text:
How can monkeys be ancestors to people when they are herbivores?
How monkeys can be ancestors to people when monkeys are herbivores but humans are omnivorous?
Maybe it is monkeys that evolved to become omnivorous gradually?
How does the generally accepted theory of human origins explain it?

Do you have a reference for monkeys being herbivores?

The first hit on Google's "similar questions" seems to refute that claim pretty solidly.  Also, humans and apes share the most recent common ancestors, the closest being chimps

The following information the first thing to face on websites about human evolution. For examples, with similar quotes:

"These and other anatomical features suggest that the early monkeys were becoming mostly diurnal fruit and seed eating forest tree-dwellers." (refer to link)
"Herbivores include gorillas, cows, horses, elephants, rhinos and giraffes". (refer to link)

Welcome to Biology.SE! You would probably get a more positive response to this question if you: 1) focused on a single clear question (e.g.s: the grammar of your title is so scrambled that it isn't even clear if it is intended as question, you have at least two questions in the body which need to be separated), and 2) state clearly in the body of the question (comments are ephemeral) what sources you are using and summarize what you think you have learned from them. ——— Please consult the [tour] and [help] pages starting with [Ask] questions effectively on this site for details. Thanks!

I have found that when learning about a new area starting with a relatively accessible and reliable source like Khan Academy is very helpful. Wikipedia is also generally a good starting point and you can then check their references. Online platforms called MOOCs offer free (or very low cost) courses on a wide variety of subjects — two I am familiar with are Coursera and edX. Finally, textbooks with a good level of detail are also freely available online e.g. from NCBI.

I also encourage you to check out some of the online resources available for learning more about evolution. For example, this a useful introduction to evolutionary theory from UC Berkeley.
——— Finally, many "herbivores" will eat other animals if given a chance — for example deer will eat eggs and chicks from birds nests — this illustrates that the premise of your first question is faulty.

Ok, so there are several erroneous assumptions here:

Monkeys are not the ancestors of humans. Both humans AND monkeys share a common ancestor: an animal species that was neither monkey nor human.
The evolution of diet specialization is one of the most common phenomena in evolutionary biology. It is totally plausible for a species to evolve an omnivorous diet from a vegetarian one, and vice-versa. So you cannot use diet-specialization as a way of inferring the ancestry of a group of species (there may be some inferences done with diet-specialization and phylogenetic evolution but it is usually to re-confirm other types of data).

So, to sum-up, monkeys ARE NOT the ancestors of humans. Both monkeys and humans have a common ancestor, an animal that could have been herbivore or omnivore.

Also we do have our own veggies.


text:
Can you please identify these yellow dot parasites which grow on non-living surface?
Little yellow dot parasites have screwed me for years and I still don't know how to fight back as I don't know what they are. I just know that they are living beings because they grow in number.
Images:

(Click the images to enlarge)
Location: North India
Size: Visible to naked eyes (one dot is approx 0.25 mm in diameter; their colony is upto 5 mm in length or diameter; their colonies aren't perfect circles as seen in the images)
Behavior: They grow on any plastic, metal and glass surfaces (but not on clothes, walls or wood) if they are stored in open (the surface is in contact with oxygen)
Can you please identify it?

' I just know that they are living beings because they grow in number' How do they react when exposed to a biozide (Triclosan, Zink-Pyrithion etc..)?

@iLuvLogix Never tried.

This looks like the work of an insect, perhaps a fly.
You can check by experimentation.
Try covering part of one surface with a fly-proof covering.
Take photos at weekly intervals of exactly the same area, compare images.
black-and-white images below from
Forensic Science International 137 (2003) 152–159
"Distinction of bloodstain patterns from fly artifacts"
Mark Beneckea, Larry Barksdale
DOI: 10.1016/j.forsciint.2003.07.012
Bar on images is 1cm

Can you expand on the reasoning behind your conclusion?

source: Stack Exchange

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

sort: votes


text:
Why are the shells of birds' eggs fragile but not those of other creatures?
In my limited  understanding, eggs of oviparous creatures other than birds have a flexible outer membrane.
Is there any obvious reason that bird eggs should have fragile shells?

Notes

I'm asking why birds seem to be a special case. If all other oviparians manage perfectly well without shells, what is it about being a bird that requires the extra resources to form a shell?

I believe birds are considered to be modern-day dinosaurs. Didn't dinosaurs have leathery eggs?

