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Are acid-fast bacteria Gram-positive or Gram-negative?
Both procedures involve using a stain, decolorising agent, and then a second stain. I am tempted to conclude that acid-fast bacteria, which resist decolorisation (eg. by strong carbol fuchsin), also resist decolorisation in the Gram staining test (eg. by gentian violet) and are thus Gram-positive.
After all, there are much fewer acid-fast bacteria than Gram-positive bacteria.
Is this line of thinking incorrect?

Image URL: http://www.scienceprofonline.com/images/science-image-library/microbiology/staining/differential-bacterial-stain-controls-diagram.JPG

Taxonomic Classification:
The most salient acid-fast bacteria are Mycobacterium spp., which are part of a phylum of gram-positive bacteria called Actinobacteria. This classification is based on 16S rRNA sequencing. However, based on genetic conservation, this paper makes the claim that they are more closely related to gram negative bacteria.
Gram Reaction:
Acid-fast bacteria are characterized by cell walls rich in mycolic acids. This characteristic causes both poor stain penetration and high stain retention which forms the basis of acid-fast stains. However, it also means that crystal violet will not penetrate the cell wall efficiently. Thus their gram reaction is variable and they generally stain light purple. The result is dependent on technique as well as mycolic acid content variation between genera (Nocardia spp, for example, are less acid-fast and stain gram positive). Needless to say, their cell walls don't fit well with the classic dichotomy of thin versus thick peptidoglycan which the gram stain differentiates between.
Example Gram Stains:

For comparison, the left image is of Bacillus subtilis, a gram positive, non-acid-fast bacilli. In the middle is M. phlei and on the right is M. smegmatis, both of which are acid-fast but show a weakly positive gram reaction. Images from Napa Valley College.

B. subtilis is again on the left for comparison. In the middle is M. fortuitum staining positive but more weakly than B. subtilis. On the right is N. astroides which is partially acid-fast but stains strongly gram positive. Images from Microbe Canvas.


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Is there any evidence for the validity of RNA/DNA supplements?
Is there any evidence for the validity of RNA/DNA supplements?
I've recently been seeing advertisements for RNA and DNA health supplements in the form of a pill, which claim to perform some rather miraculous functions within the body, though I can find no scientific validity behind this. There are some very respectable companies including Holland and Barrett selling this stuff and I can't see how this would provide any health benefits.
Are there any studies on this? If not, may someone care to speculate if there could be any health benefits to RNA/DNA supplements or is this just a terrible gimmick?

I skimmed through this website and couldn't help but laugh at this: Results of a bold new study from Kashkow University’s School of DNA and Medicine, expected to begin next year, were announced yesterday. They have been called a “breakthrough” and a “game-changer” by some of the leading scientists on the proposed study. Aside from the fact that it makes no sense... Kashkow University?

haha! Brilliant. I especially remark at the comments of Cyrus Tosine

Says it all really. I'm just looking for any particular papers that conclusively refute it as idiots are being taken advantage of

@canadianer Where did you find this blog? It's incredible. Also "Credulity, WI": where people are incredulous? (of course there is no such town, unfortunately - I'd love to live there) "University of California at Boulder" - one of the most covert of all University of California schools... And where Cyrus Tosine is about to say it could help people "concen" ---trate? Seems either Cyrus or the author really need this product! Really truly brilliant piece, rivals anything in the Onion.

@Charlie The burden of proof is on the claimant; I don't expect there to be a lot of research based solely on refuting a ludicrous idea.

Yes I suppose. It however bothers me that this is being sold not only in dodgy online markets but stores people should be able to trust.

The website that canadianer linked to is meant to be satirical about these useless supplements. Despite that, comments left on the site still shows people think he's saying DNA/RNA supplements are good. Love his wit!

It didn't take me too long to realise it was satirical

source: Stack Exchange

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What happens if you mix brain waves?
I was learning about brain waves, i.e. gamma, alpha, beta, etc., and was wondering what would happen if you mixed them together - e.g. I listened to Gamma waves and Delta waves at the same time. Would I get some sort of brain damage or is the brain able to handle that?

Your question is very unclear. What do you mean by "listening" to brain waves? Do you mean hooking someone (yourself?) up to an EEG and using software to translate the various types of waves to sound? The only damage you'll get is to your ears if the volume is too high. Why on earth would you get brain damage?

Everyone has a mix of ongoing oscillations, of brain waves, at any given point. Some frequencies of waves are more or less likely to co-occur with other types of waves.
In general, brain activity follows roughly a power law distribution - that is, there is more power at lower frequencies and that power decreases in a predictable way as you go to higher frequencies.
When researchers talk about brain waves at a particular frequency, they are talking about a deviation from power law at that frequency - if they say "gamma waves" what they really mean is "there is more energy at gamma frequencies than we would expect if things were random."
Some of these deviations are predictable with changes in brain state - for example, low frequency (delta) activity is greater during sleep, and higher frequency (gamma) activity is higher during cognition.
It should also be understood that these terms really come from a method of data analysis such as Fourier analysis that breaks a signal down into component frequencies. It isn't necessary that a signal is actually produced by combinations of sine waves to break that signal down into component sine waves and describe it that way.

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How does the body determine where to deposit fat reserves?
People's bodies store fat in similar areas, but often there are subtle differences in which areas are first or slightly more effected. This seems to also be apparent with morbidity, where certain areas are overburdened with adipose while other areas are less effected. What are the factors the determine which areas exhibit build up, while others do not?


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Why did my isolation streak of an unknown organism on Mannitol Salt Agar turn yellow where there was no growth and magenta where there was growth?
I repeated a culture twice in an entry level microbiology class for our final lab project of culturing a provided unknown organism.  One of the required tests on our dichotomous key was to culture a gram positive cocci in mannitol salt agar.  After repeating the experiment twice as instructed, and doing an isolation streak as instructed, the part of the agar with no growth was acidic while the part of the agar with growth was neutral or slightly basic.  Both cultures were incubated for around 48 hours, and the first one then refrigerated for another 48 hours while the second one was examined directly after incubation. My professor told me to disregard the results and treat it as a negative in my report, but I'm perplexed as to how this result came about.

Yeah it seems kind of impossible on first thought. The sterile plates are red, yes? Do you know what result is expected with your organism?

So she's not allowed to tell me the expected result, but I'd imagine since she told me to treat it as negative the expected result was supposed to be negative.  And yes they were certainly red when sterile.

I just realized I forgot to mention something that now seems important.  I also did a simple dextrose test that came out as orange with phenol red in it when it was expected to come out as red.  Could these issues be caused by a error in the preparation of the indicator?  It makes me wish I could incubate a sterile plate and see what happens.

In my experience, many TAs are not that thoughtful. Are you able to monitor the growth at more time points over the two days? If the plates were red to begin with, the only explanation I can think of right now is that the organism fermented mannitol and produced acid, turning the entire plate yellow. Once the mannitol was exhausted, it started metabolizing peptones which produces base and reverts the colour of the agar surrounding the growth to red.

I was going to say that, if the plate was yellow to begin with, someone might have used the wrong indicator when they were preparing the plates (eg methyl red instead of phenol red).

The orange colour you see is intermediate between red and yellow. It's likely that the pH was near the transition point (pKa)  of the indicator.

The exhausting of the mannitol and utilization of peptones was my first thought and why I was going to mark my first result as positive but the prof redirected me. My knowledge of the creation of the medium is limited however and I was wondering if there might be a simple chemical answer. Sadly I can't check at different intervals or run any other tests so I think I'm just going to write an excessive lab report and leave it in the direction the professor sent me. Thank you for your help thinking about it, though.

I can't think of a chemical explanation unless someone left an uncapped bottle of hydrochloric acid in the incubator. The plates are pretty simple.


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Which co-transmitters are released first?
I understand that a single neuron can release different neurotransmitters depending on the frequency of its stimulation (see https://www.ncbi.nlm.nih.gov/books/NBK10818/). As the frequency of stimulation is increased, what is the order in which the neurotransmitters are released (i.e., which neurotransmitter is released at lower levels of stimulation and which are released at higher levels of stimulation)?

For a specific answer, you'd have to specify a specific neuron type. However, the source you link already discusses the general pattern, did you see that?

The source does say that smaller neurotransmitters are released first followed by neuropeptides; however I am looking for more specific information. Given the following list of neurotransmitters--glutamate, GABA, glycine, serotonin, histamine, dopamine, epinephrine, norepinephrine, endorphins, and acetylcholine--is there a specific order to which is released first based on stimulation frequency?

Those are all small molecules. No, it's not a list like that and it would be inappropriate to make one.

Why are we unable to make such a list?

Because that's not how it works. Read again the source you linked: it's not indicating that neurons release a dozen neurotransmitters in some order, it's saying that some neurons might release a couple different things, and that peptides tend to be released at higher intensities.

Maybe think of it this way: if someone says "people eat more than one thing for dinner, they often have their dessert after their entree", you wouldn't give a list of entrees and ask which entree is eaten before the other entrees.

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Variance in epigenetic drift rate between different species
My question relates to the prospect of (near?) future control of biological aging.
As I understand, it has been recently demonstrated by Prof. David Sinclair's group that epigenetic drift appears to be a major driver of aging, and demonstrated it may be reversed by applying a certain subset of Yamanaka factors. In particular, upon fixing DNA aberrations, epigenetic information tends to be restored with less fidelity than the DNA itself. In the mice in the experiment, the degree of epigenetic changes corresponded well to an aged phenotype in these mice, which was also apparently reversed by applying the above said Yamanaka factors.
See https://www.sciencedirect.com/science/article/abs/pii/S0092867422015707 for more details..
My question is regarding on the existence of "Horvath clocks" that provide a certain measure of epigenetic drift that can be compared across species. That is, do we have some kind a way to measure more of an "absolute" amount of epigenetic drift, allowing to compare this amount in say, mice, dogs and humans? My hope is that this absolute amount would be much greater in shorter lived species, to an extent providing an approximate explanation to the major differences between the lifespans of these species, to further support Sinclair's theory.
Maybe this measure can not be summarized by a single number, even, but rather depend on epigenetic drift in particular DNA regions/presence of certain methylation patterns etc.?

