text:
How to calculate the conservation score of specific amino-acids or motifs in a multiple sequence alignment?
The proteins I'm interested in create disulfide bonds using cysteine pairs. In different states of the proteins, those pairs are sometimes formed, other times they stay separated.
I would like to calculate a score for the conservation of specific amino acids in my multiple sequence alignment (MSA).
The thing is that some of these amino acids or structures are irreplaceable. For example disulfide bridges must be conserved, otherwise the correct structure will not be adopted.
So, in some way, the score is already very high. But is there a way to calculate the score between different disulfide bridges?
Also, is there a way to state that a MSA shows an amino acid or motif to be highly conserved (as opposed to "just" conserved)?
Is there a quantitative way to differentiate the one from the other?

Are you looking at just the amino acid sequence, or do you have nucleotide sequences as well to compare?

there are many ways and terms that have been proposed for very conserved chunks of protein or DNA, e.g. ancient conserved region or ultraconserved region. However I think that it is more useful to just state the degree of conservation (100% identity, 99% similarity, etc.). There aren't really meaningful "conserved" vs "highly conserved" categories, and conserved in hominids vs. conserved in mammals vs. conserved in metazoans all mean different things.

nonetheless, your intuition is correct that disulfides are relatively conserved.

In my experience, many students new to sequence alignment want someone else to  put the results into a formula and produce a number that encapsulates the conservation of a sequence or the significance of an alignment or whether it is better or worse than some other one. You are correct in that a number (score) is required, but before I can provide an answer to your question (which I am prepared to do) I need you to tell me what you hope to use it for, e.g. to comment in a report, to compare two situations. And the situation for a single amino acid is different from a motif of several.

I now what you mean @David. We're looking at cysteines, some of them building disulfide bonds others not. We would like to understand how conserve this process is during the evolution of metazoan, but also of (much) earlier organisms if at all. we can see that some cysteine-pairs bond at specific conditions, other not. Is this possible (like you say) to piut a number to it? thanks

@AssaYeroslaviz If we can easily identify the cysteines involved in disulfide bonds, we can readily postprocess alignments and say that such cysteines are 90% conserved across mammals, 80% across vertebrates, 70% across metazoans (or whatever numbers), and then provide comparisons to various other residues. Is your question how do we postprocess protein alignments to give such numbers? Or is your question is it possible to define different degrees of conservation? Or perhaps even can we even estimate conservation from a multiple sequence alignment?

like the question stated at the top of this post state, I would like to know if it is possible to assign a score to specific AA (or also domains) from a Multiple sequence alignment. If the answer to this question is yes, then of course the next question would be how? thanks

I am still not clear precisely what you want to do. Look at my answer and then, if it is not on target, comment indicating precisely why.

I am somewhat disappointed after the effort I put in to trying to answer your question you have not responded to it in any way. As I believe that we are both professional scientists I find that somewhat uncollegiate.

Hi David, sorry for not responding. As we had here school vacation last week I took some time off work, so also tried to avoid reading my mails. I have not seen any posts from you. Thanks for this elaborated answer. I will read your it and let you know if I have more questions to that topic. thanks again

Preamble
I am not quite sure what the poster is trying to do, in particular the question “is there a way to calculate the score between different disulfide bridges?”. Clearly, if different bridges are completely conserved between species in two different proteins or within the same protein, that’s it. (Sort of the converse of ‘slightly pregnant’.)
Nevertheless this answer discusses ‘scoring’ multiple sequence alignments (MSA) and describing the results, so it can be updated in response to any clarification the poster makes.
The Clustal MSA program already scores positions in an alignment
I do not know what MSA program the poster is using, but the output from Clustal X (at least standalone v. 2.1 for the Mac) already presents scores of a sort. This can be seen in a sample output, below:

The height of the individual bars in the bar graph below the alignment ranges from a maximum (where all five sequences in this set align) to what I assume is the zero baseline (where one of the sequences introduces a gap).
Closer examination, however, shows that the scoring system used is not a simple percentage identity: 0, 20, 40, 60, 80, 100%.

In the detail it can be seen that (4xK + 1xN) scores higher than (4xV + 1xK), and also gets a ‘:’ comment (see below). This is presumably because it is using the same PAM or BLOSUM amino acid comparison matrix used in the alignment to compute the height of the bars. (I leave the interested reader to plough through the literature to see if this is documented.)
What can one say?
The question seems to wish to transform the numerical score into a descriptive statement. The following assumes that one is taking one sequence as reference — here 1qjo.
• The simplest possibility would be a statement of the type:

“P at position 8 in the reference sequence is completely (100%)
conserved in the data set, whereas at position 49 the conservation is
only 80%, and at position 51 only 60%”.
This could be converted to descriptions using the percentage scale in a subjective and arbitrary manner which one would have to define, e.g. >75% but <100% = ‘highly conserved’, >50% but <75% = ‘moderately conserved’

• An alternative would be to use the descriptive categories — * : . — and convert them to descriptive terms ‘completely’, ‘highly’ and ‘moderately’. This result of this would be different from using percentages. What one would really be describing here is not the conservation of a particular amino acid, but the conservation of amino type at a particular position. So the statement would be something like (choosing a different example):

“As regards the eight positions in the reference sequence where E was
found in the data set, only position 40 was highly conserved and
position 58 moderately conserved.”

Context matters
My example statements above all refer to “the data set”, emphasizing that any numbers or descriptions cannot be absolute, and their significance depends on the extent of the data set and whether it is biased towards sequences of a particular origin. The most obvious cause of bias is species e.g. a data set with 20 mammalian species and two insects. Not only species range is important, but it can happen that a problem is complicated by different forms of a protein in the same species, and that these forms may be more similar between species. A way of approaching the latter problem is to consult SCOPe, and if necessary construct a data set containing a range of SCOPe subcategories.
Other approaches to the disulphide bond problem
I am not quite clear whether any of the members of the family of proteins of interest to the poster lack cysteine at the position of the disulphide-bond forming cysteines of the references. If they do I would be tempted to use alphaFold to obtain predicted structures of these exceptional members and see if the positions at which the cysteines in the reference sequence occur are predicted also to be in close proximity in the exception.

I really appreciate your answer and I think it is a good start toward what I'm looking for. The two possibilities you offered sounds good. I'm starting to understand that it is not really easy (if possible at all) to get a number stating the degree of "conservativity".
I know about the ClustalO/Mafft/T-coffee/etc. results and the way they show how is conserve a position. But if I understand it correctly, this states only how conserved the position is by itself, and not compared to others.

I am not sure, if this is possible or even make sense at all. I'm interested though in trying to put a number to a specific position in the MSA compared to other positions. Or as @David put it. Is this one slightly more pregnant than the other one?
After thinking and searching the problem, I also see, that a structural comparison might give better (or at least more conclusive) results, as to whether or not a postion is more conserved.

The disulphide bridges I mentioned are a bit of a problem, because those Cysteines ** have to be there** in roder for the bride to exists. No cysteines, no bridge! Therefore they are always very conserved.
This is why, even though the answer is a good one to decide how to regard the question, your two suggestions will not really be helpful here, as they Cysteine-pairs will have most of the times 100%. So by themselves they will always be highly conservative. But how is it comparing them to one another?

So, maybe the question would be to see what around the bridges, maybe what is inside the loop the bridges create. If i can show that there are other, more unique AA there (e.g. W or Y), which might be needed for some kind a binding event, this might make this bridge "stronger conserved" than a bridge, where this AA is not available anymore, as the binding activity can't take palce anymore.
I'll take a look into AlphaFold and see if I can make use of it.
thanks


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How do i create sustainable readily available stock cultures to act as Gram stain controls?
My investigation on the matter
Ref #1

Staining known Gram-positive and Gram-negative organisms on either
side of your unknown organism act as positive controls for your
technique.
(Microbiology Laboratory Theory and Application (Michael J. Leboffe, Burton E. Pierce)

Ref #2

Similarly, cultures should undergo evaluation while they are still
fresh. Old cultures tend
to lose the peptidoglycan cell walls, which predisposes gram-positive
cells to be gram-negative or gram variable.
(Tripathi N, Sapra A. Gram
Staining. 2023 Aug 14. In: StatPearls [Internet]. Treasure Island
(FL): StatPearls Publishing; 2023 Jan–. PMID: 32965827.)

Ref #3

Refrigeration impedes further growth of the bacteria, so you will have
"fresh" cultures to work with during the next laboratory session.
(Laboratory Exercises in Microbiology By Robert A. Pollack, Lorraine Findlay, Walter Mondschein, R. Ronald Modesto)

Ref #4

Remember the following points concerning your [refrigerated or frozen] slant or agar stab stock
cultures:
-Do not use stored stock culture for making slides or routine inoculations.
(Laboratory Practices in Microbiology By Osman Erkmen)

Question
How do I create a sustainable readily available pair of stock cultures to act as Gram stain controls (as Ref #1), in the least time-consuming and tedious way?
From Ref #2 and #3, I can prepare two slant cultures, one is of a Gram-positive bacteria and the other is of a Gram-negative bacteria, then store them in the refrigerator or freezer. Then I can retrieve them daily and use them. After that, they are returned to storage.
However, Ref #4 argues against using refrigerated/frozen cultures for making slides.