Well, the birds have to be able to get out of them, don't they?  Can a leathery egg withstand an adult bird sitting on it?

@swbarnes2 - (1) All oviparous species have to get out of the egg (2) I don't know if a leathery egg will withstand being sat on. However, birds are not very heavy and I don't think they put all their weight on the egg - they also use their feet and legs  to support themselves.

Bird egg shells are actually pretty strong.  Although they can break from a concentrated blow (cracking an egg) they resist distributed pressure, as from the parent sitting on eggs, quite well.  Do any of the other creatures with leathery/flexible egg casings actually sit on their eggs?

I don't understand the question. How e.g. frog eggs are more resistant?

@Exocytosis - (1) A table-tennis ball is easily squashed and will not recover its shape. A hollow rubber ball can be squashed and recover its shape. Similarly with eggs. Both types of squashing may or may not damage the embryo, however the hard shell, once broken, will allow the ingress of bacteria and viruses. (2) Frogs survive as a species, so their eggs must have sufficient resistance.

I am not sure their deformability really makes frog eggs less fragile than birds' ones. There are clearly a lot of factors involved in an egg durability. And your second statement seems irrelevant to me since birds survive as a species too "so their eggs must have sufficient resistance". Feel free to clarify though.

@Exocytosis - I'm asking why birds seem to be a special case. If all other oviparians manage perfectly well without shells, what is it about being a bird that requires the extra resources to form a shell? Does it help the hen to fly better?

https://en.wikipedia.org/wiki/DDT#Eggshell_thinning may be relevant.

@chasly - supports Monica: The difference between frogs and birds is that most frogs lay many more eggs - up to 10,000 or more at a time, for some species.  So it really doesn't matter if some of them get squashed.  Birds lay relatively few eggs, and incubate them.

Your question is, I think, based upon a false presumption: that avian eggs are more fragile than those of other oviparous animals.
The paper Evolution of the Cleidoic Egg Among Reptilian Antecedents of Birds1 suggests that increased calcification of the avian eggshell is an evolutionary response to protect against predation and microorganisms, particularly in soil. The trade off was less permeability and water absorption. To offset that "cost," birds' eggs evolved the albumen or "egg white" which adds liquid content.
This is discussed more (and referenced) in Frank B. Gill's Ornithology2, which goes on to further explain that the shells additionally protect eggs from the weight of incubating parents.
Other functions, such as that of oxygen exchange, are permitted by the calcium shell due to microscopic pores. Also, crystalline calcite (the main ingredient of the shell) can be used by the embryo to form calcium in development of its bones.
1 Evolution of the Cleidoic Egg Among Reptilian Antecedents of Birds by Gary C Packard and Mary J Packard; American Zoologist, Volume 20, Issue 2, May 1980, Pages 351–362
2 Gill, Frank B.. Ornithology. United Kingdom: W. H. Freeman, 2007.

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


text:
Do all IgG autoantibodies lead to autoimmune diseases?
If there is a presence of autoantibody in our blood, does that mean that we are going to have an autoimmune disease? Are there some autoantibodies which don't cause tissue and organ damage?

As usual with biology, it's not that simple. There are autoantibodies present even in people without any signs of autoimmune disease. The immune system is a complex network of positive and negative regulatory cells and molecules - looking at a single component is unlikely to determine the state of the system. This is a major reason that it has been so difficult to figure out how to selectively act on the immune system to stop or prevent an autoimmune disease without compromising normal immune function.
Here's an article that expands on some of these aspects: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2703183/
For example, note "Despite the physiological elimination (negative selection) or functional inactivation (anergy) of high-affinity, self-reactive T and B lymphocytes in the thymus and bone marrow, respectively, there is compelling evidence that low-affinity, potentially autoreactive cells persist and that low-affinity reactivity to self-antigens is required for survival of T and probably B lymphocytes in the peripheral immune system."
It's also important to keep in mind that affinity of Abs and receptors for antigens usually depends on additional 3rd party molecules involved in the interaction, and that a single molecule may present very differently in different situations (for example, damage or inflammation may alter some self molecules into a previously unseen configuration that stimulates self-reactivity).

Can you please add some citations to support your claims?

@MattDMo hope that helps a bit

That's a good reference for autoantibodies in general, but the original question asked specifically about IgG, which as far as I know are always associated with pathology. I suggest expanding on that, talking more about normal IgM autoantibodies and what their suspected roles may be, then talk about class switching and IgGs being essentially universally associated with disease of some sort. You have the beginnings of a good answer, though.

