: I once worked for Shire, which, among other things, specializes in rare diseases including lysosomal storage disorders. I specifically worked with their Hunter Syndrome therapeutic, known as Elaprase. Other companies are also working on various therapeutics.
This is in no way an endorsement of the company or its products, it's just where I learned all of this stuff.


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What small insect is this?
Lately, lots of these little bugs have been lurking in my house in Italy. Should I worry?

I'm curious to know what they are.
For reference, the 2 cent Euro is 18.75 mm in diameter.

Possible duplicate of Bug Identification: Is this small tubular, black bug a bed bug?

Related: What kind of insect can this be?..., Can anyone help confirm this tiny insect larvae?, Bug Identification: Is this small tubular, black bug...,
How to protect my mounted insect..., What is the name of the critter depicted..., Varied Carpet Beetle Larvae, What bug is this...

It looks like a carpet beetle larvae(Anthrenus verbasci) to me. This seems to fit considering you found it in your house, which is one place they are fairly common. I would not be able to tell you if you should be worried, I am not a biologist.


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Are "constraint trees" in phylogenetic analysis cheating? How can I correctly use them?
How do phylogenetic experts evaluate results which use constraint trees? Are there examples in the literature where phylogenetic experts detail how they use constraint trees?
Here is my problem. I have 500 samples. These are five different "categories" of species A, B, C, D, E, 100 samples each.
Category A: A1, A2, A3, ..., A100
Category B: B1, B2, B3, ..., B100
Category C: C1, C2, C3, ..., C100
Category D: D1, D2, D3, ..., D100
Category E: E1, E2, E3, ..., E100

There are two classes of which these "categories" fit in: Class 1: A and B, Class 2: C, D, and E.
For the purpose of this discussion, let's say A=whale, B=dolphin, C=mouse, D=gerbil, E=hamster
When I do the analysis, there are some problems. The output tree resolves the samples into two classes which meet my expectations; it splits the samples into two groups: ( A & B) and ( C & D & E ). That's great. However, it doesn't resolve the species into separate categories, e.g. it mixes together "whale" samples with "dolphin" samples, and mixes together all the individual C, D, E . I see
(A1, B3, A27, B23, B2, A2, A3, A4, ....), (C3, C5, D72, D3, E1, E2...).

This would mean whale1 is more evolutionarily "related" to dolphin3 than whale 27.
I try to use a constrain tree instead to constrain each of these groups, using the form
((A1, A2, ..., A100), (B1, B2, ..., B100), (C1, C2, ..., C100), (D1, D2, ..., D100), (E1, E2, ..., E100))

Sure enough, my tree now resolves each "category" A, B, C, D, E into a distinct category.
Question 1: Isn't this cheating? I feel like I stipulated "resolve the tree in this manner I expected" and RAxML output that.
Question 2: How do I evaluate whether this is correct?
Question 3: For experts, could direct me to published literature which used this approach? Which papers used RAxML constraint trees?
Thanks for any help. I'm happy to clarify things.

I understand where you are coming from when you say that it feels like cheating. However, there are a coupled of things to keep in mind. First let's consider why your tree topology might not reflect concordance with intuition/species trees:
1) Presence of artefacts such as long-branch attraction
2) Lack of sufficient phylogenetic signal/presence of non-phylogenetic signal (due to, for example, convergent evolution in the sequences)
3)Horizontal gene transfer (unlikely in animals).
4) Incomplete lineage sorting/deep coalescence (hemiplasy).
Only in the case of 3 and 4 does your tree reflect true relationships among taxa that genuinely differ from the species tree. Cases 1 and 2 are artefactual. In cases 3 and 4, it would not be appropriate to use a constraint tree to get a species-tree concordant topology because the resultant topology would not reflect the 'true' relationships among taxa (i.e. would be 'cheating'). In cases 1 and 2, I would argue that it is appropriate to use a constraint tree to get the species-tree concordant topology (depending of course on what you want to use the tree for) because you know that the your current topology is species-tree discordant because of artefacts and is therefore not reflective of the 'true' relationships among taxa. Of course, you are unlikely to know a priori what factors (1-4) are causing your bad topology (though you can do some tests for long-branch attraction for example -- see Cladistics 21 (2005) 163–193).
What you can do is test whether the log-likelihood of your non-constrained tree and your constrained tree differ significantly. You can use tree topology tests such as the  Kishino and Hasegawa (KH) test. I don't know about RaxML, but IQ-TREE has excellent topology testing: http://www.iqtree.org/doc/Advanced-Tutorial. If your constrained topology is significantly different (statistically) from the ML topology, then you probably should not use the constrained tree. I am by no means proficient in phylogenetics concepts so I would take my advice with a grain of salt, hopefully some of the other members can illuminate the issue a bit further.