Just spitballing, but what if you made a stack of slides and heat fixed smears of your controls onto each slide, so that you could just grab one out of the slide box and have your controls already fixed to the slide. It would probably take some verification testing against fresh controls to determine the quality/stability, but I know I have used commercially available QC slides like this in the past.

It's not about the mean, but the end. Anything that would substitute as a Gram stain control would do. So this is an answer.

Aside from MikeyC's commented suggestion, which I think is a good idea and they should write it up as an answer.
In my experience, most species of bacteria you might use as controls for Gram staining will easily last 2-4 weeks in the fridge on a plate and still be usable as controls.  These will be genera like Staphylococcus and Escherichia, well known, readily available and well characterized.
For fairly minimal effort, one can simply take a plate of the organism wanted and re-streak/sub-culture once a week or once every two weeks. The streaking itself should only take you a minute or two, adding in time for labelling of plates and general fluffing around in the lab (opening incubator, placing plate in incubator etc.), maybe a maximum of 5-10 min per plate. I know that with pre-labelled plates and disposable loops, I can sub ~100 plates in about an hour.
For longer term storage of species, it is best to keep a glycerol stock. These are stored at -80 C (ultracold freezer) and can be used indefinitely. If you wanted to work from glycerol stock (to be sure of getting the right species), add maybe another 5 min to look up location in the freezer and get them out for streaking. There is no need to thaw a glycerol stock (in fact it is detrimental to thaw them) - just use a cooled flamed loop, or a clean disposable loop to scrape a tiny amount of the stock from the top of the tube and streak this out.

source: Stack Exchange

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

sort: votes


text:
Are these algae responsible for concrete staining the same organism?
I am interested in studying the effects of algae that cause concrete staining on the walls in my city, particularly because this green growth is widespread in my country, Quito, Ecuador.

Since I am considering establishing an in silico Genome-scale Metabolic Model (GEM), I need to determine whether this type of algae is a distinct organism or a composite of fungi, archaea, cyanobacteria, and other microorganisms.
I have some doubts, as I have successfully cultured a sample of this green algae using wastewater, NPK fertilizer, and exposure to sunlight. Moreover, these algae exhibit remarkable resilience to fluctuations in temperature and oxygen availability.

“ determine whether this type of algae is a distinct organism or a composite of fungi, archaea, cyanobacteria, and other microorganisms” have you tried using a microscope?

since its naturally occurring the answer will almost certainly be no, monoculture is a human invention.

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


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How to choose a method for upregulating an endogenous protein?
What factors affect the method that should be chosen to engineer a cell line that upregulates an endogenous protein? I am mostly asking permanent or long-term expression of nuclear proteins in mammalian cell lines, but more selection criteria for more applications would be appreciated too.
As I understand it, the possible methods are the following:

Target the regulatory factors already present in (or adjacent to) the gene of interest responsible for the protein, possibly targeting known variants that express a phenotype associated with high protein expression
Introduce new regulatory elements to improve transcription and translation
If the cell line is immortalized, expand and select for higher expression of the target protein
Introduce a non-integrative element that expresses the mRNA transcript variant

Are there any factors regarding the protein, gene, or cell type that make one of these better or worse? And are there any methods I'm not considering?

This is one of those questions that needs to be determined empirically, as it is highly dependent on the protein in question. For any one system, the best method to use needs to be determined by trial and observation. Upregulation and over-expression can be problematic, depending on the system you are targeting. Check the literature to see what others have used.
You are missing a few methods, namely those that use a lower expression cf. the already determined level in your unaltered line:
In many cases it is possible to find a cell-line that has a naturally higher or lower expression of the protein that can be used experimentally to compare to another that has a lower/higher expression, or use/generate a Knock-Out (KO) version of the cell line. Generation of KO is generally easier than introduction of a gene for stable expression if you are aiming for integration into the genome. The exception here is where the gene is used on a mobile element like a plasmid and is continually selected for using selective marker for over-expression.  Investigate CRISPR/Cas systems for these, as well as viral vector methods (lentivirus, adenovirus etc.)
You can also use methods such as siRNA to target mRNA for degradation, but this is not stable, needs to be done individually for each experiment, and may or may not work for your system.


text:
What is the difference between electrophoresis and electro-osmotic flow?
How can one explain the difference between electrophoresis and electro-osmotic flow (EOF)?
Is there also a difference in the way the electric potential is used?


text:
Do Tardigrades have an innate immune system, or any type of immune protection?
Do Tardigrades have any immune protection against bacteria and viruses?

Welcome to SE Biology. Please read the Help on Asking Good Questions. A one-liner starting with an obvious typo (repeated in the title) hardly corresponds to providing context and demonstrating an attempt to answer the question yourself.

I could not find any data on their surival following an infection compared to uninfected individuals. I could not find a proper description of their immune effectors either. However, I would be very surprised if Tardigrades did not exhibit immune reactions in the case of a sceptic wound.
They are exposed to many different bacteria in their environment, which affects their own microbial communities, and even seem to have endosymbionts:
https://par.nsf.gov/servlets/purl/10217788
Endosymbionts are usually kept under control by the immune system in insects. I expect it to be the case in tardigrades.
They do not seem to possess the classic pathways leading to antimicrobial peptides production in other ecdysozoa, although in their genomes you can find other NF-κB distantly related NFAT homologs:
https://academic.oup.com/g3journal/article/10/3/1137/6026230?login=false
In this paper : https://www.biologie.hhu.de/fileadmin/redaktion/Fakultaeten/Mathematisch-Naturwissenschaftliche_Fakultaet/Biologie/Institute/weitere_und_ehemalige_Dozenten/weitere_Dozenten/Prof._Dr._Hartmut_Greven_i._R/2005_04_2005-Greven-Dastych---Kraus-integument.pdf
there is a picture of their hemocytes, which in insects have an immune function.
I could find mention in several papers of a pigment resembling melanin, which in insects (as well as a lot of other clades) has an immune function.
More evidence might come, although I would assume their size to make experimental infections and RNA extraction  (in order to detect upregulated genes) very complicated.

Does this actually answer the question? I'm asking because I could not find any papers that actually concluded that they do have any immunological capabilities, and that the genes comparable to those of other organisms' immune systems might have been conserved for other reasons. Thanks. (My takeaway was, "They might, but we don't know yet." However, I have only the most basic understanding of immunology.)

You are right, this is more my opinion based on the information I could find. I rephrased my answer.


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Has the speed of animals changed over time?
I am not a biologist but always had the following questions:
Evolution theory says that the fittest of the fittest pass their genes on. Perhaps an oversimplification, but this would mean that slower lions would be less likely to pass on their genes. For example, lions that are slower would eat less, become weaker, be less attractive to their mates ... and therefore, be less likely to pass on their genes compared to lions that could run faster. And evolution theory also would suggest that the speed of a lion cub would be statistically closer to its parents - faster lions are more likely to produce faster lion cubs and vice versa. Obviously, there is probably a terminal speed - that is, lions wont eventually run at the speed of light, and likely plateau at some speed after many evolutions ... and then the rate of increase will likely be negligible from generation to generation.
This brings me to my question:

Do we know if animals like lions are running faster than they were 1 million years ago?
If we define a new ratio variable as R = (average speed of lions)/(average speed of gazelles) ... do we know if this variable R has remained relatively constant over the past 1 million years?

Thanks!
Notes:

These animals have mutated millions of years ago and their current form might have mutated from their old form. Therefore, a given lion from a  certain species 10 million years ago might be a new species of lion, making any comparison somewhat irrelevant (i.e. comparing apples to oranges)

We assume that animals become faster each year - but its possible that they no longer need to be as fast due to environmental changes (e.g. deforestation caused by humans has changed the habitat of their prey and the prey is easier to catch, and requires less energy to chase).

fitness is relative not absolute, thick insulation is a great adaptation in the artic and horrible in the desert. every adaptation has its cost. the more you are adapted for speed the less you are adapted for anything else, like strength or robustness, just look at cheetah. super fast but easily bodied by basically any other predator.

Modern lions are less than 1 million years old. Last common ancestor ~500,000 years ago. Also - fastest =! fittest evolutionarily speaking for lions. They are mostly stealth hunters - jump and pounce, or short charge.


text:
Can Neurons be connected in Series and will that pattern create huge voltage in human body?
We have learned in Physics that when multiple voltage sources are connected in Series , the resultant voltage becomes the summation of all voltages .
Now, my question is - Can Neurons be connected in same pattern and if it's possible , can let's say billions of neurons connected in Series , create a huge voltage in the body?
also , can the resultant voltage thus created become harmful for human body as an electrical shock?