Yes, I interpreted the question as being very basic and not intended specifically about IgG based on the body of the question. I don't have a good feel here yet about how deep to go in a response -- thank you for your suggestions.

Thanks for your input. I understand that IgM autoantibodies undergoes class switching to IgG and becomes more specific for the target antigen. Does having IgG autoantibodies indicate that at some point in future, the person is going to develop an autoimmune disease?

@Riq generally, yes. In fact, they likely have already developed disease, as it is during that process that class-switching occurs.


text:
Can anyone identify this bug, it's got six legs
Hi I live in the midwest (Wisconsin), these have recently started appearing all over my basement. Anyone know what they might be? They are about 2.5 mm long and they are quite active. I don't keep any food items in the basement they they would be able to fed on.

Please indicate size, describe behavior, and comment about any stored food in your basement or in nearby places of your home.

RelatedTiny dark-colored bug ID in Amman-Jordan

I'd look hard through your possible food storage areas; they may not be infesting the sorts of foods you'd expect, I've definitely seen some relatives here in WI. See for examples https://extension.umn.edu/product-and-houseplant-pests/pantry-pests-insects-found-stored-food#beetles-55711 https://hortnews.extension.iastate.edu/red-flour-beetle https://hort.extension.wisc.edu/articles/sawtoothed-grain-beetle/ I'm not certain which exactly you have, I'm guessing @theforestecologist can either provide a more definitive answer here or mark as a duplicate of the related ID.


text:
Can I use multiple bicistronic RBS sequences in a synthetic biological circuit?
The bicistroninc RBS sequences (BCDs) developed by Mutalik et al. [1] aim to remove context sensitivity from translation and therefore ensure more predictable gene expression. However, I have been told that having multiple transcriptional units, each using BCDs, can make cells sick. The explanation that I was given was that the toxicity is from small peptides that are produced from transcription from the first RBS sequence.
Has anyone demonstrated toxicity from multiple BCDs or is it apocryphal? If it has been demonstrated, is the mechanism of toxicity known and is there a way to use multiple BCDs while maintaining healthy cells?
[1] V. K. Mutalik et al., “Precise and reliable gene expression via standard transcription and translation initiation elements,” Nat. Methods, vol. 10, no. 4, pp. 354–360, Apr. 2013.

That’s a great question and has lot of opportunities to explore. I am not sure anyone has followed up on this original BCD work systematically. We did try cloning these elements on a medium copy plasmids, in an operon design, driving multiple genes, and now I think about it, that was not a smart thing to do. Cloning was very challenging, probably due to toxicity you mention. Didn’t have time to investigate this in depth (that it self is a cool project), but I think the toxicity is due to too much resources (ribosomes?) titrated out on these units. But that’s a hand-wavy explanation. Need mechanistic study to investigate. I think Tom Ellis’s group and others have done some beautiful work on toxicity associated with protein expression. Personally I think the toxicity is not related to the inert peptide (1st gene in a BCD operon) that’s produced. Another story we tried was to replace this first gene with something functional but not published.
Coming back to using BCDs for driving multiple genes, I would say if you clone these directly on genomes they should work like charm. We did try this and works good. Not published much (oh god, that’s so much work unpublished!) Bacterial operons have these junctions and elements of different strengths. Happy to discuss more if you have a follow up question!!
Thanks for your interest in this work. Really proud of our work on this system. Of course happy that we did this work as there were so many early effort on these BCD type elements. And love this open discussion SE platform! Don’t know how synbio survived without this system of sharing knowledge and experiences. Best wishes
Vivek Mutalik

In the documentation for this recent cloning method from Richard Murray's group at Caltech (,https://doi.org/10.1021/acssynbio.8b00060)  they include a parts library with various BCDs. I haven't tested this directly myself, but the warning they note for multiple BCDs is not that they are toxic, but that because they have long homologous regions that they are prone to recombination. This makes sense since the dummy peptide region is I think around 50bp and shared across all the BCDs. You could imagine making variants in this region to combat recombination issues, but who knows if that would affect the robustness of the BCD expression.


text:
What is meant by "opposing plasma membrane" with respect to cell adhesion molecules?
I am reading the Handbook of Neurochemistry and Molecular Neurobiology and I am learning about cell adhesion molecules (CAMs) and I have come across the following:

CAMs are involved in homo‐ or heterophilic interactions with molecules
positioned on opposing plasma membranes, and such interactions are
referred to as trans‐interactions. In addition, CAMs are often
involved in homo‐ or heterophilic interactions with other
membrane‐associated molecules positioned in the same plasma membrane.
Such membrane‐lateral interactions are referred to as
cis‐interactions.