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Tools that take a kinship matrix for phylogenetic decorrelation
I have plant genotypes that have been classified as Invasive, Wild or Domestic. I am trying to investigate what explanatory variables (such as "leaf size", "width of petals" and other continuous variables) affect the probability of being classified a sone of the three groups. I therefore have to perform a multinomial logistic regression. However, I would like to account for phylogenetic non-independence using a kinship matrix.
Are there R tools that can perform such regression?
I considered lmekin for example but I don't think it manages to take a response that can take 3 different categories. Is there some function I would be interested in (in the ape package for example)?

If you willing to do Bayesian model fitting, this is likely possible but will take some tinkering to make sure the models are what you think they are. Stan (via rstan or brms), can fit multinomial logistic regressions (A demo from Thinkinator).
If you can convert these models to pure stan code, then you can incorporate phylogenetic/kinship/arbitrary correlation structure into the model following this example on github (or this one). I have had better luck getting phylogenetic regression to work correctly in pure stan than via convenience functions.

Thanks, that was helpful! Here is also an explanation for similar analysis with MCMCglmm


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Features of phosphatase
I was wondering if you would be able to help me with discovering what the main regulatory feature of a phosphatase is. I understand many have separate catalytic and regulatory subunits, however, so do kinases so I feel that there is a different answer that I am not understanding. Thank you,

Your question is a bit unclear. What do you mean by feature?

there are LOTS of different phosphatases - and LOTS of different regulatory   mechanisms - this is too unclear of a question

Maybe OP is asking about the role of phosphorylation/dephosphorylation in signal-transduction by covalent modification.

I answered assuming the OP was unclear about the difference between phosphatases and kinases, based on the statement "I understand many have separate catalytic and regulatory subunits, however, so do kinases" - that seems to suggest that the OP thought kinases and phosphatases did the same thing and that OP was looking for how they differed from a regulatory standpoint.

@AlwaysConfused I'm not familiar with the specifics of the catalytic activity anymore, and you may very well be correct, but from a regulatory perspective the modified protein doesn't much care about the extra water. :) But importantly: phosphorylase and phosphatase are not the same at all, and phosphorylase does not cleave phosphate, so I think you have a typo in the comment since it seems clear you are meaning to talk about phosphatase.

@BryanKrause Ahhh. it is purely typing error I'm very sorry. That would be phosphatase. I did it completely subconsciously because plausibly then I was reading some article on phosphorylase in wikipedia.

I'm deleting that comment and copy-pasting and correcting it so that people do not get misguided.

@BryanKrause as I had been taught, there is a basic difference between working mechanism of kinase and phosphatase... kinase do not release H2O when it adds phosphate to something. But Phosphatase takes H2O (i.e. hydrolysis) when it cleaves the phosphate... i.e. their work is not the exact reverse.

@WYSIWYG. firstly: a. that is a trick question... features are defined according to the object definitions in a given standard, and definitions of the past may be obsolete, for example a feature may be a field in a .gff3 file, or a .gff2 file, or see this example glossary, in accordance with the EnsEMBL database schema: https://www.vectorbase.org/glossary; b. how do you maintain so many posts, are you a bot?

Kinases phosphorylate, or add a phosphate group.
Phosphatases remove a phosphate group.
Beyond that, the concepts for regulating them are the same, though the precise factors of course are different.


text:
Can different bacteria strains of same species have different genomic sizes?
Can two different strains of a single species have different genomic sizes? I am not asking about plasmid. Can they have different sizes of actual chromosome?