In a typical nervous system, no, that's not how neurons are connected at all. Neurons have a voltage across their membrane, a potential difference inside versus outside of the cell. A "connection" between neurons either involves a chemical synapse where there is a gap of "outside" between the two neurons that neurotransmitters are released into (so relative to outside the potential is zero between the neurons) or electrical synapse where the insides of the neurons are directly connected (so relative to each other there is no potential difference). Think also of all the other surface area of two connected neurons: to have an accumulating voltage these surfaces would also need to maintain that full voltage across the membrane. I would recommend trying to draw out a circuit diagram along the whole membrane of two connected diagrammatic neurons and I think you'll discover the problems quickly.
However, the configuration you describe is roughly how an electric eel operates to generate voltage (particularly for a strongly electric fish that is capable of damaging shocks), not with neurons exactly but with a special electric organ.


text:
What bird species were featured on this album?
I am very curious about the identity of the feathered subjects on the cover for Susumu Yokota's 2000 Album "Sakura."
The one on the left seems to be some kind of hummingbird. Not sure what family the two on the right belong to, let alone genus or species.
Assuming they aren't fictional species created in an ad-hoc manner for the album art, which I hope isn't the case, does anyone recognize them?

There are two species of bird shown in the illustration.  The one on the left is Eupetomena macroura, the swallow-tailed hummingbird.  This bird lives in eastern South America, primarily Brazil.
The species on the right I can't identify.  From the style of the illustration, it appears to be  a 19th-century zoological illustration, and is not likely to be an original for the album cover.

It looks very much like the work of ornithologist John Gould's wife, Elizabeth.

@ mgkrebbs Wonderful. I had a feeling the hummingbird was real. As for the other, perhaps you might be right. It has to be a passeriform at the very least. I find unsolved mysteries rather troublesome so perhaps I'll try to get a definitive answer elsewhere.

@anongoodnurse I looked at her illustrations on Google and the birds she drew bear a striking similarity to these little ones. There's no artist credited for the cover on the album's Wikipedia page or Discogs, so who knows who created it. I don't think it's likely that he had some other artist's work copy/pasted though.

Perhaps Sunbirds of some type?


text:
Anatomical separation of body components
What separates the organs and parts of the body, for example, the intestine and the spine?

This image shows what makes this separation, but what would be represented in orange and yellow?

In vertebrates at least, organs are contained within body cavities, delimited by serous membranes. Here you seem to be pointing at the limit between the abdominal body cavity (delimited by the peritoneum) and the spinal body cavity (delimited by the meninges).
Take a look at the Wikipedia page (and related links):
https://en.wikipedia.org/wiki/Body_cavity

I imagined it would be the peritoneum, but in the image I sent, it wasn't evident, thank you very much!


text:
How can one store non-sterile culture media in dissolved form in the refrigerator?
How do I store non-sterile culture media in dissolved form in the fridge in a clean but non-sterile container?
The powder of the media (Broth, Nutrient agar, MAC, or MH agar) will be put in a glass bottle filled with distilled water and then dissolved/mixed in the microwave.
Would a 12-hour to 16-hour storage in the fridge prior to sterilization, thereafter, affect the media performance?

So long as you are careful in making this, so as to not add gross+ contamination (hair, don't put your fingers in it, etc.) and use clean glassware, then a storage at 4 C will inhibit almost all bacterial growth from almost all common species, and those that are capable of growing at 4 C tend to grow very slowly.
You don't need to microwave before sterilization generally - the autoclave will melt the agar much better than you can do in the microwave and is easily mixed in by a swirl of the bottle after removing from the autoclave.
+ This means bulky or heavily, not "ewww disgusting". See definition 4: https://www.merriam-webster.com/dictionary/gross

I'm melting to mix. Do you mean that i generally don't need to mix prior to autoclave, just add powder + water, then autoclave and swirl after its out?

@FreezingSoul you should dissolve liquid media in cold water, then autoclave. Media with agar, you should dissolve the soluble components in cold water add the agar (if separate), then autoclave. No need for microwave to dissolve the agar.

I meant to ask, generally, is there no need to mix prior to autoclaving? I think i had pimpled MacConkey agar when i didn't boil it prior to autoclaving.

I didn't swirl, to be honest after receiving my autoclaved media, but it was clear.

@FreezingSoul I usually keep a magnetic stir bar in the flask when autoclaving media. Makes it easy to mix while cooling, which is especially important when I have to add heat-sensitive amendments (like vitamins or certain amino acids). I honestly wonder why every SOP ever tells us to dissolve agar with heat before autoclaving, since every lab person I know just mixes it in cold and lets the autoclave do the heating/dissolving.

Media performance in terms of what? What are the temperatures in the fridge?
Assuming you are storing sterile media, refrigeration will not affect anything. What might be affected is the media and culture. Your question sounds like you are storing media without cells, and nothing will be affected.

"Non sterile", not "sterile"


text:
Identification of invertebrate
Found on mattresses/walls in France. Size about 3mm long.

The duplicate suggestion unfortunately gives the answer. Leaving you, some cleaning to be done.... sigh


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Why are dogs descendants of Wolves but humans are not descendants of chimpanzees?
From here

The dog, Canis familiaris, is a direct descendent of the gray wolf, Canis lupus:

But from here

Human and chimp DNA is so similar because the two species are so closely related. Humans, chimps and bonobos descended from a single ancestor species that lived six or seven million years ago. As humans and chimps gradually evolved from a common ancestor, their DNA, passed from generation to generation, changed too.

 Same is said for cats and dogs that they evolved from a common ancestor that is neither dog nor cat.
Why are dogs "friendly wolves"? but humans not " intelligent chimps"? Why are dogs descendants of wolves (with wolf ancestor) but humans and chimpanzees different species (with common ancestor)?
I don't think reproduction is the basis for this because dogs and wolves don't mate to produce fertile progeny in the wild.

Welcome to pets.SE! I think, this question would be a better fit in biology.SE, because the sience of descendants belongs there. Also the rule for "child of someone" vs. "descendant race/species" is part of the biology field of science.

The very simplistic answer is that dogs and wolves belong to the same genus and are so closely related that they are often considered to be parts of the same species. The genus is Canis (Latin for dog) and the species are lupus (Latin for wolf) with domestic dogs being the subspecies familiaris (...the familiar one) to make the dog's name Canis lupus familiaris and the wolf's Canis lupus lupus. Being this closely related, dogs and wolves can interbreed to produce a hybrid wolfdog, which can themselves be fertile. Fertile interbreeds is one of the characteristics that are used to determine the separation of species. This means that things like mules, which are a cross between a horse (Equus ferus) and donkey (Equus africanus), and are different species within a genus aren't fertile.
Wikipedia has a good illustration of the relationships between dogs and wolves on the page on the genus Canis. Basically the genomes of dogs and wolves will be very very similar, much more similar than that of humans compared to chimpanzees. The last common ancestor (LCA) of dogs and wolves is about 10,000 years ago, at the domestication of dogs.
On the other hand Humans; Homo sapiens (Latin for "same" and "wise-one") and chimpanzees; Pan troglodites (Pan was a god of the forest in mythology and Troglodites were mythical cave dwellers), are not even in the same genus, though we are in the same family grouping, known as the Hominidae, meaning that we are closely related in terms of body shape.
We don't actually have fossil evidence of the LCA for chimps and humans, so we don't know exactly what it looked like. However, for some frame of reference, I refer you to the excellent and informative A Short History of Nearly Everything by Bill Bryson, which has a line on hominid remains which goes something like this:

If you took all the ancient hominid remains you could comfortably fit them into the back of a pickup truck with room to spare.

While our genomes are similar, the genetic similarity is about 98.8% - which in a genome of about 3.2 billion bases, this equates to about 35 million differences. The similarity between wolves and dogs is 99.9%, which, with a genome of 2.4 billion bases, gives about 2.4 million differences, far fewer than between humans and chimpanzees.
The LCA of humans and chimpanzees is about 10-13 million years ago, which is about 1000x longer than that for dogs and wolves. If you could go forward about another 10 million years, dogs and wolves might be similarly separated to humans and chimpanzees.
Another problem here is the concept of relatedness - the LCA of humans and chimpanzees isn't a chimpanzee or a human, rather it is a species with similarities to both.  On the other hand, we know the LCA of dogs and wolves, and know that it was a wolf, because of their close relationship. Thus we can say that dogs are the wolf's little sibling or are friendly wolves, but we can't say that humans are brainy chimps (or that chimps are less intelligent humans)

+1 for the balance between details and "understandability" :)

also wolves is a group which the ancestor of dogs would still definitely be in, while chimpanzee is not even the only Pan species.