I am not an expert, but having a clear definition / source cited of what you mean by "epigenetic drift" and "Horvath clocks" would be helpful. E.g. in some organisms there is no DNA methylation. What do you do then? Also, my (out of date) recollection was that epigenetic clocks are not uncontroversial as a method of measuring age. Is that really so good of a measure of age? Clarifying and citing sources would again be helpful here.

The fact that some species have no DNA methylation indeed complicates the picture (so lets focus on mammals). I am not an expert either, just a longevity enthusiast.. Regarding a definition and utility of "epigenetic drift" - this is in a sense part of my question. I know that the amount of change relatively to youthful patters ("Horvath clocks") are problematic for estimating age, especially following some intervention, even inside a given species. My question is whether there is any work trying to explain inter-species lifespan differences by such "drift rate".

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Resemblance of a child towards mother or father
Often we see that a child resembles more closely towards either the father's facial structure or the mother's facial structure.
I want to know what determines this resemblance and is it possible to not have any resemblance at all? What is the science behind this?
PS : I am not a biology or medical student. Just a curious mind here.

Welcome to Biology SE! Unless you know of any research suggesting otherwise, I would guess that the impression that a child tends to resemble only one parent is just the result of our bias to only notice when that is the case, and not a real phenomenon. If you are curious about the biology of resemblance, I would suggest reading a primer on genetics and inheritance.

Or, to put it another way, I've my dad's nose and my mum's hairy legs, but people generally see the nose first.

@Eonema : Can you please share the link to a primer on genetics and inheritance?

To put it simply, the resemblance is because of genetics (your DNA). You have 23 pairs of chromosomes, or a total of 46 individual chromosomes. Half of those come from your mother, the other half your father. In some cases, you will get the same copy of a gene from both parents, this is called being homozygous. Having two different copies is referred to as being heterozygous. Blood types are the simplest way to explain this, if both parents give you the gene coding for type A, your blood type will be A. If both give you B, then you are B etc. If you get the type A gene form one parent and the type B from the other, then you are type AB.
Now to finally answer your question on why resemblance varies, some genes are dominant and others are recessive. That means that if we suppose a gene for brown eyes (this is much more complicated) is dominant over blue eyes, then a child will always have brown eyes if they inherit the "brown eye gene" from one parent, regardless of wether they get the blue eye gene of the brown eye gene from the other parent.
So if hypothetically one parent has a lot more traits that happen to be dominant, the child will more closely resemble them. But statistically this will typically be more even. If you want to learn more then you need to pick up a high school biology book.
Sources to explain some of this
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5289863/
https://www.hudsonalpha.org/the-genetics-of-eye-color/


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What is the energy of activation of uncatalyzed ATP hydrolysis reaction? Say in aquous solvent?
By ATP hydrolysis, I mean the chemical reaction: ATP + Water -> ADP + Pi. Focusing only on the reaction, this is a nucleophillic substitution reaction, most likely occuring in SN2 mechanism. But so far, I haven't found a single paper reporting the energy of activation of this reaction uncatalyzed. So, does anyone actually measured/estimated the activation energy of uncatalyzed ATP hydrolysis reaction?

I have searched the literature and found an answer to your question, which I have posted. However in future I suggest questions of this type should be posted to SE Chemistry as it really has no biological content (relevance yes, content no) and that SE site has more users who are specialists in this area.

@Chris and I shave provided answers. If you have a problem with them you should say so, otherwise you should accept one (his is more recent). That’s how this site works.

The activation energy of ATP hydrolysis at in the pH range 3–9 was determined by Kahn and Mohan in 1974 and found to be 28.0 to 20.7 kcal/mole. At neutrality (i.e. uncatalysed) it would appear to be:
approx. 23 kcal/mole
A subscription is required to access the paper, but I reproduce the key table as fair citation under copyright laws:

I imagine that redeterminations or confirmations have been performed more recently and can be found by searching the chemical, rather than biological, literature. (And @Chris would seem to have confirmed this in his answer.)

The 2014 paper of Wang and colleagues found the activation energy of ATP at 32.5 kcal/mol. See the reference for details. The image is figure 3 from the reference.

Reference:

QM/MM Investigation of ATP Hydrolysis in Aqueous Solution


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Spiral lichen forms
I recently spotted many examples of a bilaterally symmetric lichen with a spiral form. This was on Navajo sandstone at the Utah-Arizona border. I found one paper that indicates this is likely Lecidea tessellata [https://www.colorado.edu/asmagazine-archive/node/933]. But I have found no indication of why a spiral pattern should form. It looks like the lichen first forms in an oval shape and then the center of the oval gets eaten away. Any ideas of why the spiral should form?


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What does q stands for in Gq/11 alpha subunit?
Sorry for asking, I am not capable to find what does the q stands for in Gq/11 alpha subunits.

I know the term must have shown up somewhere between this paper in 1989 and another in 1995 referencing it.  The latter paper defines Gq as a broader class of proteins, and uses G alpha q for a formerly numbered clone.

@Mike Serfas Thank you. I am very appreciate that. :)

@MikeSerfas Since your comment seems to have been useful to the OP, do you want to turn it into an answer?

@LukasChumchal To make your question more useful for others, can you expand a bit to give context?

@jakebeal Thank you for noticing my question. I am actually studing for molecular farmacology exam right now and i know that my profesor said that she doesnt know that reason for this abbreviation. So this made me more curious about the it (i am very used to that abbreviation in biology have usually quite important reason behind it). I tried my best to actually find out the answer myself but failed horribly. Thats all what i can said.

@jakebeal I really can´t think of more specific reason/context for this question. It´s just really about the abbreviation. Nothing else. Nothing more.

@LukasChumchal This site has a very broad audience and subject matter, so explaining a bit more of what you're talking about would be useful. What is a Gq/11? What is its alpha subunit? Is this a protein? Is it a drug? Does anybody know what a Gq/11 alpha subunit does? Why would anybody care about it?  If you give a couple of sentences like that, it will help people who aren't sitting in class with your professor understand what your question is about.

@jakebeal you got a poit. However if you have no clue about stuff you mentioned, you are not capable of answer it anyway. So what is even point of adding more information about mechanism/role of Gq/11 in this case?

@LukasChumchal It will improve the information that you get, because it will demonstrate to people that you actually understand the subject you are asking about, rather than just being a lazy student who is pretending so that you can get somebody else to answer your homework. It will also help other people in the future who may be wondering about the same or similar questions.

@jakebeal I understood your point from your first comment. However do you thing that this question is really suitable for homework? I understand your life philosophy. However not everybody is in this times lazy individuals, who does not wont to work to archive some goal. Right now i feel like i am getting yelled by you becaus i was curious about this topic. Just you may try to actually find the meaning behind Gq yourself. I faild after reading 5 articles about it.

@LukasChumchal Apologies, I'm not trying to be rude, but to provide guidance on the typical expectations around question asking at StackExchange. You can read in the help center for more details: https://biology.stackexchange.com/help/how-to-ask If you're not interested in improving your question, that's fine, but be aware that as a result you may receive downvotes and the question may end up closed and deleted.

@Lukas while I disagree that it should be necessary to explain in your question all the details of how GPCRs work, what would have made the question better would have been to include references to the 5 articles that you have read for instance... It's not so much that we want you to make a 10,000 word essay on everything you know as we want to know where you're coming from and what you've tried so far.  It might not make much difference in this particular case, but for future reference, questions will be better received with such information included.  Thanks! Oh, and welcome aboard!


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Amount of carbon captured in photosynthesis by a plant
Is it more proportional to the mass or the volume of the plant? I thought it might be helpful to think on the cellular level here. Even a reference to an external explanation would be useful.

Welcome to Biology.SE! Unfortunately, I'm having some difficulty understanding the context of your question. Can you please elaborate on the background of this question and why the standard description of carbon capture hasn't solved this problem for you?

I guess I'd loved a unified explanation on the level of cell biology. I mean I've phrased the question in what I thought was a pretty good way. Why can't I find it? Even a link to your favorite technical resource would be lovely. Search engine optimization is not doing it for me

The effective carbon capture of a plant involves not just the plant itself but the system that it is part of. Perhaps start by reading up on carbon farming and see if what you find either answers the question behind your question or else allows you to refine it to be more answerable? https://en.wikipedia.org/wiki/Carbon_farming

Welcome to Biology.SE! I am not entirely sure what your are asking but here are some places you might want to start:
Photosynthesis Molecular Biology
If you want to know about the number of sugar molecules created 'per photon' by photosynthesis you can explore the light-dependent and light-independent reactions used in photosynthesis. In particular you might want to look at the Calvin Cycle and how NADPH is used there and how NADP is reduced to NADPH in the light-dependent reactions.
Carbon Capture Efficiency
You might be interested in the variation between plants in carbon capture efficiency, i.e. not all plants are equally 'good' at photosynthesis. To think about this you might want to look at different photosynthesis mechanisms (C3 vs C4 and CAM; different forms or amounts of Rubisco enzyme) or you might want to look at sunlight 'capture' mechanisms (photosystem I and II and the accessory pigments like chlorophyll and carotenoids) or even at adaptations to different light environments (trichomes, leaf shape, etc).