Yes, and one could argue that the differences between two strains of the same species are entirely due to their collections of genes (and therefore different genome sizes).
Take the plant pathogen Pseudomonas syringae, for example. There are many different strains, categorized by the plant hosts they cause disease on. This host range is determined by different collections of virulence genes in their genomes. So although they are the same species, they can be remarkably different in their genomes. See this (open access) paper by Baltrus, et al for more information.
A point to remember... "species" is a manmade concept, and there can be different definitions. Some species can have less than 90% similarity at the genome level!

This answer seems decent, but I'm curious what example you have for that last sentence.

I guess there are two ways to look at it... at the genome level, or homology of orthologous proteins. To keep with the example above, we found that several P. syringae strains have less than 80% similarity of orthologs.
The same figure shows that there are on average 26 SNPs per KB, which is only 2.6% differences at the genome level, but that also is across only the genome portions that are actually comparable, and the overall differences at the nucleotide level are much higher.


text:
How to find mutations related to disease for a protein?
I have done research on the protein (CYP3A4). I have its function, purpose and diseases (breast cancer, prostate cancer, testicular cancer, lung cancer). I am however having trouble finding the mutations of the protein and how it correlates with the diseases, specifically breast and prostate cancer.

What is your question? If you want to know more about the protein the way to go is to read papers about it.

Where do I find such papers

Does anyone know about my question and can help?

Pubmed, Google Scholar... As it is written, your question is just too broad (also unclear because there is no real "question"). Please clarify and narrow it down to focus on a specific issue.

I think I understand what you are asking so I will make a little guide to find what you need:
NOTE  the mutations you are searching for are probably on gene level so you can search your protein on Uniprot and then use the gene name to search on DisGeNET, you typ in the gene you are searching for:

Then you hit the search button and this will give you a result like this:

You can see that this site uses a sort of text-mining, in other words it is searching for the gene name associated with disease in articles. The score is an indication for how good the text-mining "worked". As mentioned in the manual:

We have developed a score to rank the gene-disease associations
  according to their level of evidence. DisGeNET gene-disease
  association score takes into account the number and type of sources
  (level of curation, model organisms), and the number of publications
  supporting the association. The score ranges from 0 to 1.

Then you have to click the browse details... in the down right corner. This will guide you to another summary page like this:

(NOTE I omitted a lot of rows to avoid huge images in the answer, so there will be more rows in your result). Because you were interested in prostate cancer I will click on Prostatic Neoplasms:

You can click on the 3 to obtain the 3 articles where the combination of the CYP3A4 and Prostatic Neoplasms was found. This will give you a list like:

As you mentioned in your question

"where do I find such papers"

You can easily click on the PMID this will guide you to the article, for example the first article:

CYP3A4 polymorphisms--potential risk factors for breast and prostate
  cancer: a HuGE review(link).

I think this will help you to find the papers related to the protein + disease, you can further read the papers to find mutations which cause these diseases.


text:
Does anyone know of a study supporting predictions #2 or #9 of the Extended Evolutionary Synthesis?
Regarding the 12 predictions made by the Extended Evolutionary Synthesis (http://extendedevolutionarysynthesis.com/about-ees/), does anyone know of a study that supports #2 or #9?
It seems like #1, #3, #5, #8, #10, #11, and #12 do not violate the modern synthesis.  #2 and #9 would though.  Agreed?  But I know of no study that supports them.  Not sure about #4, #6, or #7.

Note that the title ask for a study that support two given predictions while the content of the post (and your comment below my answer) ask whether the two given predictions given predictions from another set of knowledge. You might want to clarify that.

I'm essentially asking two questions in the post.  A primary question:  whether there's a study supporting #2 and #9.  A secondary question:  whether it violates the modern synthesis.  I think I overlooked the distinction the EES authors are making between genotypic variance and phenotypic variance and that #2 and #9 are probably exemplified by facilitated variation.