@Allerleirauh Thanks, it's a difficult line to walk and the biologist in me is screaming to add commentary on the not quite true bits

@John Good point, also not to mention that there are a bunch of other hominina, with many extinct species, of which we are the only surviving species, not just of the genus Homo but of all genera within that clade.


text:
Could the inability of adult mammals to digest lactose be partially explained by the loss of lactose-metabolizing bacteria from the microbiome?
BACKGROUND:
1. Lactase persistence
Lactase persistence is the continued activity of the lactase enzyme in adulthood, allowing the digestion of lactose in milk.
According to Wikipedia, only a small proportion of human mammals keep the ability to digest lactose when reaching adulthood:

In most mammals, the activity of the enzyme is dramatically reduced after weaning. In some human populations though, lactase persistence has recently evolved as an adaptation to the consumption of nonhuman milk and dairy products beyond infancy. (...) Worldwide, most people are lactase non-persistent, and are affected by varying degrees of lactose intolerance as adults.

The scientific consensus is that the enzyme lactase is encoded by the mammalian lactase gene (LCT), and that Hypolactasia is known to be recessively and autosomally inherited. Most mammals lose the ability to digest lactose once they are old enough to find their own source of nourishment away from their mothers, and there is still debate about the selection mechanism which yield  the   human excepcion:
Lactose malabsorption is typical for adult mammals, and lactase persistence is a phenomenon likely linked to human interactions in the form of dairying.
2. Gut Flora inheritance
Our understanding of the gut microbiota has recently evolved
(the study of gut flora began in 1995): the digestive tracts hosts a whole population of microbiotes, each with their own DNA, playing active (positive and negative) roles in the digestion process and co-evolving with their host. The composition of human gut microbiota changes over time, when the diet changes, and as overall health changes.
The gut flora are believed to be inherited, in particular from the mother and from people living around the infant:

During birth and rapidly thereafter, bacteria from the mother and the surrounding environment colonize the infant's gut. The exact sources of bacteria are not fully understood, but may include the birth canal, other people (parents, siblings, hospital workers), breastmilk, food, and the general environment with which the infant interacts. (Wikipedia)

QUESTION
Could an environment selecting for lactase persistence phenotypes select both human and gut flora genotypes in paralel, so that the survival or disappearance of gut flora able to hydrolyse lactose to glucose and galactose play as important a role in the ability of selected humans to digest or not fresh milk as the various genes previously identified?
PERSONAL REMARKS
I wonder if  these hypothesis have been previously ignored because the gut was considered "neutral" rather than "active" in the digestive process (the alternative being that theses hypothesis have been already proven wrong beyond questioning, which I am curious to learn about).
I understand that this is not the scientific consensus, and I am not claiming that the scientific consensus is wrong. But the scientific consensus was once that the earth was flat, or that the sun was rotating around the earth, and it evolved. I am wondering if there is place for doubt in the current scientific consensus about the genetic causes of the ability or inability to digest lactose in human adults (from a scientific point of view).

What brings you to the conclusion that this is not (as it is the fact) caused by our genetics?

Just a thought, but try looking up the LCT gene. It's a human one, producing lactase. I'm not sure how your experiment tests the hypothesis - wouldn't that work equally well if the enzyme continued to be produced by the growing organism because of continued milk intake due to something in the milk interacting with the organism directly? Do you mean to suggest that the LCT gene expression is regulated in some way that's mediated by gut flora?

@Chris: The intestinal flora has genetics (distinct of our own), is transmitted from parents to children (as our genetics) and evolve under the same selection mechanism as our genetics. I am aware that the current state of scientific knowledge is that the ability to digest lactose is based on genetic, but I wonder if an alternative or complementary theory based on the genetics of the microbiome could also explain the ability and inability to digest lactose in adult mammals. (Sun and stars rotating around the earth used to be a scientific fact too!)

Scientifically spoken, tt was not a fact - it was a hypothesis. Which was proven wrong. Besides this the mutation which leads to persistent expression of lactase nicely explains the mechanism.

I suggest reading this paper: "Human adaptation, demography and cattle domestication: an overview of the complexity of lactase persistence in Africa".

@mgkrebbs I will, thanks!

Preamble
The original version of this question has been edited, so the first part of my answer, which addressed certain arguments and proposed experiments has now been removed. The question now incorporates material accepting the role of the enzyme lactase in determining whether humans can continue to digest milk after weaning, but I retain the section I wrote on that point, as it presents some precise genetic evidence and points to a useful review. In my update in response to the changes in the question I have extended my consideration of the role of gut bacteria.
The mechanism of lactase persistence has been established to be genetic
A recent (2017) review in Annual Review of Genomics and Human Genetics covers the topic in detail. There are five separate genetic variants and details of one of these are:

In 2002, a study of Finnish families by Enattah et al. (30) identified the first mutation associated with the LP [lactase persistence] phenotype: −13.910:C>T (rs4988235).

A further study showed that the −13.910:T variant creates a new binding site for octamer-binding protein 1 (Oct-1), a transcription factor that interacts with human hepatocyte nuclear factor 1α (HNF1α) to bind to the LCT [lactase] promoter (77). This allele therefore leads to an alternative path for LCT expression that is not downregulated, as the original path is.

There are questions about lactase persistence that still have not been answered — primarily why it arose in some human populations, but not others. However experimental evidence and scientific logic lead to the conclusion that cessation of expression of the gene for lactase ([lactase non-persistence) results in loss of ability to metabolize lactose. Any “scientific consensus” rests on this experimental and logical basis and the absence of any experimental evidence for a different or additional explanation.
Intestinal flora and lactose tolerance
The poster now accepts the role of genetics, but posits that the microbiome might be an additional factor in lactose tolerance. I shall now consider studies in this area.
CORRELATION OF LACTASE PERSISTENCE WITH PARTICULAR MICROBIOTA
The review already quoted does provide some information on Bifidobacterium, a bacterial constituent of human microbiota able to metabolize lactose:

Interestingly, although most of the focus has been on the cost of drinking milk for LNP [lactase non-persistent] individuals, arguments can also be made that consuming milk or dairy also has advantages for these individuals. Indeed, recent studies have shown that the gut microbiota of LNP individuals differ from those of LP individuals from the same population in that they have a higher prevalence of Bifidobacterium (11, 15, 47), which is explained by the larger amounts of lactose available for bacterial fermentation. In fact, this represents one of the strongest associations to date between genetic variants and variation in gut microbiome composition (11, 15, 47).

Thus, humans who for genetic reasons do not expresses lactase (a trait that correlates with the inability to digest lactose) have a larger intestinal population of lactose-metabolizing bacteria. This is consistent with their having unabsorbed lactose in the gut. However it provides no evidence in support of an additional role of such bacteria in lactase persistent individuals, even assuming that there was a mechanism by which these bacteria could contribute to lactose tolerance. (This latter point will be considered next.)
LACTOSE-METABOLISM IN BIFIDOBACTERIA
The implicit assumption — now made explicit in the title of the question — is that bacteria possessing a lactase (generally known as β-galactosidase in bacteria) could or would supply the products of lactose hydrolysis (glucose and galactose) to the human host. This is by analogy with ruminant bacteria, and perhaps the supply of vitamins by human bacteria. Unfortunately there is no evidence to support this idea. It has been demonstrated that bifidobacteria take up and utilize lactose for their own growth, employing the (anaerobic) fermentation pathway known as the bifid shunt, which also involves glucose. The products of this are lactate, acetate and ethanol.
THE MICROBIOTA & THE PATHOLOGY OF LACTOSE INTOLERANCE
It is worth recalling that lactose intolerance can be a pathological condition if the subject consumes dairy products. This is not my area of expertise, but it would appear that this results from the fermentation of lactose by bacteria other than bifodobacteria, with the formation of different products — fatty acids, hydrogen, methane and carbon dioxide. The gas produced causes various problems (flatulence, bloating etc.), and the acidification of the intestinal contents can cause diarrhoea — a major problem in this condition.
It should be noted that bifidobacteria are regarded as beneficial (‘probiotic’) in lactose intolerant individuals, although the basis of this is not known. (Perhaps they compete for the lactose with the bacteria whose metabolism produces more harmful products.)

I am confused: you seem to equal "Lactase non persistent" humans and  "humans who cannot digest lactose", when my understanding (from your own quotes) is that humans with a higher prevalence of Bifidobacterium do indeed digest lactose without producing lactase?

Thanks a lot for the pointer to the survey! I am sorry if my question seemed unscientific to you: if no biologist, I am nevertheless a scientist, and a "believer" that science progresses by asking the right questions (and that stack exchange is a good engine to make science progress). I am not sure than mine are the right ones to progress, but at least they are the right ones for me (and others) to learn!

@J..y B..y — I have now modified my answer. I did not read your original point properly. "when my understanding (from your own quotes) is that humans with a higher prevalence of Bifidobacterium do indeed digest lactose without producing lactase". The quote says nothing about digesting lactose only "beneficial effects" which may be due to the protein or fat content of the milk. All this implies is that they tolerate some milk — i.e. don't show the lactose intolerant pathology. As I mentioned in my wild speculation, the bifidobacteria may outcompete those responsible for the pathology


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Is crossveinless in Drosophila melanogaster example of condition mutant or phenocarpy?
This is the original question -
Ques - A researcher exposed Drosophila larvae to 37°C during their growth. One of the adult flies that emerged had a crossveinless phenotype. When this crossveinless fly was crossed to a known crossveinless mutant fly all the progeny had normal phenotype. The options had both condition mutant and phenocopy.
What is the difference between condition mutant and phenocopy?
Any specific points I can use differentiate between them in such a question?