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DNA Design for Multi-Site Restriction Enzymes
I have to use the SacII restriction enzyme, which requires multiple recognition sites to efficiently cut DNA, for a DNA assembly. From my understanding, multiple copies of DNA holding only a single restriction site can still lead to digestion through bridging interactions between molecules and enzyme. However, this appears to require digestion optimization I would rather avoid. Can I place two SacII sites in tandem on my insert DNA to enhance my digestion? How far should these be spaced to allow efficient enzyme interaction between the sites?

You've got a very nice answer from @acvill, but for future reference the NEB website is a good first place to look when you have questions about the specifics of RE usage (and for many other enzymes as well).

Hi @tyersome, that's where I started but they are not clear on design.

In its active form, SacII (also called Cfr42I) is a homotetramer that must bind two copies of its recognition sequence in order to efficiently hydrolyze its substrate.1 Upon binding two sites on a single molecule, the interstitial sequence is "looped out" and cleaved. The efficiency of cleavage is a function of the length of the intervening sequence due to the sterics of DNA bending (see resources concerning the persistence length of DNA 2 to better understand the energetics at play). One study on the effects of DNA tension on the cutting frequency of two-site restriction endonucleases (including SacII) suggests that the optimal loop length is hundreds of bp.3

In each case the DNA template contained multiple recognition sites for the enzymes being tested with separations ranging from ≈200 to 1,000 bp, predicted by theory to be favorable for looping.

A different study notes that EcoRII, another two-site enzyme, can cleave its target with as little as 10 bp between the 5′-cytosines of its two recognition sites.4
As an alternative to designing a construct with multiple SacII sites, you could supplement your digestion with a dsDNA oligonucleotide containing one SacII recognition site.3

...stimulation of activity upon addition of short oligonucleotide duplexes containing the recognition sequence has been reported for Eco57I, HpaII, Cfr9I, and SacII. Such stimulation provides evidence that an enzyme complex can bind in trans (i.e., across two sites on different molecules).

If you go this route, I would recommend first incubating SacII with your construct for some time, then add the oligos and continue incubation. This way, SacII will associate with the cut site on your target, and you will reduce the frequency of events where SacII binds and cuts two oligos at once, which would reduce the available oligo concentration and possibly lower your target cleavage efficiency.

References

Gasiunas G, Sasnauskas G, Tamulaitis G, Urbanke C, Razaniene D, Siksnys V. Tetrameric restriction enzymes: expansion to the GIY-YIG nuclease family. Nucleic Acids Res. 2008 Feb;36(3):938-49.
Manning GS. The persistence length of DNA is reached from the persistence length of its null isomer through an internal electrostatic stretching force. Biophys J. 2006 Nov 15;91(10):3607-16.
Gemmen GJ, Millin R, Smith DE. Tension-dependent DNA cleavage by restriction endonucleases: two-site enzymes are "switched off" at low force. Proc Natl Acad Sci U S A. 2006 Aug 1;103(31):11555-60.
Reuter M, Kupper D, Meisel A, Schroeder C, Krüger DH. Cooperative binding properties of restriction endonuclease EcoRII with DNA recognition sites. J Biol Chem. 1998 Apr 3;273(14):8294-300.

Thank you @acvill! I think I better go with the dsDNA oligos in this case, it's a shame Benchling doesn't highlight these enzymes.

@JEJS I've updated my answer with a methodological tip.  I hope your experiment goes well.

Oh great thanks @acvill!

Update for future reference: I actually had no problem with standard digestion conditions being 1ug DNA (~170 pmols) to 1ul SacII. However, I did leave digestion for 16+ hours which I imagine to be critical.


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Could you recommend literature regarding non-coding RNA and micro RNA?
I am familiar with the Alberts and Watson textbooks, but they are quite general, not specific.
I would be grateful if you wrote down books or even in-depth reviews/papers regarding the topic.


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How can I learn botany/plant ID by myself?
I am interested in sources and methods regarding botany and plant ID, and being a self-taught person. Textbooks, sites etc.
Thank you all in advance!

Welcome to the Biology Stack Exchange. Thank you for taking the [tour], but please carefully read through the [help] to learn more about the site, including what is on-topic and what is not, and [ask] a good question. In particular, questions that are inherently opinion based are not appropriate for this site. You can try asking for advice in the [chat], but please delete this post. Thanks!

Your local public library should have books, including field guides to local plants.  For a more general view, there are lots of on-line resources, for instance a couple of OpenStax texts on biology: https://openstax.org/subjects/science

Thank you for the useful answers!

Really, start with identifying the most common plants in your area, especially weeds. try to learn family as well as genus and species - then you will see similarities within families. When I was a horticulture student I learnt ten plants each week.


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What is a good book to start with if I'm interested in Gene clustering analysis?
As a beginner, I would like to learn more about gene clustering analysis, namely discovering groups of correlated genes potentially coregulated or associated to some conditions or finding patterns in gene expression data, identification of coexpressed genes from microarray data.
I was looking up for some books, but all of them are a little too much biology-heavy for me, given the fact that I have a Computer Science background. I would like to dive into algorithms such as hierarchical clustering, k-means algorithm, pattern-based clustering and other methods, so a book addressing these would be of real help.
If you have any suggestions, I would be grateful.

Usually, people do not ask for book recommendations on this site. Quora, Researchgate, Reddit, or maybe Biostars are the perfect choices to look for such questions. Still, to give you a clue to continue, If you've previously read some books about "Biostatistics", "Bioinformatics", "R/Python programming" and have a general understanding of what is a protein and what is DNA ("General Biochemistry"), the next step should be reading research papers, indeed. If you lack the mentioned principles, then the best strategy would be reading those first.

Just one more thing. In the case of Bioinformatics, always, always read books that are recent and new. Do not read old books (before 2005 or even 2010) as the area has evolved pretty much in recent years and many old links and websites are not available now


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Is “random arousal” in humans still caused by/connected to “background” sex drive?
I’m not sure if the title is the best way to word the concept but I don’t know how else to put it briefly; though honestly this question itself might be a bit hard for me to communicate concisely in text so if any more clarification on my thoughts or question is needed, then just ask.
So what I’m curious about is the origin of spontaneous erections (e.g. those not caused by conscious sexual stimulation of any kind be it visual, mental, or physical; for example “morning wood”, or other “random” erections that can occur during the day unprompted) and how libido plays into those, since a drop or loss of libido is typically reportedly accompanied by a lack of these spontaneous erections including the “morning wood”. Even though this behavior of the body isn’t directly and consciously caused by active sexual stimulation (but seems to generally still link to overall reproductive activity and function?), is it still tied to general sex drive and libido levels, as its absence correlating to low libido—and its seemingly higher quantities/strengths occurring with particularly high libido—suggests?
For a particular example, asexual people are a diverse group with varying properties regarding their individual sex health or habits, but there are many who report having a naturally low libido for most of their life (without distress). A level as low as, or lower than, the level at which a typical person experiencing a sudden drop in libido—and a lack of spontaneous erections as a result—would “fall” to. Would these asexual people with naturally, consistently low libido (so not a sudden change, as in the context of the people with typical libidos experiencing a new and temporary drop, but instead a default and non-distressing state) just as a result of that low libido naturally experience these spontaneous erections less—less often, weaker, both?

I think that libido and spontaneous erections could possibly have a correlation as you say, since usually the explanation for spontaneous erections is a surge of estrogen, progesterone, and testosterone which could cause a high sex drive. Low amounts of those hormones could possibly cause low libido and thus cause low spontaneous erections, although if your interested in primarily testosterone and their effects on men, their are different forms with their potentially varying effects on libido. I think these studies could help you get a better look at this topic:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5649360/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2586969/


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Bug/larva identification
What do you think these could be?

The photo was taken today from the inside of a bin liner, which contained waste from fruit and vegetables (carrot skin, banana peel, salad leaves, etc.), and (normally) nothing of animal origin.
Size: about 3-4 mm (body length).
Location: Europe/Belgium.
Behaviour: did not seem to move at all, or only extremely slowly.
Any ideas?

Possibly juveniles of the Clausiliidae family, of which there are many, many varieties. I'm having trouble pinning down the exact one, as pics of adult snails dominate the web. Unless an expert comes along, perhaps you can look after some 'till they grow-up, then take another picture?

Thanks! So maybe they are not even insects... :D They did look like mini snails to me, when I saw the photo, but I did not mention that in the post, as I did not want to sound silly. That worked, didn't it(!). As for your suggestion to follow their development, hmm, I don't suppose they will get the chance to 'grow up', unfortunately :/, but I will ask.


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Why are these ants emerging from underground?

Every spring through summer season, I see these ants emerge from beneath my driveway and form these thick swarms on the surface.  They typically do this once or twice per day, and after a few hours they go back underground.
After they are gone, there are often some dead ants laying around.
What is the best explanation for this behavior? Why do the ants come to the surface as a group and then seem to later disappear underground?

type of ants and or a location had been helpful.

Some hypotheses:

depending of the species, this could be because ants from another colony attack this colony from outside, then many ants inside go out to defend their colony. This could be coherent with the fact that you see dead ones after they quit the surface.
This can be supported if you see some of them which are fighting and if you see a line of ants coming from another place.

They are disturbed and think they are attacked, e.g. if you see this everyt ime after you can pass on it, or after you play basketball here, etc. Just try and check if they respond to it.

They are disturbed because of environmental reasons, e.g. after watering your garden, water could suddenly flood their nest.

Less likely:

They just choose the best time of the day (temperature, ...)  to clean their nest, including dead ants, but they look too numerous for this.

They may prepare the nuptial flights of the winged ants and group to protect them, but I can't see any on the photo, so probably not.


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What is the evolutionary origin of euphoria and dysphoria?
What kingdoms from the three domains haven't evolved something like the reward system in us? Couldn't we feel neutral all the time and undergo an involuntary push towards the right behavior instead, without the need for joy or distress?