There is no debate
The so-called Extended Evolutionary Synthesis (EES) is just a new term for a whole lot of knowledge that roughly speaking everyone acknowledge to be true. EES is really just an extension but does not say anything that conflict with previous theory. There is no conflict and no contradiction.
The only debate stand upon whether or not our current understanding of evolutionary processes deserve a new name or shall we just stick with what we call the modern synthesis.
Shall we use the term ESS?
I talked about this renaming with about 20 evolutionary biologists and all of them consider such renaming useless. However, by the end of the day, they all mainly did not care much.
My personal opinion about the renaming
IMO, one reason such naming is silly is that there has not been a major work that have completely and suddenly changed our understanding. We just keep discovering more and more as we always did. All the new things we discover we just used to integrate it what we already called modern synthesis. Those advocating for a renaming define the modern synthesis not as most people do (that is everything we know about evolution so far) but as the set of knowledge that existed in 1950.
It is funny that even the discovery of DNA did not bring about a renaming of our theory of evolution as we only considered that it added up to our current understanding. I doubt that the emergence of new fields (such as niche construction and its heritability or developmental noise) would be in any way sufficiently revolutionary to cause a renaming. And I say so even though I also work in the field of mutational and developmental noise.
Unclarity
The points listed in the link are rather unclear and it is therefore impossible to comment on them. Take the #2 you are interested in

heritable variation will be unbiased

The term variation has no strict definition. The term variance is clearly defined. However, a variance in itself cannot be biased, only the distribution it comes from can. So, this simple sentence mainly makes no sense (to me at least). If it does make sense to those who wrote this list, then, OP, you will need to provide explanations from other source or ask for its meaning before asking for its validity.
Further reading
This paper will offer you opinions from both sides. As implicit from the above, one side (namely, the "counterpoint" side as referred to in the paper) seems to me to represent the vast majority of evolutionary biologists.
Addressing your comments

Thank you for the clarification. I think by "heritable variation," the authors mean mutation. You feel it's still true that they are unbiased?

"mutation" is not a variable, it does not follow a distribution. It cannot be bias or unbias.
Mutational effect on fitness is a variable and follows some distribution which is most definitely biased (deleterious mutations are much more common than beneficial mutations; usually modelled with a double gamma distribution; see here).
Mutational effect on the phenotype is a variable and follows some distribution. It may well be biased indeed. The distribution of mutational effects on the phenotype were mainly unconsidered by evolutionary biologists who contributed to place the first bricks in the modern synthesis (Fisher, Wright, Haldane, Muller, etc...).
These "early" evolutionary biologist never made predictions about the distribution of mutational effects on the phenotype that would contradict today's predictions. They just had little understanding and did not talk about it much.
Again, in your question you are opposing EES with Modern Synthesis as if they were to be opposed. But by doing so, you need to clearly define Modern Synthesis. By default, one just consider the Modern Synthesis to include all the knowledge we have in evolutionary biology and therefore by definition, elements like niche construction, biased mutational effects of phenotype and other field of knowledge that one might want to specifically associate to EES only.

Do you still feel it's true that natural selection is the only source of the evolution of adaptation?

This question depends only on the definition of adaptation. If, for example, you consider a lineage being poorly adaptive becoming adaptive as the environment changes to match their phenotype (and not the other way around) to be an adaptation, then typically nobody would have never thought that only natural selection would cause adaptation. I would personally be happy to call that an adaptation.
The question is not a question of evolutionary process but only a question of the definition of adaptation.
Note, as an extra source of confusion, when talking about adaptation one may refer to the changes yielding to higher fitness (whether the change is genetic or not is up to you) and/or to the resulting state of having a high fitness.

For example, if there is an epigenetic modification that is transgenerationally stable and adaptive, is it an adaptation?

Again, it depends upon what you call adaptation. I would be happy to call that an adaptation.

the discovery of DNA would not cause a reconceptualization of the modern synthesis because it was consistent with it.

Everything from the EES is consistent with the modern synthesis. Most of it are just add-up subjects that brought little consideration before. Some of it might break some simplified generalization that may have been done before though. Many does affect our view of the grandeur and complexity of evolutionary process but none is contradicting what we previously thought.

what you mean by "becoming more adaptive as the environment changes." Would you give an example?

Imagine a population is perfectly adapted to live at an environment where the temperature is 18˚C. The current temperature is 15˚C though. Let's imagine a case where the population does not change much through time (eventually due to a lack of genetic variance to select from, eventually due to a low mutational variance or a recent bottleneck) but the environment is getting warmer and after some time the environment is at 18˚C. The population is now perfectly adapted.

I appreciate it and I've already read the paper.  Irrespective of renaming, the question is whether those predictions violate the modern synthesis.