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Why do many plasmids for Flp-mediated Flip-Excision only flanked by one FRT site on each side and not two non-homologous?
I'm trying to build some molecular gene switches into a model, and want to use both Cre and Flp. I understand how to invert gene segments with Cre, double floxing (e.g. with loxP and lox2272, like in this plasmid for example). To do the same with Flp/frt, I was looking at Plasmid constructs on Addgene, but most results are only flanked by one (inverted) FRT site on each side. From my understanding, this would lead to flip-flopping back and forth, so when FLP is not expressed anymore, you'd get a 50/50 distribution.
Can somebody explain to me why they do not use two frt sites, but instead one?
Thank you very much!


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Can a neuron produce electric or magnetic effect?
According to my view,As a neuron is an electrical impulse generating cell and through this impulse it carries information from brain to whole body or vice-versa, As here a very small electricity is generated so there must be some electrons which can produce an electrical or magnetic effect !

Any time charges move (current), electric and magnetic fields are created.
Neurons involve quite small voltages, on the order of 100 mV as well as small currents. Neurons process and transmit information through small changes in voltage, but they generally return to rest. That means, over a long time scale, the net electric and magnetic field is going to be zero: everything averages out to some steady state. Neurons and their fibers are made up of roughly spherical or cylindrical compartments, and voltage is going to be roughly constant within those compartments (because a solution with dissolved ions is a good conductor). That means the changes occur along the edges, and think of a sphere: if the same change occurs all around the entire surface, once you get sufficiently far away you're going to see all those fields as cancelling each other out. For a cylinder, the cancelling will occur in every direction except along the long axis of the cylinder.
That said, populations of neurons that have synchronous activity and are arranged in favorable orientations (like that of pyramidal cells in neocortex) can create detectable electrical and magnetic fields. Electroencephalography and magnetoencephalography are commonly used techniques to measure this brain activity (electrical and magnetic, respectively) from outside the skull.


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Can humans metabolize D-malate?
Only the L-isomer is produced naturally, while racemic mixtures are produced synthetically and used commercially as food additives and energy supplements.
So what happens when we consume D-malate? Does it just partake in the Krebs cycle, the citrate-malate/malate-aspartate shuttles, and such like the L-isomer?
Or, does it just bioaccumulate and/or inhibit these processes? Until it gets excreted out?

An interesting fact that is probably of no physiological relevance, but nonetheless interesting, it that the product of the reduction of oxaloacetate by isocitrate dehydrogenase is D-malate! (see Reduction of oxaloacetate by pig liver isocitrate dehydrogenase) OAA is a very good substrate for ICdh.

I do not have specific proof, but I strongly suspect that the answer to this question is NO on the basis of the following arguments.

The overwhelming majority of sugars, amino acids, carboxylic acids
and other metabolites with and asymmetric carbon atom have been long
known to occur in only a single enantiomeric form within living
organisms. This was established long before the nature of the enzymes that catalyse their reactions were characterized.
Since the 1950s and 1960s we have understood that the stereo-specificity of enzymic reactions reflects the weak but binding of (co-)substrates to specific chemical groups of amino acid residues in the active site, and the subsequent flow of electrons between the bound components (often including the amino acid residues). The overall three-dimensional structure of the interactions that allow such catalysis only occur with one form of the enantiomeric metabolite.
The fact that malate (e.g. in fruit such as apples) only occurs in the L-form indicates that the reactions which involve it (predominantly malate dehydrogenase and fumarase) conform to the principle just expounded.
Although racemases (enzymes that interconvert enantiomers) exist for certain compounds in certain species, malate racemases have only been reported in obscure bacteria. They are not known to be present in man.

The problem is that this is so well established that studies with D-malate of relevance to the question are hard to find. One thing to do would be to examine the three-dimensional structure of malate dehydrogenase with a suitable malate analogue bound and model the enantiomer. This requires some work — a cursory trawl shows that usually the enzyme is crystalized with the product, oxaloacetate bound.
I have not looked at the mitochondrial transport system involved in the shuttle: something else for the poster to try. Nor can I find information on whether D-malate is taken up by the gut, and what its fate is if it is.

Interesting! Just found https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1185386/ (back from 1970, found to inhibit gluconeogenesis from malate but without any effect on the TCA cycle otherwise)

@ManRow — The problem with this type of paper is that it's all "what" and little "how". That's not to criticise the work, which in the context of the time provided data to test hypotheses about the pathways. However if people sell malate as a supplement you would think someone should do experiments following the fate of radiolabelled  D-malate in, say, rats. Not the cutting edge of science, but you would think the FDA would demand something of the sort.

@ManRow — In case I did not make myself clear, the interest here was not in D-malate per se, but in what inhibitors might reveal about L-malate metabolism.

The existence of D-amino-acid oxidase (discovered by Krebs) is surely an exception to this argument

@user338907 — You need to explain more clearly which of my points it negates, and it would be of interest if you could mention what is known of the function of that enzyme. At the moment I don’t see any connection with D-malate.


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How do plants that grow underground legumes/nuts distribute their seeds?
It makes perfect sense to me when plants employ some sort of method of distributing their offspring some distance from the mother plant. If the mother plant dies due to that location not being ideal, the offspring could potentially find somewhere better. Though, plants like peanut plants that grow their seeds in the same location don't make sense to me. How do their seeds travel distances and spread across land? How is this method effective enough to be passed down through evolution? It seems awfully counter intuitive to me. I tried figuring this out on google but couldn't find anything that answered this.

How do other seeding plants spread their progeny - might this still apply?

the plants you mention in your question uses bacteria to convert nitrogen to nitrate,so the plants provide fertilizer to the soil where it places the seeds.

Searching for "how do peanuts spread" lead me to http://bioweb.uwlax.edu/bio203/s2012/steinmet_vero/reproduction.htm, an excellent site where your question is answered (considering peanuts).


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White oak germination in autumn — Leaves or just roots?
I collected fallen acorns from a white oak tree in Toronto, Ontario, in mid-September 2023. The acorns were germinating at the time, so I planted them (in a cage to protect them from rodents).
So far, only roots have grown, no leaves. Is it normal for only roots to grow in this case, saving leaf growth for the spring?

All seeds start by putting down roots, which allow the first set of leaves to absorb water/swell, splitting the seed capsule. How much time this takes depends on conditions, but it's weeks for acorns, not months.

@anongoodnurse It's Nov 13 and still no leaves: https://i.stack.imgur.com/CUxic.jpg

Clearly they have germinated, so that's good. Is it very cold? is there sufficient moisture? I don't know how many weeks, but if you like, you can google the time span for the Toronto area. Maybe (maybe) it's different up there?

@anongoodnurse You might find Falko's answer interesting. And my comment on that answer to.

Nice to know. Thanks!

Nice that you started observing so early, so I can complete this here while learning something. I usually only get aware of the new oaks when stem and leaves are sprouting in the lawn, and, yes, that's in spring. I always asked myself why they already have such a large root. This makes it clear.

I brought the pot of acorns into the house a couple of months ago. To be honest, I forget why; maybe to protect from freezing temps. I dug up one of the acorns just now to see how much roots it had. And I removed the acorn's shell to see how it looked inside. Here's a photo. https://i.stack.imgur.com/nxZqj.jpg It's hard to tell, but the main root actually broke off when I dug it up. So it was likely a few inches longer. Also, here's a photo of my pot/cage setup: https://i.stack.imgur.com/bID5L.jpg. I screw the wire waste basket onto the bucket to protect the actorns from mice, squirrels, etc.

A friend took some of the acorns at exactly the same time/place. But he planted his indoors right away. Here's a photo from Oct 14, 2023: https://i.stack.imgur.com/OXHVn.jpg. His leafed out, I guess due to the warm conditions.

@User1974 - Oooo, nice little oak there!

I wonder. Generally it seems that acorns, as chestnuts, don't survive a dry out. So these are seeds that work differently than, say, peas or corn. I don't know any general distinction of plant groups along this difference. Yet :-)

@anongoodnurse and Falko: The acorns/roots now have leaves (indoors): https://i.stack.imgur.com/5A6Yv.jpg


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Troubleshooting direct sandwich ELISA
I am validating an ELISA measuring A1c (also called glycated hemoglobin; target for humans) for use in another species. It is a direct sandwich assay. The standard and my sample (whole blood) were both serially diluted twofold.
I am wondering if anybody can help diagnose what I am seeing in my parallelism graph. As you can see, the curves are near inverse of each other (linearity R2 = -0.91). Since it is a direct assay, I would of course expect this correlation to be positive.