One question at a time, there are at least 4 separate questions here in only three sentences.

"involuntary push" towards certain behaviors to satisfy biological needs sounds like a reasonable description of mesolimbic system we do have. Like how else would such drives manifest in cognitive beings? We'd need to retain cognitive mechanisms for prioritizing conflicted drives in real time such that we don't just drop everything when we get a little thirsty or tired, but also so those drives can increase based on the severity of the need. Without varying degrees of discomfort and contentment, what would that even look like?

Perhaps it's best to equate euphoria with dopamine, because if it can be found to control sex, food choice and foraging of invertebrates, that a major piece of the puzzle:
Dopamine is believed to have evolved around 600-700 million years ago in simple organisms like bacteria. At this stage, dopamine likely had basic functions related to cellular signaling and regulation.
For worms and insects, dopamine played a role in various physiological processes, including locomotion, feeding, and mating behaviors.
In bacteria, it has pretty simple functions in several species like Escherichia coli (E. coli) and Pseudomonas aeruginosa. Although dopamine levels in bacteria are relatively low compared to those in mammalian systems, its presence suggests potential physiological roles.
Bacterial dopamine biosynthesis pathways are similar to those in mammals, involving the conversion of the amino acid tyrosine into dopamine through a series of enzymatic reactions. Key enzymes involved in this process include tyrosine hydroxylase, which converts tyrosine to L-DOPA, and aromatic L-amino acid decarboxylase, which decarboxylates L-DOPA to dopamine.
In E. coli, dopamine is produced in response to oxidative stress caused by exposure to reactive oxygen species (ROS). Dopamine acts as an antioxidant.
Studies have shown that dopamine can enhance the production and stability of the extracellular matrix, promoting biofilm formation in various bacterial species.
Dopamine can modulate flagellar rotation and affect the motility of certain bacteria. In Pseudomonas aeruginosa, dopamine has been shown to enhance twitching motility, a form of surface-associated movement.
in the honeybee (Apis mellifera), dopamine is involved in associative learning and memory formation related to foraging. Dopaminergic pathways are activated when the bee receives a reward, reinforcing behaviors associated with finding food sources.
in insects like fruit flies (Drosophila melanogaster), dopamine is involved in fine-tuning flight behaviors, such as wing movements and flight initiation, and also in arousal.
Dopamine contributes to reproductive behaviors in many invertebrates. It can influence courtship behaviors, mate choice, and mating success. For instance, dopamine affects mating behaviors and receptivity in the nematode Caenorhabditis elegans.
Nematodes are some of the simplest invertebrates, so their use of dopamine for sexual reproduction suggests that the evolution of mammalian euphoria could go back 570 million years ago.

This is kind of a  philosophical question in my opinion.
First of all, what is 'right' behaviour?
Something that may be right in one culture may not be right in another.
It highly varies from individual to individual as well.
For example if you think focussed and planned studying is a right behaviour and your brain is caught in some kind of a reward loop in a useless activity like browsing the social media which is causing you distress.
So the question arises that does studying give humans some kind of an evolutionary or biological advantage such that nature may try to evolve our minds in such a way that it is consistently able to focus on studying? I don't believe it does. We are basically same from the survival point of view whether we are browsing social media or studing as your body is surviving and functioning appropriately which is the entire point of evolution itself. If hypothetically studing gave you better survival instincts then maybe evolution could take place in that direction.
However lets take another case;
Lets suppose certain variations exist in genes coding for muscle enzymes and proteins such that some people have better stamina or strength. Over the course of evolution they are likely to be selected as it gives them some kind of an evolutionary advantage.
But the development of the complex human brain is a huge evolutionary accomplishment in itself. Maybe the development of this reward system is itself a beneficial thing and helps us to focus? It basically puts the brain on autopilot mode where we don't have to think much and keep doing things repetitively, it could have evolved to save energy and maybe nowadays we have created things that take advantage of this exact same thing.
It could be that this reward system was actually evolved for our benefit but we humans have themselves learnt to take advantage of this in other humans.

Reward is a natural process during which the brain associates diverse stimuli (substances, situations, events, or activities) with a positive or desirable outcome. This results in adjustments of an individual’s behavior, ultimately leading them to search for that particular positive stimulus.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8992377/#:~:text=Reward%20is%20a%20natural%20process,for%20that%20particular%20positive%20stimulus.

If we follow along the lines of this definiton, then reward sytem development seems highly beneficial from the biological point of view.
It readily helps to distinguish between desirable and non-desirable stuff.
I strongly believe that evolutionarily it is in our best interests, it is we who are misusing it.
Another remarkable property of our brain is to get conditioned to what can trigger this response and what cannot.
Thank you.

It's not really philosophical. I wanted to ask what species did emotions like joy, sadness originate with. By "right behavior" I simply meant the things we naturally tend to do or avoid which increase our chance of survival and reproduction.

If you meant that by 'right' things then we are constantly evolving towards it. The development of senses of vision, hearing and smell and the development of reflexes are all directed towards it. Emotions are usually related with the frontal lobe and although other mammalian species and some other chordates feel emotions, humans are the ones with the most complex and complete set of emotions with the required capability and anatomical structures to express them as well. I would suggest you should read the development of frontal lobe, that will really help as well.


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How long does it take for a gene to be switched on or off through the process of epigenetic expression?
I understand that in our lifetime, our experiences affect the expression of our genes. Some get switched on, while others switched off. Our experiences, diet, lifestyle etc. determines this expression of genes, but my question is, how long does it roughly take for such an expression to take place? Let's say you are a raging alcoholic suffering from chronic stress. Because of this lifestyle, certain genes get turned on. Then after a decade or two, you decide to change. You start eating healthy, you exercise, you change your lifestyle completely. How long would it now take for your new lifestyle to cause a different gene expression?
I realize this could be a silly question, but this is my understanding of how things work.

Have you Googled this question searching for an answer? One of this site's requirements is that the OP show evidence of searching for an answer (which usually means a quote with a link to the source.) Strange, maybe, for a Q&A site, but it helps us know where you are in understanding a topic. Not all epigenetic changes are alike; many are permanent, and some are even passed on to offspring!

If I had found an answer to my question, why would I be posting here? I'm sure the answer can be found somewhere, it's just that I don't want to read 100 pages of hard core research just to find a short 1 sentence answer to my question. Isn't that why Q&A sites exist? I still don't see the answer to my question in the link you provided. I also don't understand what you mean by being epigenetic changes being permanent. My question is not whether they are permanent, but how long does it take for such an expression to take place. Just give me some rough estimate.

"Isn't that why Q&A sites exist?" Not this answer site, obviously. And if you didn't find the answer in the link I provided, you can't have read it. It addresses your question about smoking exactly, and the other is easily inferred. There are few one-sentence answers in Biology. If they could be answered in one sentence, you should be able to find it very easily.

The smoking was just an example. I am mainly interested in chronic stress, and what genes could get expressed because of it, and if hypothetically your situation changes, how long would it take before bad genes get muted again.

Read the link!!!


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When an action potential reaches an axon terminal
I came across the following question in my study of action potentials in neurons:
When an action potential reaches an axon terminal:
A. Na+ channels close.
B. K+ channels open.
C. The interior of the cell becomes positively charged with respect to the exterior.
D. Options A and B are correct.
The correct answer is apparently C. But I want to know, how?
I know that action potential causes part of membrane of the axon to become positively charged with respect to the external environment, moving across the membrane (such that when it reaches another part, the previous part returns to its previous negatively charged state) toward the axon terminal.
This question seems (as far as my understanding goes) to refer to the repolarization of the membrane (as the action potential has already passed through the entirety of the axon, so it cannot to my knowledge cause a positive inner charge in the neuron anymore). If that is so, then the peak of depolarization has already been reached. In order for the neuron to reattain its resting potential, repolarization has to occur, which includes the closing of Na+ ion channels and the opening of K+ ion channels.
I might be mistaken, but I would say the answer is D.

You are mistaken. The question is asking you about what happens in the axon terminal when an AP arrives there.

Think about how neurotransmitters are released into the synaptic cleft. Whenever something is being released from the cell, think about increasing intracellular $\ce{Ca++}$ level similar to what happens with platelet release reactions.


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What actually kills a plant that requires winter dormancy if it is kept indoors all year?
In bonsai practice, beginners will commonly purchase a juniper (often Juniperus procumbens 'Nana'), which is an outdoor tree, and keep it inside all year.  The tree invariably dies.  It is commonly explained to the beginners that this is because junipers are outdoor trees and require a winter dormancy.
My question is what exactly goes wrong that leads to the death of the plant?  Let's assume that the person gives the tree appropriate care, e.g. assume that desiccation or root rot or other more direct causes of death are not the reason.  (Of course, a valid answer is that it is impossible to give "appropriate care" for some specific reason.)
I have two strong hypotheses, in more detail but not in a rigorously scientifically biological detail.

The first is that the warmth and low humidity of the indoor environment cause the plant to continue to transpire water and attempt to grow or maintain foliar mass, while the reduced daylight hours signal the plant to "do something" (what, though?) that results in lower metabolic action.  And so the tree expends its stored energy (starches and sugars?).  Then in spring, the when the tree tries to put on a strong flush of growth, it has nothing left to build on.  So it struggles and eventually dies.

The second is that there is a daily metabolic cycle that is disrupted when the tree is kept in the more or less constant indoor environment.  That is, there is a cycle that depends on the daily differences in temperature and humidity the tree experiences during daytime and nighttime.  Through my own measurements, I have found, for example, that the vapor pressure deficit (VPD) reduces to near zero outdoors during the night in springtime as temperatures drop and relative humidity rises.  This, I think, means the respiration demands on the tree are near zero.  That is not the case indoors, where the VPD is more or less constant.