I know that cell adhesion molecules are proteins mediation cell-cell or cell-extracellular matrix interactions. However, in the above excerpt from the book in the following statement: CAMs are involved in homo‐ or heterophilic interactions with molecules positioned on opposing plasma membranes, I am not sure what exactly is meant by "opposing plasma membranes". I think that this refers to the plasma membrane of a neighbouring cell the CAM is interacting with, however I am not fully certain.
Any insights are appreciated.

Opposing means facing each other, so the two outer surfaces can interact. Like two opposing armies.
I found an article:
"Pharmacology of cell adhesion molecules of the nervous system"
at
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2644493/
doi: 10.2174/157015907782793658
"...CAM-induced intracellular signalling is triggered via homophilic (CAM-CAM) and heterophilic (CAM - other counter-receptors) interactions..."

Thank you for your reply. Just to clarify, do homophilic interactions between CAMs always join two surfaces of the same cell? In the same book, I have read that the cell adhesion molecule NCAM2 interacts homophilically in trans, and the book states that trans interactions happen when CAMs interact with molecules positioned on opposing plasma membranes. Any insights are appreciated.


text:
Is the phrase "transmembrane segment" equivalent to the transmembrane domain of a protein?
I am reading the Handbook of Neurochemistry and Molecular Neurobiology  and I am learning about the cell adhesion molecule NCAM2 and I have come across the following:

The overall structure of NCAM2 is similar to that of NCAM. Thus, NCAM2
consists of five Ig‐modules (supposedly of the C2‐type) followed by
two Fn3‐modules. The protein exists in a GPI‐anchored isoform and in a
transmembrane isoform that contains a 20–25 amino acid transmembrane
segment followed by a 106–119‐amino acid cytoplasmic tail (Alenius and
Bohm, 1997; Yoshihara et al., 1997).

I know that NCAM2 is located at the cell membrane and has an extracellular, transmembrane and intracellular domain. However, for the above statement: The protein exists in a GPI‐anchored isoform and in a transmembrane isoform that contains a 20–25 amino acid transmembrane segment followed by a 106–119‐amino acid cytoplasmic tail, is the term 'transmembrane segment' equivalent to the transmembrane domain? Further is the term 'cytoplasmic tail' equivalent to the intracellular domain? Any insights are appreciated.

Yes
I'll admit defeat in trying to find the section in the text you linked - if there's any one thing Google can't do, it's search.  But questions like this are better put to Uniprot, which gives quite a bit of information.  Following that link, you'll see they identify 21 AA of transmembrane topology from 698 to 718, with a cytoplasmic domain afterward.  So the cytoplasmic tail is the intracellular domain.
In a sense there is a second transmembrane domain - the signal peptide from 1-19 - but because it is cleaved little attention is paid to it.  The extracellular domain starts at 20, with an N terminus outside the cell.
To quote Wikipedia, a transmembrane domain "usually denotes a single alpha helix of a protein".  You should probably listen to them on such an issue because nobody is more fixated on semantics (it's a sort of vote).  Philosophically, you can picture that multiple transmembrane segments could operate as a functional unit - but each of these segments would be separated by some region of extracellular or intracellular sequence from the next.  A "domain" in a protein is a self-contained unit in the primary sequence, not just a series of helices that turn out to be near each other, so that wouldn't work.  And in fact if you look at a GPCR paper they speak in standard terms of seven transmembrane domains even while analyzing how they function together.


text:
How standardized is lab-grade skim milk?
I was surprised to learn in the answers to this question that in many cases the preferred cryoprotectant for many organisms is skim milk, rather than something more simple and well-defined like glycerol. And indeed, Sigma will happily sell you lab-grade dried non-fat cow's milk for lab-grade prices.
It seems to me that this could potentially cause significant variability and reproducibility issues. Milk is pretty sensitive to the condition of the producing animal, and when dealing with a cow we're talking about a very large and complex source that's not hyper-standardized like lab-grade rodents.
I don't seem to be able to find anything much about specification on Sigma's site, however (the spec sheet for milk has only the obvious like "opaque white fluid").
Does anybody know to what degree lab-grade milk is actually standardized, and if this should be a concern for protocols like cryoprotection?