I have gone over my plate map and how I set up my dilution rack a hundred times in my head, and I am quite certain that I did load my plate in the correct sequence as my plate map - ie, having both standard and sample increase in concentration down their respective column. Is there any other possibility (besides me incorrectly loading my plate according to my map) that could cause this "perfectly incorrect" parallelism correlation?
I would love to be proved wrong and find out that it was indeed my error in loading - but I'm pretty sure I loaded it correctly...so I just wanted to check if there was any biological answer to this (matrix effect?)
I plan to run another plate tomorrow to check- but just wanted to ask.
Thank you!

It might be that there is a molecule present in your whole blood samples that masks your target epitope. Diluting the sample would also dilute the masking. But this is only one possible explanation, I guess there are more variables to consider to find a complete solution.


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Are there two different senses of the word 'heritability' in use?
Target Height as Predicted by Parental Heights in a Population-Based Study states:

The heritability value was taken as the regression coefficient between
final height and midparental height

Is this the same sense of the word 'heritability' that is in use in https://en.wikipedia.org/wiki/Heritability and in answers on this site, namely Var G/Var P? Or are there two different senses in use simultaneously?
Edit: see https://www.jstor.org/stable/2531017 ... heritability h^2 is defined as follows:

Note the superscript (1/2) in the equation, indicating a square root. So the slope of the regression does not seem to be a ratio of variances.
FWIW, Wikipedia cites the S.E.P., which cites Behavioral Genetics by Plomin.

Possible duplicate https://biology.stackexchange.com/questions/59053/heritability-in-population-genetics, https://biology.stackexchange.com/questions/112552/is-heritability-just-slope

Does this answer your question? Why does the slope of parent-offspring regression equals the heritability in the narrow sense?

Actually this question answers your question. Basically if you do a bunch of math, the slope reduces to the (narrow-sense) heritability. Var(G)/Var(P) is usually broad-sense heritability, but it's hard to do infinitesimal math with the broad sense heritability.

@MaximilianPress I'm not sure that it does answer my q. It cites https://web.archive.org/web/20210420073545/http://userwww.sfsu.edu/efc/classes/biol710/heritability/heritability.htm#Oosterhout, which states (without proof or reference) that "The slope of regression of offspring on parents will tell you about resemblance between relatives, h^2". The maths in the Q/A don't add anything to that assertion.

The page you cite https://en.wikipedia.org/wiki/Heritability expresses the general concept in the first sentence:

Heritability is a statistic used in the fields of breeding and genetics that estimates the degree of variation in a phenotypic trait in a population that is due to genetic variation between individuals in that population.

This is a conceptual definition, not a mathematical one. Variance is only one statistical measure of variation; see also https://stats.stackexchange.com/questions/88348/is-variation-the-same-as-variance
I would consider a statement like "Heritability = H2 = Var G/Var P" to be not a different sense but rather an operational definition that says "in this context, we'll use this mathematical representation of the concept".
There are multiple ways to estimate or compute heritability, some of them addressed in that same article under the heading "Estimating heritability", including methods based on correlations and regression. For a simple, univariate relationship, the Pearson correlation r and the coefficient of determination are related, in that the coefficient of determination is r2 and the same as R2 and the same as the "variance explained".

So... when you see in a paper a statement like "___ has a heritability of 0.7", how on earth are you meant to make sense of that? What about meta-analyses which look at the heritability of different traits?

@Mohan In a paper producing numbers, they should be clear about what the number means; in a sense, it's a lot like how you could say something "weighs 60", but this isn't really something you can make sense of, they need to provide the units, too, so you know they're talking about 60 kg or 60 g or 60 lbs. In this case, there are no units, but you still need to know what the quantity is to make sense of it, and especially if some people are giving you a square-root version of what other people are giving you (e.g., r rather than r^2).

Thank you. Having looked into this further, I think what's confusing in this case is that not just the term 'heritability' but also the specific expression h^2 is being used to denote two different quantities, one of which is the square of the other.  [See my edit to my Q.] Sometimes a single paper seems to use both senses -- see e.g. the Plomin textbook I cited. I almost wonder whether someone looked at eq(5) in the paper I quoted and missed the square root symbol, and then that error has propogated through the literature?

@Mohan I don't know enough about the history of the term to know why h^2 is used; on the statistics side, R^2 is useful because it's interpretable as the fraction of variance explained, and also because it doesn't make sense for sign to enter into it; a squared quantity will always be positive, when you take a square root it's ambiguous whether you started with positive or negative numbers.

Another place it comes up a lot for some overlapping reasons is in variances versus standard deviations; standard deviations are useful because they are on the measurement scale. Variances are useful because that's the scale on which variation sums.


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Water consumption of the average housefly
So, I have this question:
How much water does the common fly consume in its lifetime?
I was able to find the following facts:

Born from swine waste under 40% (waste to water ratio)
Lifespan of 15-25 days
They are 40-45% water (the flies)
avereage weight (in mg) 0.005 to 0.01 (the flies)

Also, I'm not sure where, but, I heard that flies defecate whenever they land, but I'm not sure on size or frequency.
Here are my resources:
https://en.m.wikipedia.org/wiki/Housefly
https://www.arrowexterminators.com/learning-center/pest-library/flies/house-flies
https://www.researchgate.net/figure/Average-weight-of-flies-Each-bar-represents-the-mean-and-range-thstandard-deviation-The_fig3_318433682

Welcome to the Biology Stack Exchange. Please take a [tour] and visit the [help] for more information on this stack and what makes a good question and answer. That being said, we need a bit more information in your post (edit these into the question) - What are your units for the values 0.005 and 0.01 in the list. What is under 40% in point 1. Were you able to find anything on how frequently they drank?

Please don’t waste space telling us you have a question. We’re smart enough to work that out as this is a question and answer site. More to the point, explain why you wish to know something that most of us would find completely uninteresting, and why you think modern biologists would clog their minds with such things. Houseflies, bedbugs, moths, dung beetles… What next?


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What factors allow some species to outcompete species formed by the local environment and become invasive?
If an invasive species is introduced to a new environment, why can they outcompete local species in the same nische, if they specifically evolved in this local environment and are adapted to it, whereas the invasive species would have evolved in a similar, but not identical environment?
What factors determine wether a new species will become invasive or nor be able to survive in the new environment, and can we predict that beforehand?
What does this mean for future space exploration? Lets say, we find life on mars and bring it back (or accidentally bring it back with the sample return mission), what are the chances that it could survive on earth, and what is the probability it could pose a threat to native life?

one of the best examples about  invasive species is iceland,it once had forrests covering large parts of the country and then sheep was introduced,you can read a bit about it here: https://www.skogur.is/en/forestry/forestry-in-a-treeless-land/history-of-forests-in-iceland

Interesting! Thank you very much :)

In this case, the competitive advantage of sheep is obviously that they are useful to humans. But that is quite a special case. I am more interested in the general case. What determines if a species is well adapted, and why are local species not even better adapted to the local environment?

You are right, most species cannot invade most new environments, they have to be specially adapted to the new environment. For example, a jungle frog can't invade a desert; it'll dry out and die.
You are also right that a newly introduced (invasive) species is (almost) always going be less adapted for the new environment than the local species already living there.
So why can introduced species out-compete the locals despite not being as well adapted?
-->Most of the scientific evidence seems to point to a lack of predators in the new area for the invading species.
-->This can make some sense if you think about the power dynamic between predator and prey.  If predator and prey have been living together and evolved to have relatively equal hiding and hunting ability, then they can coexist.  But if a prey and predator have never encountered each other, it's possible there'll be a power imbalance.  Perhaps, the predator is really good at hunting the new prey, or maybe the prey is really good at avoiding the predator.  If the prey is invincible, then it becomes an invasive species in the predator's habitat.  If the predator is invincible, it becomes an invasive species in the prey's habitat.
I love that you're thinking about space, but science can only really answer testable questions. -- Mars Aliens -- aren't really testable right now.
That said, probably the Mars aliens would win since their incompatible chemistry would be to their benefit.  If we assume the aliens are made of weird chemicals that nothing on Earth has evolved to digest, then we wouldn't be able to eat them and derive energy, so they probably wouldn't have any predators at all.  But why would they be able to eat us? Well, just like astronauts on Mars could live off the ice we find at Mars' poles, probably the Mars aliens would be able to find something similar, some of their chemicals here on Earth that they can still use for themselves to take over.
--> But I don't think they'd be eating us humans any time soon! :)

Oh, I was thinking about Bacteria from Mars (either by bringing back soil, or even naturally, through Panspermia). The predator-prey relationship is certainly interesting! Would it be correct to say that invasive species usually do well in environments, if those environments themselves have undergone radical changes recently (for example, certain predator species dying out, recent changes in climate, ...)?

Because what confuses me: If there is an obvious niesche, like animals that can kill turtles on an island, where before, they had no natural predator, why did no other animal evolve to fill that niesche? Is it just a question of time? (iE would there have been canivorous dodos hunting other dodos if we had left them alone for another couple million years? Or are environments like that stable without outside interference?)

And since you mentioned predictability: Is there any way to quantify what environments are "at risk" of invasive species surviving there, vs environments, where most introduced species would not pose a threat? Is there a way to quantify if a specific species would pose a threat to a local ecosystem if it was introduced there?