Is either of those at all consistent with what really happens?  And what does really happen from a biological perspective?  That is, what part of the plant's metabolism fails?  Is there something that happens during dormancy that doesn't happen when it doesn't get a cold dormant period?  Is there something detrimental that happens when it should be dormant but isn't?
If anyone has any pointers to resources where I could do further research on this question, that would be much appreciated, too, and I will update here with any further information I can find.

Here's a link with a discussion that is a step in the right direction.  http://www.omafra.gov.on.ca/english/crops/hort/news/orchnews/2016/on-0216a2.htm  Specifically, it says that there is an endodormancy period where the tree will be dormant of its own volition and will stay dormant until it has been cold long enough.  This is followed by an ecodormancy period where the tree remains dormant so long as external conditions are not favorable to growth.  It references a paper called "(Westwood, 1993)" but with no corresponding bibliographic entry.

Some plants that naturally survive frost periods outside, produce antifreeze proteins and shed any leaves to prevent actually freezing during this period. The production of antifreeze proteins requires a decent amount of energy (not sure how much i couldn't find any bio-energetic stuff) and when they are housed indoors you warm them up enough to signal that they can stop the production of these antifreeze proteins but you don't keep them at an ideal temperature all the time (such as during the night when you're asleep things cool down again and when you wake up you might put a heater on and warm them up again) and so they end up producing more antifreeze proteins. So this constant cycle of production -> loss -> production of antifreeze proteins coupled with no leaves to make more ATP starves them and kills them.
NOTE however, this is also just a theory and i have not seen/couldn't find any papers or info about experiments directly for this question and it is likely that the reason for plant death have many factors, potentially including your theories. I encourage a read of this which is all about antifreeze proteins and goes more into detail about the biology.
https://link.springer.com/chapter/10.1007/978-3-030-41929-5_7

Please better indicate which of the statements are covered by the reference.


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Are there any organisms that perform photosynthesis-like processes with thermal energy alone?
The closest I can find are thermophiles, but it seems they use the chemicals present in the hot environment for energy, not the heat itself.

Welcome. Photosynthesis means synthesis fueled by photons. As a consequence, thermally driven 'photosynthesis' is technically impossible. Can you elaborate on your Q, add relevant considerations and your own findings so far? One-liners are discouraged.

@AliceD - heat(infra-red radiation) is composed of photons too, just longer wavelength than visible light, so it isn't technically impossible. You can certainly generate fluorescence from IR range, and fluorescence uses similar electron stimulation to photosynthesis

@bob1 - Heat isn't the same as IR; objects can release IR and more so when their temperature rises. Objects can absorb IR and increase in temperature. Heat in itself is a vague term; it describes perceptually high temperatures. But that's subjective - what is high?

@AliceD, my understanding is that anything above 0K will emit IR. Conceptually IR is how a potential thermoautotroph could work, not that we know of any organisms that do work this way.

Thermophiles are organisms that are capable of surviving high temperatures. It doesn't mean they use or harvest the thermal energy in any way. Normally proteins start to unfold and degrade at temperatures above about 41 °C and all other organisms have a hard time coping with the effects.
Usually biology uses chemical energy. Photosynthesis is the one exception of a biological system converting the energy of photons directly into chemical energy stored in complex biomolecules for all others to use as nutrition.
Organisms that do not rely on those complex biomolecules but can support themselves are called autotroph. So photosynthetic organisms are  photoautotroph and micro organisms that use chemical energy from inorganic compounds are chemoautotroph. The inorganic compounds used can be as simple as decomposed water by radioactive decay.

Welcome. OP asks for thermally-fueled 'photo'synthesis (thermosynthesis?), not for a definition of thermophiles.

OP wrote "it seems they use the chemicals present in the hot environment for energy" and OP is right about this. OP asks for "photosynthesis-like processes" and not for miraculous "thermally-fueled 'photo'synthesis". There is nothing wrong with asking if life is known that directly converts thermal energy. An to my knowledge the answer is: No!

@AliceD Heat is certainly not a "vague term" but directionless energy not able to perform work.


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Can Eskimos be regarded a distinct species from Kalahari Bushmen based on morphological differences & geographic isolation?
I was motivated to ask based on the answer to another SE Biology Question that uses the following argument to conclude that two varients of snake are indeed a different species:

To test whether [Dendrelaphis ashoki and D. girii  were a separate
  species of snake] they (Vogel and van Rooijen, 2011) compared 9
  individuals of D. ashoki with 34 individuals of D. pictus, and found
  statistically significant (p<0.05) differences in five morphological
  characters....

Further:

The authors didn't rely just on morphological evidence: they note that
  D. ashoki, which is found in the Western Ghats, is also geographically
  isolated from other populations of D. pictus, which are found in
  Northeast India, Myanmar and South East Asia.

Minor differences in morphology of a snake: Why designate it a different species?
My question is, why can't we on the bases of an analogous argument conclude that (say) Eskimos & Kalahari Bushmen are, forget the race debate, but two entirely  distinct species?
I mean if "number of infralabials touched by the first sublabial" can count as a legitimate species-distinguishing morpohological factor, then so can heights, eye colors, hair texture, skin color etc. right? And we won't even have to fish too hard to gain statistical significance given how different Eskimos are from Kalahari Bushmen morphologically.
Further, the geographical isolation must have been pretty strong too.

The quick answer is "because not all characters are equally informative". A great example of this is classifying dogs on the basis of their coat colours -- I don't think you'd think of a fawn-coloured chihuahua as similar to a fawn-coloured Great Dane. However, this is a great question for delving into derived characteristics, and I'm hoping someone comes up with a really great, detailed answer!

@Gaurav Thanks for humoring all my questions. To pick your brain a bit more, when you say "not all characters are equally informative" that begs the question (to a layman like me): Informative of what? What's the basic attribute that we are getting down to here? In other words, the "morphology" is means to what end?

@DavidBlomstrom Thanks! Is it though? Then it would be more straightforward but then why do we get so much elaboration & statistical significance testing of morphological differences & geographic isolation?

@curious_cat I may be wrong, but I think the general idea is to look at overall similarity, i.e. over all possible criteria. Of course that's impossible, but I think the traits that are chosen as relevant are those that have been observed to correlate with differences in other traits. So when mammals are defined based on milk or a specific bone shape instead of, say, color, it's not because traits were picked arbitrarily, it's because it was observed that plenty of very different animals share a color and nothing else, but all animals that give milk are also similar in many, many other ways.

@RozennKeribin Thanks. When you talk about features like "animals that give milk" sure that's a substantive criterion. It's at the level of individual species-defining criteria that I'm skeptical. e.g. When two snake species are differentiated on the basis of the feature "number of infralabials touched by the first sublabial" can we be sure this wasn't something picked arbitrarily? Is that a relevant trait for snakes?

@curious_cat "animals that give milk" sounds substantive but does "three middle ear bones"? That's also a criterion for defining mammals. The criteria for defining a clade will obviously get finer and finer as the clade gets smaller, and species are (almost) as small as clades go. The thing about species (or any other clade) is, there is no reason for there to be a single factor that uniquely defines them. All members of a clade will be more similar to each other than they are to any other member of the clade, but that's across all traits overall, not a single one (...).

For example, almost all mammals are land-based... except for cetaceans, but cetaceans are still more like other land-based mammals in way, way more ways than they are like other things. It so happens that you can usually find a trait that does include all members of a clade and excludes all non-members, but it isn't a logical inevitability; it could be that it so happens that all the traits are like "land-based" for mammals, or "four-limbed" for tetrapods. It also means that in the search for "that one defining trait", you might end up coming up with something that looks totally arcane (...)

@curious_cat not because that trait is more important than all the others, but because it's the one that happens to uniquely characterize that specific group, and "number of infralabials touched by the first sublabial" is still easier to work with than "shows up in this cluster of the principal component analysis on these 1024 measured traits".

I think that species delimitation is not a science, or at least not a coherent one. Different fields use different criteria, for practical or historical reasons. For instance, in plants, loads of fertile hybrids exist between species. It seems that botanists do not split based on the traditional biological definition of what a species is: they apparently tend to split more (see the splitters and lumpers notion).
My intuition is that humans are generally interfertile. There even seems to have been interfertility between H. sapiens and H. neandertalensis which have been (or maybe still are?) considered as distinct species. But how are the actual genetic exchanges across the human populations?
In my opinion, if it were proven that genetic exchanges between human populations living very far apart and having evolved very different ecological adaptations (like populations from the arctic and from the Kalahari) were almost reduced to zero, then it would not be absurd to call them different species. Humans would form a continuum that can be considered a unique species (if interfertility is to be taken as a criterion), but with isolated extremes being in the process of forming separate species, somewhat like the extremes of a ring species. Maybe there even is some degree of reproductive incompatibility between very divergent human populations. The thing is that it is not ethically acceptable to experiment with this. We need to rely on "natural" experiments happening. Globalization could potentially tell us in the future, by facilitating encounters between individuals from very distant populations, whether such reproductive incompatibilities exist or not. That said, I doubt that the origins of parents are recorded in a scientifically usable manner when a couple has problems having children.

Thanks. If species definition is not a science is it even relevant to modern biology? e.g. When someone conducts a statistical analysis of a sample of snakes and publishes an article that purports to establish a different species of snake based on some set of distinguishing features like "number of infralabials touched by the first sublabial" is that useful? Or does it just get the guy a publication? Do we make progress by defining  Dendrelaphis ashoki seperate from D. girii?

@curious_cat Giving distinct names to distinguishable subsets of a species is definitively useful. Giving these names species status may not necessarily be a scientific progress, but it can have practical implications. I remember having heard at a conference a case where the issue was whether some particular edible bivalve on the coast of Brazil and Africa was or not a single species. I don't remember the details, but this had implications on whether or not the species could be used in aquaculture or something like that, due to Brazilian environmental laws.