The answer is "No, because nothing in the EES contradicts the modern synthesis. EES is just an extension (but most people don't really like the idea of renaming our theory based on this extension)" I edited my answer. Hopefully that will clarify my point.

Thank you for the clarification.  I think by "heritable variation," the authors mean mutation.  You feel it's still true that they are unbiased?

Also, do you still feel it's true that natural selection is the only source of the evolution of adaptation?

For example, if there is an epigenetic modification that is transgenerationally stable and adaptive, is it an adaptation?

Also, the discovery of DNA would not cause a reconceptualization of the modern synthesis because it was consistent with it.  If anything, it confirmed the principle of the modern synthesis that inheritance occurs through genes.

@sterid I addressed your comments in an edit in my answer.

I appreciate your view a great deal.  Thank you.

"This question depends only on the definition of adaptation. If, for example, you consider a lineage being poorly adaptive becoming adaptive as the environment changes to match their phenotype (and not the other way around) to be an adaptation, then typically nobody would have never thought that only natural selection would cause adaptation."  I do not think it's purely a semantic issue.  It is also the conceptual issue of which definition for adaptation making sense.   I'm also not clear about what you mean by "becoming more adaptive as the environment changes."  Would you give an example?

Re "becoming more adaptive as the environment changes" : Is this what you feel occurs during niche inheritance?

@sterid See edit

I see.  That part is clear now.  Thank you very much.


text:
How is NAD+ used in lactic acid fermentation after it is oxidized from NADH?
I am confused with the whole process of glycolysis and the fate of the products of this reaction. So, I understand that anaerobic glycolysis results in 2 pyruvate + 2 NADH and 2 net ATP. Is the whole anaerobic purpose of glycolysis to make the 2 net ATP? Then pyruvate and NADH are waste products? Also, pyruvate then reduces to lactic acid. What is the need for this? NADH is oxidized to NAD+. How is NAD+ used? Also, lactic acid is eventually converted back to pyruvate through Cori cycle. How is that pyruvate used?

I have altered your question to indicate that it applies to anaerobic glycolysis.

Anaerobic Glycolysis
As this question refers to glycolysis in the context of lactic acid fermentation it clearly relates to anaerobic glycolysis, which is why I added that to the question.
I believe it is correct to regard the primary purpose of anaerobic glycolysis as being to generate ATP for the anaerobic organism or tissue.
To understand the roles of NAD and lactate in this process you need to consider the chemistry. The conversion of glucose to pyruvate is an oxidative process, with the oxidizing agent being NAD+, which itself is reduced to NADH. For glycolysis to continue the NADH must be reoxidized to regenerate NAD+. This is the primary purpose of the reduction of pyruvate to lactate and is summarized in my own diagram, below.

So, the answers to your (paraphrased) questions “what are NAD and lactic acid needed for?” and “are they waste products?” are:

NADH isn’t needed for anything — it’s the consequence of the oxidative function of NAD+. No, it is not a waste product — it has to be reoxidized otherwise glycolysis would stop for lack of oxidising power.
Lactate also is not needed for anything, as evidenced by the fact that other reduced products of pyruvate are produced in different organisms, most notably ethanol in yeasts. Ethanol can certainly be regarded as a waste product, although the carbon skeleton of lactate is salvaged in multicellular oxygen-breathing organisms.

The so-called cycle of Cori & Cori
In my opinion it is best to approach glycolysis as I have done above, without reference to the tissue or organism, so as to understand the essential features of the process.
In the specific case of mammals, some tissues perform glycolysis anaerobically, e.g. the red blood cell (which lacks mitochondria) or rapidly excercising muscle (where the blood supply and number of mitochondria are not sufficient to generate ATP for muscle contraction. The liver, in contrast, has a plentiful supply of oxygen and hence NAD+, and so can reoxidize lactate to pyruvate if the former is transported in the blood from the anaerobic tissue to the liver, salvaging the carbon skeleton.
Under conditions of low blood sugar (e.g. starvation) it is important that the pyruvate be reconverted into glucose in the liver by gluconeogenesis, rather than be converted to other products, and the glucose is released into the blood. In this case one goes full circle, this process is generally referred to as the Cori Cycle. I always avoided this term myself in teaching students as I found it caused confusion with cycles such as the tricarboxylic acid cycle and the urea cycle, where all the chemical interconversions take place in the same tissue.
Footnote: Glycolysis under aerobic conditions
Under aerobic conditions (e.g. in the liver after a carbohydrate meal) the purpose of glycolysis is not primarily to generate energy but to utilize the glucose, storing it as fat (after glycogen capacity is reached) or using it to synthesize intermediates. There are different fates for the pyruvate (acetyl-CoA is shown), but lactate is not one of them as the NADH can be reoxidized far more efficiently in the mitochondria, with molecular oxygen being the ultimate oxidizing agent.