I don't know too much about the evidence on recently disturbed environments, but it is well studied by ecologists worried about human disturbance,  I'm sure you can find lot's of information about it.  Maybe even post it here as answer afterwards.  I remember hearing about it once in class, and I think it depends how the environment is disturbed,  some disturbances open up new niches, while others just destroy the environment, lol.

re 2nd comment: no! environments are not stable without outside involvement.  Look up the experiments on trying to establish a mars or moon style colony prototype here on earth.  they can't do it because inside the locked away biomes, nature does it's thing and the ecology comes crashing out of balance.  Also look at the rabbit fox/wolf simulation experiments where they show the expected predator/prey boom bust cycles.  all that said, yes, I do expect eventually we would see dodos evolve to eat other dodos. and then once that new animal evolves, new parasites would evolve to parasitise it...

re 3rd comment: yeah, definitely investigate the literature for all that,  I don't know much, but I think it's well studied.


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Primer dilution verification
I just received a primer (details are displayed in the picture). Since this is my first time doing this, I want to do it correctly. My goal is to make a 10µM primer.
So, If I get it right and based on the paper I received, should I have to add 665μl Sterile distilled water (Inside the primer tube) and then aliquot 90μl Sterile distilled water with 10μl of primer tube mix?

Yes, this is correct. Note that it is not important that the water has been sterilized, it needs to be nuclease free.
Also, for long term storage TE buffer might be a better choice. This will not result in inhibition of your PCR by the EDTA component of the buffer, since the amount of it in the final reaction is neglectable.

Thank you very much for the response as well as for the tip!!!!

@KGee If this answer helped, make sure to accept the answer by clicking the checkmark


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When Rain Lilies Bloom
I have had the Pink Rain Lilies in a large pot for over 10 years. In that time span, I have noticed it doesn't matter how much water, or what kind, is given to them, I water them daily in warm weather. They do not ever bloom unless there is a storm. For instance, I am in subtropical Queensland, Australia and a few nights ago, we had an electrical storm. It started 4 nearby fires. I heard a couple of drops of rain on the roof, but it stopped as fast as it started. Where my pot of lilies is sitting, I doubt a rain drop even fell on them. I have experienced these kinds of dry storms many times in the past, it's very typical here. The next morning, there was a Pink Rain Lily flower, as is the case after every storm, rain or dry. So, my question is, could it be the nitrogen released in a storm that they are sensitive to?


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Does the duration of the head-hair growth phase differ between men and women?
I found one website which claims the following

The growth phase of the hair is called the anagen phase. It lasts
about 3 years in men and 5 years in women.

Another website makes a very similar claim.
The problem is I can't find any journal article which supports the idea. Is it true that the anagen phase lasts longer in women than in men? And is there published research to prove it?

Both these articles are from companies that sell cosmetic products. If their "research departments" have any data to support any scientific statements they make they are unlikely to be interested in publishing it. It sounds uncontroversial and may be old observations or old wives' tales nobody has cared enough about to investigate. Not where modern biology is, for sure, but you never know whether your bounty will bring something out of the woodwork.


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What is the most accurate polygenic score for Alzheimer’s disease?
To date, which polygenic score (i.e. which study) has produced the largest effect size for Alzheimer’s prediction in out-of-sample validation?


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Can the complement of the start sequence occur in a gene?
Put another way, I suppose I'm wondering if the start sequence of a gene always actually starts a gene. If so, I assume it means that the complement of the start sequence in one strand would always start a gene in the other strand, but forcing some prefix of two genes to be complements of each other seems like it would make things a bit messy (but then again, when is biology ever not?).
I gather from this answer that this is more complicated than ATG (ie, AUG's complement's complement) occurring in the middle of the coding strand, but even if the start sequence is ATG + some other stuff (or rather, the other way around) it seems like the same problem with a longer sequence.
If not, then how is the start of a gene distinguished from a sequence that coincidentally happens to be the start sequence? One step further, how is that mechanism (which must not be part of the DNA sequence itself) reproduced?
Edit: After some snooping around it looks like the sort of "mess" I imagined can and does occur and is called "divergent gene overlap". So I guess the answer to the question I put in my title is yes. (?)

(Disclaimer: In case it wasn't abundantly obvious, I'm very new to all this so apologies if this doesn't make sense and please let me know if there's context I'm missing I need to do some reading up on! Thanks!)

Welcome to Biology StackExchange! You have to differentiate between transcription and translation. Start codon has nothing to do with the initiation of transcription, it is the promoter.

Further to @Domen, please do some reading to clarify for yourself the start of a gene (DNA) — the promoter, specifing the start of its transcription to RNA; the start of the mRNA (which in eukaryotes is capped by a methylation sequence), and the start of the region translated into protein — the initiation codon (most frequently AUG). You will then realize that your question and title need clarification at the very least — "start sequence of a gene" has nothing to do with AUG (or ATG). Also, "complement" is  wrong — the complement of AUG is CAU. You mean same sequence on the opposite strand.


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Validating Generative Models for 3D Conformations of Inactive Dopamine Receptors in Protein Design
Considering a dataset comprising 3D conformations of Dopamine receptors in an inactive state, we aim to train a generative model capable of capturing the distribution of these receptors and generating new 3D conformations. How can we ensure that the generated 3D conformations correspond to valid representations of Dopamine receptors, particularly in the context of protein design?

The hardest but most robust method would be to express, crystallize, and solve structures for the proposed dopamine receptors. Are you specifically interested in bioinformatic methods?


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What kind of spider is this (from Bangladesh)?
I just saw this spider in my bathroom. I was wondering what kind of spider is this and if it is venomous.
Country: Bangladesh

Only three Sparassidae (huntsman spider) species have been observed in Bangladesh on iNaturalist. Only one looks anything like the individual in your photo: Heteropoda venatoria. I venture it's a male based on the dark brown patterns on its prosoma and the overall body's lighter brown color. Most spiders are venomous, but according to a University of Florida IFAS publication, this spider isn't dangerous to humans. Hopefully this helps.

Thank you. This is the answer I was looking for.

Glad I could help!

This is a huntsman spider , which is venomous but it's affect on humans is not so reactive , it's not can cause several symptom like itching, swelling,in more severe vomitting and nausea like ,
It was a coincidence to identify it because my cockroach also have the same upper structure like it so. I thought it should have some relation and the results were **these are cockroach eating ** I didn't know the exact reason behind this unique relation


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Does recombination occur in both chromatid of a chromosome with homologous chromosome? Or only 1 chromatid participate in crossing over?
A chromosome has two chromatids. In meiosis weather both chromatid participate in crossing over or just only 1 chromatid does?

So, I am asking whether 1 turquoise and 1 purple chromatid participate in crossing over or both chromatid of turquoise and purple chromatid participate on 1 to 1 basis?

The diagram you provide is just a schematic, showing a simple version to clarify what is happening in a crossover. It seems that at least once crossover has to occur in each bivalent for normal chromosome segregation to take place. This is called obligate crossover. Multiple crossovers do take place, but in eukaryotes this is usually limited to be four crossovers or less for each chromosome pair.

I think like that , different alleles coding for different traits are present on different positions on two chromatids
So both can participate in the recombination  only when chromatids of torquoise and purple have contrasting characters present on each chromatid
Conclusion :- both chromatids of a chromosome will participate in recombination but at different time

Different time means in different cell cycle? So in same cell cycle can both chromatid recombine?

Different time means in one cycle as there are no only one  trait to recombine in one cycle , for eg. If two genes coding for blonde hair and tall height separately but present on a same chromatid then they will recombine with the chromatid having respective alleles on non - homologous chromosomes at different time , as one chromatid can not perform two recombination at a same time , it was my opinion!


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I learnt that anterior axillary folds are formed by pec maj but I can palpate and feel a hard tendon like structure
What is that hard tube like structure that I can feel in anterior axillary folds? I think it can’t be pec major because it’s tendon is bilaminar not like a tube? Is it suspension ligament formed by clavicpectoral fascia in anterioinferior axillary part? I am just curious

Flex various muscles in your arm while feeling the structure. The action which causes the tension to increase should give you the answer. Please note that we ask that you show evidence of searching for an answer when you ask a question. You've asked a number of them without doing so, and I even answered an early one. Please follow the site's requirements. It will get you the answers you want.


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What protein or other process does the peptide BPC-157 come from?
BPC-157 is a peptide for which there were some studies that suggest that it can help with wound healing and gastrointestinal problems in some animal models. In 2022 the World Anti-Doping Agency added it as a forbidden substance.
A patent suggests that it can be extracted from human and animal gastric juice, but it was from the time before the human genome project, so they don't mention the actual protein it comes from.
My attempts at running BLAST only bring me to the synthetic Usp-BPC-157 and not to any protein that could plausibly be the source in humans or other animals.
Can someone tell me how the body creates BPC-157 naturally, either from what protein it's a breakdown product or otherwise how it gets into human gastric juice?