Though globaluzation has/will also increased gene flow :p.

Welcome to the difficult concept called "Species".
Let me ask a simple question are tigers and lions different species?

They look different (Lion is a solid light brown. Tiger is a darker
  brown with stripes. Male lions have a mane. Male tigers do not)
They are socially different. (Lions live in prides. Tigers are
  solitary)
They are behaviorally different. (Tigers climb, Lions do not. Tigers
  love water and swim. Lions do not. Tigers always attack from behind.
  Lioness have elaborate ambushes as they hunt in groups.)
They live in different environments (lions in Savannah, Tigers in
  forest)
They rarely interbreed.
Yet when they do...tiger-lion offspring are viable. The males are
  sterile. But the females are fertile. So gene flow between the two
  population is possible although limited.

So are lions and tigers different species?
This is the problem with the concept of species.
A lion and tigers are clearly different species of animal.... but why? Is it because they look different? Because of historical reasons? Perhaps because they cannot freely interbreed. Or is because they do so rarely or with difficulty?
If yes, to rarely... how difficult/rare does it need to be for it to be a different species not not simply different populations?
Biology as a field has not come up with a comprehensive answer. The botanist have their own criterion (Because plants can tolerate polyploidy relatively and thus make hyrbid easily). The microbiologist have their own (because DNA can move from wildly divergent bacteria very easily). And so forth.
As to your question (paraphrased) "why scale structure and not hair colour?"
Not all biological traits are equal in the ability to change. Some traits are virtually impossible to change (number of limbs) while others are relatively easy (fur colour).
The reason boils down to the genetic programming of those traits. How interdependent one trait is with other traits. So an extra set of limbs... would also require changes in the brain to control said limbs, it would also change the walk cycles of body for a 4 now 6 legged animal. etc.
Hence traits like fur color is not useful as it changes easily with the time.
Thankfully, we now have genetic testing... and we can determine the degree of genetic flow between two populations to help make the final call if a population is one species or possible two or more.
But genetic testing takes time and a lab. So if there is some visual aid that would be helpful in the field. And these is where counting scales comes in.

Thank! Compelling explanation. What is your opinion on the alternative: We keep speciating on minor differences because it gets people publications and taxonomists a way to justify their existence?

The best I alternative I like, is that two species is defined as two population having biological or behavioral barriers that limit gene flow between the two to a level below Y% per generation (And there is big debate of how much Y should be). However... this definition would make every cell of some bacteria (which rarely exchange DNA or mate) different species. So it does not quite work either.

I like this quantitative approach you mention but it will be a cataclysmic change in the current taxonomy I am sure. Taxonomists won't like a DNA-based definition, right? It would put them out of business. The scale-counting on snakes would become redundant.

Actually they are slowly going out of business as it were. DNA based definition is moving in. This is why we now consider the orangutan to be 2 species even when morphological they look nearly the same. The problem with a DNA based definition is that it was very expensive to do until very recently for a single genome. Far outside the budget of most labs. Probably still is as you have to genome sequence not one animal but a population. Funding to study a specific plant or animal species is also very limited. So counting scales if backed by DNA sequencing (even if limited) would have its place.


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Minor differences in morphology of a snake: Why designate it a different species?
I was motivated to ask based on an answer to another question that I read on SE-Biology:

You can differentiate this species [Ashok's Bronzeback (Dendrelaphis
  ashoki)] from closely related D. girii based on it having a longer
  "postocular" black line than D. ashoki -- in D. ashoki it stops
  shortly caudal to the eye...

When the differences are so minor (e.g. "longer "postocular" black line") what's the reason for designating them as two different species?
Is there a objective reason when to call them different species? Would those two not interbreed?
Note: I'm not just asking "If they interbreed why is it a different species?"
I'm more in the vein of asking: "If two species so similar are still different species why are they different? Is there an objective metric to draw the line at which point we differentiate as different species."
Edit:
I've asked a related question over here:
Can Eskimos be regarded a distinct species from Kalahari Bushmen based on morphological differences & geographic isolation?

While it is not obvious from the title of the other post, your question is possibly a duplicate of How could humans have interbred with Neanderthals if we're a different species?.

@Remi.b I disagree. That question asks specifically about how interbreeding could take place between 2 species. This question is focused differently and asks why differentiate two species that look so similar.Though your own answer from the other question could fill in the OP immensely about the concept of a species, I still think more specifics could be said about this instance.

@theforestecologist Fair enough! There are two questions though; 1) what's the reason for designating them as two different species? 2) I'm more in the vein of asking: "If two species so similar are still different species why are they different? Is there an objective metric to draw the line at which point we differentiate as different species.". IMO, the second question is a duplicate, the first question is not. If you agree, I let you edit the question to narrow it down to a single question.

Remi.b Yup, I agree. But I encourage @curious_cat to edit the question on their own in a way that narrows it down appropriately but still satisfies their original curiosity.

@Remi.b I feel like your answer to that question is comprehensive enough to apply to this question, but the questions themselves don't really seem to be duplicates - I'm not sure what the agreed SE meta is in that situation. I feel like the title of this question conveys a broader curiosity so it has some value beyond the value of the Neanderthal question.

Short explanation
According to the papers I could find, Dendrelaphis ashoki and D. girii aren't as closely related as you suggest: D. ashoki appears to be closely related to D. pictus, a Southeast Asian snake species, while D. girii appears to be closely related to D. bifrenalis, a Sri Lankan/South Indian snake species. They were distinguished from their sister species largely on the basis of morphological differences and geographical isolation.
How do we know D. ashoki is a distinct species?
The key to this answer is in Vogel and van Rooijen, 2011a, the scientific article in which Dendrelaphis ashoki was first described. Before their work, these snakes were thought to belong to the species Dendrelaphis pictus. To test whether this was in fact the case, they compared 9 individuals of D. ashoki with 34 individuals of D. pictus, and found statistically significant ($p < 0.05$) differences in five morphological characters: SUBC (number of subcaudals), TAIL (tail-length), EYED (horizontal diameter of the eye), SUBL (number of infralabials touched by the first sublabial, left and right added) and STRIPE1 (ventrolateral stripe bright/dull/absent). Here's the statistical analyses they ran:

The south Indian form that has previously been referred to as D. pictus (e.g., Wall, 1921; Smith, 1943; Whitaker and Captain, 2004) differs from Indochinese D. pictus in the characters SUBC ($F_{1,25} = 17.7, P = 0.0003$), TAIL ($F_{1,25} = 30.0, P = 0.00003$), EYED ($F_{1,35} = 22.5, P = 0.00003$), SUBL (Mann-Whitney U, $Z = −4.6, N=40, P < 0.00001$) and STRIPE1 ($\chi^2_1 = 42, P < 0.00001$).

They also compared the 9 individuals of D. ashoki with 48 individuals of D. proarchos, and found statistically significant ($p < 0.05$) differences in five morphological characters: VENT (number of ventrals), SUBC (number of subcaudals), TAIL (tail-length), EYED (horizontal eye diameter), SUBL (number of infralabials touched by the first sublabial, left and right added) and STRIPE1 (ventrolateral stripe bright/dull/absent).

[The south Indian form] differs from D. proarchos in VENT ($F_{1,49} = 24.1, P = 0.00001$), SUBC ($F_{1,28} = 13.7, P=0.001$), TAIL ($F_{1,28} = 40.1, P < 0.00001$), EYED ($F_{1,47} = 16.8, P=0.0001$), SUBL (Mann-Whitney U, $Z = −4.7, N=52, P < 0.00001$), and STRIPE1 ($\chi^2_1 = 53.0, P < 0.00001$).

The authors didn't rely just on morphological evidence: they note that D. ashoki, which is found in the Western Ghats, is also geographically isolated from other populations of D. pictus, which are found in Northeast India, Myanmar and South East Asia. Therefore, they concluded (emphasis mine):

The distinct morphology and coloration as well as strong geographic isolation of the population from the Western Ghats imply a unique evolutionary history that does not allow application of either the name D. pictus or the name D. proarchos. Consequently, we describe this form, previously referred to as D. pictus, as a new species, D. ashoki sp. nov., endemic to the Western Ghats.

How do we know that D. girii is a distinct species?
For this information, we need to look up another paper published that same year,  Vogel and van Rooijen, 2011b. Interestingly, the authors don't compare this snake with D. ashoki at all, but with Dendrelaphis bifrenalis:

Due to their double loreal shield, D. girii sp. nov. and D. bifrenalis occupy a unique position within the genus. A congeneric species with a double loreal shield has been described in the past, namely Dendrelaphis biloreatus (Wall, 1908). However, the presence of a double loreal in D. biloreatus appears to be based either on an anomalous specimen or on a misjudgement (Vogel & Van Rooijen, 2011b). Furthermore, D. biloreatus differs from D. girii sp. nov. and D. bifrenalis in its number of dorsal scale rows (13) and its number of ventral scales (190-199).
There are several differences between Dendrelaphis girii sp. nov and D. bifrenalis. The most obvious one is the light ventrolateral line, which is present in D. bifrenalis and missing or very faint in
  Dendrelaphis girii sp. nov. (see Fig. 3, 4).
The postocular stripe is much broader in D. bifrenalis. In D. bifrenalis there are black oblique bars in the neck region of some, but not all specimens (8 specimens out of 12 in our data) (see Fig. 3-5). This pattern is not sex related. It is absent in D. girii sp. nov. For Dendrelaphis girii sp. nov. we had only 1 male, so it is not possible to compare the sexual dimorphism in this character. The snout of Dendrelaphis girii sp. nov. is much broader than that of D. bifrenalis. Dendrelaphis girii sp. nov. has, on average, fewer subcaudals and more ventrals than D. bifrenalis, but the ranges broadly overlap.