Text References
Berg et al. Section. 16.1 (5th ed.) covers glycolysis in great detail under aerobic conditions. The lactic dehydrogenase reaction is given little emphasis, but can be found in section 16.1.9.

You understood exactly what my question was even when I myself was confused about what my question exactly is. Thank you so much.  Your diagram helped. Now, I understand your diagram and why different steps are needed, but can you please help me understand the bigger picture. So the cycle in your diagram occurs when there is a lack of oxygen, i.e while exercising. But what happens where O2 is present (when we are not exercising) then there shouldn't be any lactate (b/c we dont get sore when we are sitting), if there is no lactate, means NADH doesnt get converted to NAD?

@JagmeetSingh — Happy to be of help. I've added a small section with a diagram indicating what happens to the NADH under aerobic conditions. The various possible fates of pyruvate (and glucose 6-phosphate) belong in an answer to a different question. If you have not yet met oxidative phosphorylation and the TCA cycle, then you will need to take your time learning about them — very important, but lots of detai.

So just to clarify: Glucose gets converted to pyruvate and in absence of O2, it goes through fermentation BECAUSE it produces at least 2 ATP(?), and when there is O2 available, it proceeds to carboxylation of pyruvate --> Citric acid cycle and so on. My only confusion now is that why does glycolysis need to occur (anaerobically) if it can not even proceed to cellular respiration.

I meant "decarboxylation" above and not "carboxylation".

Actually, I saved you some headache.
http://antranik.org/cell-respiration-part-1-anaerobic-respiration-glycolysis-and-fermentation/
This website it explained it well.

@JagmeetSingh — Note that under aerobic conditions in the liver there are at least two other pathways glucose may be metabolized by other than glycolysis. Also it is precisely 2 net ATP in anaerobic glycolysis — the ones generated through the capture of phosphate in the GAPDH reaction.

The whole purpose of glycolysis is to make the 2 net ATP, right?

No, actually it's breakdown of glucose as the name suggests, so as to provide pyruvate, whose fate depends on cells need and environment.

Then pyruvate and NADH are waste product?

Why? They are just intermediates which can be utilised in tca, or cori cycle or in any other metabolic pathways as cell needs.

Also, pyruvate then reduces to lactic acid. What is the need for this? NADH is oxidized to NAD+......

Wikipedia says:

The production of lactate is beneficial because it regenerates NAD+ (pyruvate is reduced to lactate while NADH is oxidized to NAD+), which is used up in oxidation of glyceraldehyde 3-phosphate during production of pyruvate from glucose, and this ensures that energy production is maintained and exercise can continue. (During intense exercise, the respiratory chain cannot keep up with the amount of hydrogen atoms that join to form NADH, and cannot regenerate NAD+ quickly enough.)
  The resulting lactate can be used in two ways:
  Oxidation back to pyruvate by well-oxygenated muscle cells, heart cells, and brain cells
  Pyruvate is then directly used to fuel the Krebs cycle
  Conversion to glucose via gluconeogenesis in the liver and release back into circulation; see Cori cycle
  If blood glucose concentrations are high, the glucose can be used to build up the liver's glycogen stores.

Also, lactic acid is eventually converted back to pyruvate through Cori cycle. How is that pyruvate used?

In cori cycle lactate is finally converted to glucose via intermediate- pyruvate.

In response to comments , relation between glycolysis and fermentation:

I think it would be nice if you add this picture: https://www2.estrellamountain.edu/faculty/farabee/biobk/BioBookGlyc.html (scrol a little bit down) , a nice graphical relation between glycolysis and fermentation

I didn't mean that figure, I meant the 3th figure @David

@RickBeeloo Is it correct now?

yes this will show the relatedness between fermentation and the need of NAD+ in glycolysis