As far as I can tell, it's a made-up scam.
Almost all of the research on this peptide is done by one person, Predrag Sikirić, who also discovered and patented it.
The claim is that this is the "important part" of some other, larger protein that he claims to have isolated from the gut. E.g. from Jelovac, N., Sikiric, P., Rucman, R., Petek, M., Marovic, A., Perovic, D., ... & Prkacin, I. (1999). Pentadecapeptide BPC 157 attenuates disturbances induced by neuroleptics: the effect on catalepsy and gastric ulcers in mice and rats. European journal of pharmacology, 379(1), 19-31.:

We have identified a new human gastric juice protein with mucosal protective properties and a huge range of organoprotective effects, and with MW 40,000 (determined by gel chromatography), code-named BPC.
...
In line with this, a 15-amino acid fragment (BPC 157), with amino acid sequence, Gly–Glu–Pro–Pro–Pro–Gly–Lys–Pro–Ala–Asp–Asp–Ala–Gly–Leu–Val, MW 1419, and apparently no sequence homology to known gut peptides, thought to be essential for activity of an entire peptide, was characterized and synthesized

Okay, so apparently this MW 40,000 protein has a "huge range of organoprotective effects", except... it doesn't seem it's actually been studied, ever. Let us follow some citations... The earliest paper those passages refer to is this one:
Sikirić, P., Petek, M., Ručman, R., Seiwerth, S., Grabarević, Z., Rotkvić, I., ... & Karakas, I. (1993). A new gastric juice peptide, BPC. An overview of the stomach-stress-organoprotection hypothesis and beneficial effects of BPC. Journal of Physiology-Paris, 87(5), 313-327.
From the paper:

A new gastric juice peptide, Mr 40000, named
BPC has recently been isolated (in preparation)
and its huge range of organoprotective effects has
been described. In this, a 15 amino acid fragment
(BPC 157) thought to be essential for its activity
has been characterized (Sikiri6 et al, 1991a,b,
c,d,e,f,g, 1992a,b).

Okay, so they've already got this peptide from gastric juice, already found and "fully characterized" (quote from the abstract) it, all in just 2 years. I can't think of anything in biology that is fully characterized and it takes decades to do this kind of work with modern methods, yet this was done by one group in a couple years! Within just those a,b,c,d,e,f,g references in 1991 they've already shown that this peptide cures kidney lesions, pancreatitis, colon hypersensitivity, diabetes, liver lesions, and stomach ulcers. And all of this work on the peptide was completed and published before the discovery of the original MW 40,000 protein was ever published (that's the "in preparation" note from the quote; I can't find evidence that the "in preparation" manuscript was ever published). All of these papers with the same lead author. This is not credible, at all: no one can perform all this work. My best guess is that it is made up entirely. The "1991a" reference is this one:
Sikiric, P., Petek, M., Rucman, R., Rotkvic, I., Seiwerth, S., Grabarevic, Z., ... & Udovicic, I. (1991). Hypothesis: Stomach stress response, diagnostic and therapeutical value: a new approach in organoprotection. Exp Clin Gastroenterol, 1, 15-16.
Along with several of these other papers, it makes up the first volume of the journal "Exp Clin Gastroenterol", which appears to have been created solely to host this new, influential work. I can't really find any trace of it. Google Scholar can't find any of these papers. There is an (also sketchy) journal with a similar name hosted at "gastrossr (dot) org" that only took that name in 2002 but does not seem to have any relation.
So, let's review...
A larger protein, never before described but supposedly isolated from the stomach, cures everything. Before this protein is described in the literature (nothing published on it at all), one person has already identified and synthesized the important 15 amino acids from it that are responsible for all of its activities across all body systems. All further research is done with this peptide.
The peptide and precursor protein are unrelated to any other protein (e.g.: your BLAST attempt; also, there is no mention of any related protein in any of these papers, including recent ones).
The peptide is patented by the person who publishes all the papers about it's benefits.
The original work describing the peptide was published in a brand-new journal; I haven't found any evidence that the journal actually exists. I suspect it's a creation of the person who "published" all of its content, including a dozen first-authored papers in the first year that this peptide was discovered.
The name: BPC, stands for "Body Protective Compound". So, before doing this research categorizing all the ways that it protects the body, it was already pre-ordained with the name "body protective compound". I assume this is because the author already knew what his results were going to show, because he planned to make it all up.

Can someone tell me how the body creates BPC-157 naturally, either from what protein it's a breakdown product or otherwise how it gets into human gastric juice?

I can't find any evidence that it does; in a 'research' context it's an entirely synthetic peptide. The papers supporting it seem to be entirely synthetic, as well. As of now there is only one result for a search of "BPC 157" as a treatment/intervention on clinicaltrials.gov; this was a Phase I study that was cancelled; it's not clear whether a single patient was ever enrolled. You can find sources that sell or claim to sell it, in some cases labeled as "for horses", in others as a dietary supplement for humans while repeating some of the dodgy claims in these papers, despite never being studied in people. I won't link to any of these sources for what I think are obvious reasons.

Nice work Bryan!

Even when I hoped for a different kind of answer, this is likely the right one. I sent Examine.com a message over their contact and it will be interesting to see whether they retract their claims.

@Christian I'm not familiar with that website, I don't think I've encountered it before your link here, but I would not really consider it a reliable source, though I'm also not immediately seeing anything there that is wrong, rather that it's misleading merely because it does not provide sufficient context. That's why we have regulatory authorities rather than letting patients decide from direct marketing based on studies: the quality of published evidence requires professional expertise to interpret.

Wow, such a rabbit hole to fall down. I don't understand the economics of all this. This person has published an article about this made up peptide every month for 4 months straight in an MDPI journal this year. They seem to make the rounds every year to different open access publishers.

@IanCampbell It's pretty remarkable, isn't it? And the papers will claim "no conflict of interest" when the author is the guy who has a patent on the main study ingredient... It must be sold by someone for it to catch WADA's attention enough to make a banned list, but it doesn't seem popular enough that anyone reputable has gone after it. I didn't find any press about any accusations of fraud or similar though I didn't look extensively.

I was also surprised by the WADA's action. Could it be guerilla marketing? Fake peptide person convinces friend on WADA to add it to the banned list. Potential customer sees that it is banned and so must be useful and then buys it to get ahead?

@BryanKrause : Examine.com is an independent subscription-based website that hires people with professional expertise. That makes it business-model very different than all those websites that make money with affiliate commissions to sell supplements. The particular article was written by someone with a MS in nutrition and fact-checked by two other people who also have credentials. When it comes to nutritional supplements it's normally one of the better sources. That's why I cite it in the OP instead of citing on of the supplement sale websites.

@Christian Still, their business model sounds like it favors selling supplements: if people subscribe to find out "none of these supplements are supported by actual evidence; if they were, they'd be sold as medications and recommended by doctors", they're not going to hold a subscriber very long who is convinced these things work and looking for someone to tell them that.

@BryanKrause : There's a market for people who do believe that some supplements work and at the same time there's a lot of crap in the supplement market and who want someone they can trust instead of listening to Mercola.


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How does the area under the curve mean the total exposure to the drug?
I was wondering how the area under the curve in the case of a conc against time plot would be equal to the total exposure in the body? I know that this area is integrated using

AUC = ∫C dt

However wouldn't that mean - according to my understanding - that the product of this is the sum between the total conc of the drug and the time as the latter is a part of the calculation? And if it's the case, wouldn't that mean the AUC isn't just the total exposure?

can you post a reference for this, whatever the materials you're looking at? a diagram might also be helpful if you can post one. It also isn't clear to me what your logic is. To me, it makes sense that if I've had 10µM drug at time 0, 8µM at time 1, 2µM at time 2, that overall my body has experienced 20µM of the drug if those are the 3 (hypothetical, infinitesimally short) times that we care about. Can you be more specific why this doesn't make sense to you?

I would think of this as a definition: the definition of "total exposure" is the product of concentration and time, in other words, the area under the curve if the curve is time versus concentration.

Welcome to SE Biology. Please finish reading the [Tour] and edit your title so it has some meaning. Referring to “the curve” just will not do. You need to say what the curve plots, and if that seems too long-winded, give a title that expresses the concept involved. In any case the curve should be described in full (preferably as an illustration) in the question itself.

Wikipedia has an article on [AUC] (https://en.m.wikipedia.org/wiki/Area_under_the_curve_(pharmacokinetics). You should read it. It represents the total drug concentration the body was exposed to. Per the Wiki article, it can be used to compare tissue exposure to different formulations (capsules/tablets) of drugs.

If by you, you mean me, there is no obligation on me to read an article that some anonymous person has written on Wikipedia to clarify a phrase in plain English that is so vague as to be useless in a title. In your actual question, where you use the abbreviation AUC (the codon for isoleucine, I presume) you do not define it. You still have not done us the courtesy to finish reading the [Tour] of this site which explains how it works, but presume to tell us what we should do. Read it, then you will learn what you should do.