Thanks Gaurav. But to play the devils advocate suppose I analyzed 9 individuals of the Eskimo tribe and another 34 belonging to the Kalahari bushmen I'm sure we could find a statistically significant morphological difference in at least five characteristics. e.g. Hair Color, Eye Color, Heights etc. Would that make the bushmen a distinct species from the Eskimos? Why not? Also, we wouldn't be relying on purely morphological evidence. The Eskimos are found in regions of the world geographically isolated from the parts where the Bushmen are found.

Even shorter, if perhaps overly cynical, explanation: if you've discovered a new species (or can 'split' an existing species), you can get a paper published.  Might even get grants if your new species are now rare enough to be considered endangered.

@jamesqf Actually, that's exactly the sort of explanation my reading is pointing to. But I just want to get other perspectives on things. Maybe I (and you) are overly cynical & we are missing something? I am no expert on this.

I've asked a related question here: http://biology.stackexchange.com/questions/56945/can-eskimos-be-regarded-a-distinct-species-from-kalahari-bushmen-based-on-morph?noredirect=1&lq=1

@curious_cat You could, but "Eskimos" (e.g. the Iñupiat) have only been separated from the Bushmen (San people) for around 15,000 years; D. bifrenalis and D. pictus are different enough that several species can be found in between, and are likely separated by millions of years of evolution -- so in some way these 5/6 snake characters are more revealing of evolutionary-scale patterns than human populations. IF that is your ultimate goal.

@Gaurav OK, that's useful to know. So if I interpret your argument correctly, mere morphological differences don't matter as much but the time period of separation on an evolutionary scale?

@Gaurav  Out of curiosity, if Eskimos vs Bushmen were separate for "only" 15,000 years; how many years have the Dendrelaphis ashoki vs D. girii been separated? Any idea? To get a relative comparison.

@curious_cat Yep, morphology is a way of getting at evolutionary relationships, which most (but not all) taxonomists agree is the best way to name taxa. But taxonomists often differ on where to draw the line (http://markscherz.tumblr.com/post/85470834478/a-not-so-brief-lesson-on-species-and-species has a nice diagram about that), and of course the line might move: other taxonomists might show that Vogel and van Rooijen about one or both of the species we discussed, in which case those species might be merged with others.

@curious_cat The closest I can find is http://www.sciencedirect.com/science/article/pii/S1055790315003127, which -- if I'm reading Supplementary Fig. S3 correctly, which I may not be -- suggests that Dendrelaphis bifrenalis and Dendrelaphis caudolineolatus shared a common ancestor 18.52 million years ago.


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Can simultaneous double pathogen infections happen, or are they prevented?
Is there something in immunology that prevents a simultaneous infection with a 2nd pathogen? For example, I've never heard of someone getting both dengue and malaria together. Or, say, Ebola and Marburg fever.  Of course, sheer probability makes it unlikely but is there something more fundamental that prevents it?
Maybe a more tractable version of the question is within the class of viruses or one type e.g. respiratory viruses. Is there something that prevents getting infected by multiple pathogens at once?

You can absolutely have two infections occurring together.
One term which is used is 'co-infection'. Also 'secondary infection', in case where either the first infection or the treatment made it more likely for the second infection to occur. For example, secondary infections causing pneumonia were a big issue with Covid19.
I have done a quick google search on 'dengue malaria co-infection', and cases do exist. In this paper (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3614227/ - Concurrent malaria and dengue infection: a brief summary and comment), the authors comment on the fact that for this particular combination of diseases, the co-occurence is indeed quite low. They have various hypotheses:

The vectors for either disease are specific to geographically distinct areas, e.g. mosquitoes that prefer city vs rural areas.
(I've seen it contradicted in another paper but no time to search).
Pure statistics: the likelihood of getting both diseases is much less likely than getting one, especially if getting one disease results in behaviour modification (e.g. staying at home sick).
Underdiagnosis: if you go to the doctor with one obvious disease, you probably will not get tested for other co-infections you might have.

It is possible that, for other pairs of diseases, immunity may play a role (your body is already on high alert from one infection) but that can also provide a risk (your body is so exhausted from fighting infection #1 that you can't fight infection #2). I am not aware, though, of any general statement that would apply to all diseases.

Another particularly good example would be the hepatitis D virus, which requires the hepatitis B virus to be present for it to replicate (though not all cases are coinfection, HBV carriers can also get HDV for example).

Something from not too long ago - man diagnosed with Covid, Monkeypox, and HIV: https://www.webmd.com/covid/news/20220826/italian-man-covid-monkeypox-hiv-same-time

Another related term is "superinfection". Especially common in immunocompromised populations and/or when antimicrobial therapy was inappropriate.

I've got COVID and a bacterial chest infection as we speak... Feels a very relevant example

Another factor factually making a secondary, subsequent infection less likely is that the immune system is all revved up already. The second pathogen encounters a really hostile environment. During an acute infection the body is in an exceptional state which it is not able to maintain in ordinary times (I guess because of detrimental side effects -- think fever --, auto-immune issues and resource issues).

@ScottishTapWater Wishing you a speedy recovery! May your body kick the butts (and other body parts) of all relevant bacteria and viruses.

@ScottishTapWater Yup:  Back in college I had strep throat and mononucleosis at the same time.  Doctors are looking for one diagnosis, it confused them at first.

There are viruses that require coinfection.  The Hepatitis D virus is incomplete and can only reproduce in a host who is also infected with Hepatitis B.

Very interesting point, although quite a special case.


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Non-toxic reporter gene or other transgenic DNA integration verification method that does not kill/damage organism?
I have been thinking that I will just use EGFP to know whether my attempted transfection was successful, but I've been coming across some publications that over expression of GFP can cause cell death. I need to create a stable line of transgenic organisms that have rather delicate embryos, and the organisms themselves are mildly fluorescent, so I am concerned that I need to hit a sweet spot of fluorescence that may be difficult to achieve. Too much and my cells die and too little and its not detectable. Does anybody know of another method that doesn't require expression of fluorescent proteins and doesn't require me to kill my organisms for sequencing?  Thanks.

Have you investigated low copy expression vectors? If they are mildly fluorescent; which colour, and have you thought about RFP or another colour vs GFP?

beta gal, maybe? https://www.google.com/url?sa=t&rct=j&q=&esrc=s&source=web&cd=&cad=rja&uact=8&ved=2ahUKEwi00O7ggN_8AhWVADQIHZTzAQEQFnoECBEQAQ&url=https%3A%2F%2Fwww.sciencedirect.com%2Fscience%2Farticle%2Fam%2Fpii%2FS0141022921001435&usg=AOvVaw2eymUOIzNHuPITIS2yVzHp


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How can saliva neutralise acids produced by bacterial cells in our mouth if it is itself acidic in nature?
My school textbook makes the following claim:

This means that saliva must be basic. However, I learnt that the pH value of saliva is about 6.8, which would surely make it acidic. How can the above point be correct then?

even if an acid is 6.0, it's reaction with other acids depends on the quantity, so a lot of the mild acid can react with an amount of the stronger acid.

Saliva is neutral, not acidic (6.8 is very barely acidic), and is a means to carry the acid away physically, and is also much less acidic than acid produced by bacteria, so is still effective in neutralizing.

Also substances with higher pH can act as bases against substances with lower pH. If I remember right, alcohol acts as base when warmed with carboxylic acid in esterification reaction. Enzymes are very sensitive to change in pH so that probably reduces bacterial activity.
https://youtu.be/UGs0hrIkjss

Saliva also has anti microbial properties and might kill bacteria or hinder their growth. https://en.wikipedia.org/wiki/Wound_licking


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How to name this bacterial gene when running out of letters?
There's a gene in some bacteria that I have to name.
My (very limited) understanding is that for bacteria, naming conventions are based a lot on Demerec et al. 1966 (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1211113/pdf/61.pdf). Essentially, the point is to have a group of three letters designating a pathway or process (e.g. abc) and an additional uppercase letter identifying individual genes in a pathway (e.g. abcA, abcB, abcC...). Different alleles would be given numbers (abcA1, abcA2...). No Greek letters, superscripts, etc.
Now my problem is that for my pathway (let's call it abc) basically everything from abcA to abcZ exists already (some only in eukaryotes, and some were later proven to not be actually part of the abc pathway, but I think it would be confusing if I repeat those with a totally different gene).
I was initially thinking about using a Greek letter for it, but that's not allowed.
Does anyone know what is usually done when running out of alphabet? Thank you for your time!

I would guess that as you have an alphanumeric code already set for the pathway, using abc as the pathway name and A as the initial with alleles as numerics; that you would add an additional capital letter e.g. abcAA.

@bob1 Not unreasonable, but I wonder if it has ever been done.

I favour the suggestion from @bob1. It's up to you to see if it has ever been done. I had a quick go myself, but it needs some effort as on GenBank genes tend just to be numbered. What I would try is Streptomyces coelicolor and related strains, which are known to make complex antibiotics, or other bacteria which can make exotic molecules. Good luck!


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Can I have LAMP on the bench / in the field?
I am interested in LAMP for detecting small amounts of DNA (loop-mediated isothermal amplification and yes, I know the initials don't match).
I am trying to figure out exactly how clean/(sterile?) everything needs to be.
On one hand:
-papers repeatedly stress that the assay is very sensitive and to avoid contamination
-these very nice guidelines (https://www.rtlamp.org/get-started/rt-lamp-open-access/) include the requirement for a PCR hood. I think this website is otherwise reasonable and thorough as it mentioned that HNB dye should be in its trisodium form (which most papers do not mention)
On the other hand:
-I'll be working with DNA, not RNA; less fragile
-the point of LAMP is supposed to be that it requires more basic equipment than PCR. If it still requires a clean bench, that sort of flies out of the window.
-a quick search for 'field LAMP amplification' found a publication (https://pubs.rsc.org/en/content/articlelanding/2022/ew/d2ew00433j - 'In-field LAMP assay for rapid detection of human faecal contamination in environmental water'). But I don't have enough experience in the field to tell whether this is a reasonable approach.


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Compatibility between spytag/spycatcher versions
Background
SpyTag and SpyCatcher are peptides which can associate via a spontaneous amide bond. Because of this, they can be fused to proteins of interest as tags to cause the proteins to bind. There are (currently) three versions of the spytag-spycatcher system, where each system contains a different version of spytag and catcher (i.e. system 1 contains spytag1 and spycatcher1, system2 contains spytag2 and spycatcher2, and system3 contains spytag3 and spycatcher3).
Question
My question is, how compatible are the spytag and spycatchers between different versions? So, for example, would spytag1 bind with spycatcher2?
Prior Research
I found the following statement from this paper:

The new variants showed backwards compatibility, reacting efficiently with parental versions (SpyTag002 with SpyCatcher: 1.0±0.06×104  m−1 s−1; SpyTag with SpyCatcher002: 5.5±0.03×103  m −1 s−1;..

But these numbers don't mean a lot to me. Would you expect to see near complete binding as with spytag2-spycatcher2?

I have worked with the coupling of SpyCatchers and SpyTags of different iterations and can confirm that they are all backward compatible. While SpyCatcher003 and SpyTag003 pairs have the quickest reaction rate, reactions of all pairs (including SpyCatcher and SpyTag version 1) should go to completion under the right conditions.
The SpyCatcher002-SpyTag1 is no exception. As you quoted in the Angewandte Chemie paper, the rate of reaction is 5.5x103 M−1 s−1. Rate = k[A][B]. This means that 10 μM of SpyCatcher002 and 10 μM SpyTag will react with a t1/2 (50% coupling) of 18 seconds at pH = 7.0. However, 10 μM of SpyCatcher002 and 10 μM SpyTag2 will t1/2 of 5 seconds (rate constant is 2x104 M−1 s−1). If you are reacting 0.1 μM of each, their respective t1/2s are about 8 and 33 minutes, respectively.
To get the reaction to go to completion (>90% coupling), you'll need to wait ~12 times as long as the t1/2 (since every subsequent t1/2 doubles in a second-order reaction). This will, of course, depend on your concentrations. However, when using low concentrations (0.1 μM), complete coupling of SpyCatcher002 to SpyTag002 will take 1.5 hours, whereas SpyCatcher002 to SpyTag will take 7 hours at 25C. SpyCatcher002 to SpyTag1 will take 3x as long to go to completion; therefore, I'd recommend using at least 1-2 μM of what you want completely coupled with an equal or 2-4x excess amount of either Tag or Catcher and run the reaction overnight. Higher concentrations (>=10 μM of both Tag and Catcher) should go to completion in 30min-1hr. When performing coupling reactions for more than a few hours, I'd recommend you perform them at 4C. Loading 10 μL of 1-2 μM of your protein should allow you to see the band shift on an SDS-PAGE gel with Coomassie stain.
In my experience, temperature and pH are important factors when performing coupling. pH > 8.0 tends to reduce the rate of reaction significantly, as does pushing the temperature upwards of 37C (the protein prefers 25C and pH = 6.0). Most of the reactions I perform in the lab are at 4C overnight at pH = 7.4 between SpyCatcher003 and SpyTag1, and coupling is nearly complete. However, others in our lab have worked extensively with SpyCatcher002 and SpyTag1 reactions, which also tend to go to completion under the right conditions. Moreover, sometimes the protein that the SpyTag is fused to will alter the kinetics of the reaction, and short linkers to SpyTag may reduce your coupling efficiency.
While others are certainly more qualified to answer this question, hopefully this gives you enough information to work with!

Very nice answer! Want to help support the proposal for a SynBio StackExchange site?

I am currently working with these tags, so going off experience here. The binding efficiency is not 100% even when the correct versions are mixed e.g. version 2 spytag and version 2 spycatcher. I believe this is the original paper (https://pubs.acs.org/doi/pdf/10.1021/ja910795a) it reported 60 % binding efficiency after an hour (I presume for version 1) and this paper (https://www.pnas.org/content/pnas/109/12/E690.full.pdf) revealed 40 % binding efficiency in the first minute (unclear whether version 1 or 2 but I presume 1).  In terms of between versions I can only speak to a mistake I made once by accidentally mixing version 1 spycatcher with version 2 spytag. There was visible binding that could been seen by SDS-PAGE however, it was very faint and required significant amounts of protein to view (~10 mg/ml). I never did any sort of quantitative measurements on binding efficiency as it was a mistake. But from subsequent correctly run experiments, I could see it was significantly lower so I would always use version 2 with 2 and version 3 with 3 etc as they were designed to have maximum binding efficiencies.


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Assembling small DNA parts using Golden Gate
Background
I've always been told that DNA assembly can be tricky when using very small DNA parts due to low efficiency. I've also seen this when using 3A biobrick assembly to assemble promoters and RBSs together. However, there doesn't seem to be any information that I can find which definitively shows what the minimum DNA part size is that can be used before the efficiency becomes so low that assembly is unfeasible. The most I can find are warnings that small DNA parts are problematic (e.g. https://blog.addgene.org/plasmids-101-golden-gate-cloning).
The Question
What is the minimum DNA part size that can be used in DNA assembly before it becomes unfeasible? I'm specifically interested in Golden Gate assembly, but information for other digest-ligate assembly methods could also be helpful.

Purely going off experience here having used golden gate assembly methods for 5+ years now, there is a definite lack of literature regarding small part assemblies. In my current lab, we use CIDAR MoClo (a golden gate method) and have assembled 100's of constructs successfully with parts as small as ~ 70 bp. However, when we assemble smaller parts we tend to increase the amount of this part compared to bigger parts. For example, we dilute each part to 10 fmol ready for assembly as a basis for all assemblies, this then allows us to play with the ratios and quickly optimise reactions. So as a standard, when the part is small we automatically start with at least a 3:1 instead of 1:1, where we put 3x the volume of the small part compared to others in the assembly. This usually helps, but on top of that we try to increase transformation efficiency by using SOC media and generally avoid building parts < 100 bp. e.g. we don't tend to use promoters and RBS separately we make larger combined parts containing both.

I don't have hard data to share regarding you question, but I can provide some anecdotal evidence. I have used golden gate assembly to build hundreds of plasmids using ~20bp annealed oligos, as well as hundreds of plasmids using ~70bp promoter+RBS, 720 bp eGFP, and ~70 bp terminators encoded on plasmids into a ~6kb backbone. In these cases I use 40 fmol backbone (1:3 backbone to insert molar ratio), and I typically get 50-100 colonies. In my experience it is the number of fragments more so than the minimum size of the fragments that has reduced efficiency. I have, however, seen reduced efficency with larger inserts. For insertion of 15-20 kb insertions into a ~6kb backbone I see far fewer colonies, however I haven't teased out if this is lower reaction efficiency, or (what I expect to be the case) reduced transformation efficiency.

It may also be worth considering how you are amplifying and isolating your small part. Gel extraction kits sometimes have an optimum DNA size ranges that may prevent recovery. Or if your part is similar to your primer length you may see considerable contamination in your 'purified' product if say the size of a single RBS.


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What's the best way to find a Tardigrade
So I have a school science project on the best sample to look under a microscope, so I want to bring in a Tardigrade. It's winter here in Ohio, although Tardigrades are freeze tolerant I don't think there's a high chance of finding one in a cup full of snow. I heard Tardigrades live on certain fruits such as strawberries and lettuce. I just want to be 100% sure I'll bring in a Tardigrade.

P.S: It's snowy so I can't make a tardigrade habitat.

google where to buy tardigrades,you can get them online

Have you searched for where Tardigrades usually live? (should be easy to find). Please do so (since we require question askers to demonstrate some research effort, and a simple Google or Wikipedia search would likely give you a couple of starting points). Update your post with any updates and where you found the info, and then let us know what you still can't figure out. Thanks

Alright, Thanks.

If the ground wasn't frozen I would have not posted this question.

I have heard they live in moss, so one time I got some moss and tried to find tardigrades in it. This did not work. I upvoted your question because I would love to find tardigrades too. It's not fun to "get them online."

Maybe greenhouses? or Houseplants? Indoor botanical gardens (which is basically a greenhouse in museum form)? You could ask the staff there if you have one.

Alright, thanks for the help everyone.


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What causes puberty to begin?
I understand that puberty begins when hormones are released from the pituitary gland as instructed by the hypothalamus, but why does the hypothalamus instruct this to occur?
How is this process timed by the body?

Too broad, sorry.

partial answer: https://biology.stackexchange.com/a/3609/460

Possible duplicate of How are long time periods measured in biological systems?


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Do humans secrete and detect pheremones?
Many animal species are capapble of secreting and also detecting pheremones from members of the same species, which relay messages and signals such as indicating sexual readiness.
Do humans do the same thing? Are humans capable of communicating in this subconscious fashion?

Yes, humans can secrete and sense pheromones, e.g. female tears dampen male sexual arousal.
Science 2011, 331(6014), 226-230
But then on the other hand, a key gene in mouse sex specific behavior (TRPC2) is a pseudogene, i.e. it is inactive, in humans.
Nature 2007, 448, 1009-1014
If you look at the references in those papers you will probably find a lot more examples.


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Does iris color effect the amount of light that reaches photosensitive ganglion cells?
Does eye color (of iris) have any effect on the amount of light reaching retina cells and hence effect melatonin production?