There is a degree of variability in milk, and in some cases this cause problems in protein work. Despite being a standard for ELISAs, it's not known to be the most reliable blocking buffer. As far as cryoprotection goes, variability doesn't seem to be a major concern.
Standardization varies depending on manufacturer. The Sigma link you included reports a quality level of MQ 200. The MQ level is something Sigma created in an attempt to increase clarity about quality controls. Products rated MQ 200 are for non-regulated applications. For this level they will provide a site-quality self-assessment, a certificate of quality/analysis, and specifications. They also have a notification system that customers can opt-in to for updates on quality control features. There's information on what each quality level meansand a breakdown of what they will notify you about on the Sigma website.


text:
How is the surface tension of water related to transpiration?
My textbook mentions the following :
• Surface Tension – water molecules are attracted to each other in
the liquid phase more than water in the gas phase.
I can't understand how that would help in transpiration.

I think the question needs more clarity: the quote given does not fully define surface tension - it is merely a correct statement about difference between a liquid and a gas. It is also not clear why the author thinks that it plays a role in transpiration.

My textbook actually mentions three things. Cohesion, adhesion and surface tension. The first two, I can understand is to maintain the continuous stream of water but I can't understand the role of surface tension.

surface tension plays a role in liquid moving up the pores, and also in gorming droplets on the skin, but it is hard say more without knowing the context.

Is the textbook abour plants? Surface tension is inmortant in plant laefs.

Complete reference:

The transpiration driven ascent of xylem sap depends mainly on the
following physical properties of water:

• Cohesion – mutual attraction between water molecules.

• Adhesion – attraction of water molecules to polar surfaces (such
as the surface of tracheary elements).

• Surface Tension – water molecules are attracted to each other in
the liquid phase more than to water in the gas phase.

The ascent of xylem sap is aided by surface tension since it allows the water to hold together and create a continuous column of water. Otherwise, the capillarity would be affected (the water column could 'collapse' under it's own weight, for example) and plants would be unable to conduct water via the xylem. Surface tension, cohesion and adhesion are common to capillarity occurring outside of living systems as well.
Recommended read:  https://www.usgs.gov/special-topic/water-science-school/science/capillary-action-and-water?qt-science_center_objects=0#qt-science_center_objects


text:
Are there any epiphytic plants that pull water from the air and supply terrestrial plants with excess?
Do you know of any epiphytic plants that pull water from the air and supply the excess to other terrestrial plants?

This isn't worthy of an answer but offhand I would HIGHLY doubt it. Pulling water from the air is harder than getting it from the ground; epiphytic plants are typically the type of plant that can survive on comparatively little water for that reason. I honestly don't see a circumstance where a terrestrial plant would need water from them, and where they could afford to spare the extra (but it's been awhile since I studied plants, so could be wrong).


text:
Can a trait be too successful? Wouldn't overwhelmingly successful traits limit variability, which is one of the requirements of NS?
Can a trait be too successful?  Wouldn't an overwhelmingly successful trait soon limit the gene pool, and if so, how would the process of natural selection react to that?  If an individual is born with a trait that allows it to reproduce unimpeded, and it passes that trait on to its offspring, wouldn't the variability be quickly reduced in the population?  And if so, then would NS limit the trait so that it isn't overwhelming?
And thanks to everyone who contributed here, you have been very helpful and I am very grateful.

Welcome to Biology.SE! Please clarify and research your question. In particular, why do you think that a "overwhelmingly successful trait" would limit the "gene pool"? ——— Please also take the [tour] and then go through the [help] pages starting with [Ask] questions effectively on this site and delete or [edit] your question accordingly. Thanks!

I have found that when learning about a new area starting with a relatively accessible and reliable source like Khan Academy is very helpful. Wikipedia is also generally a good starting point and you can then check their references. Online platforms called MOOCs offer free (or very low cost) courses on a wide variety of subjects — two I am familiar with are Coursera and edX. Finally, textbooks with a good level of detail are also freely available online e.g. from NCBI.

Finally, I encourage you to check out some of the online resources available for learning more about evolution. For example, this a useful introduction to evolutionary theory from UC Berkeley. This will give you a better understanding of evolution and perhaps allow you to frame your question more clearly.

This information is very helpful and I am looking forward to using these resources to find the answer to my question.

I think you could expand the question to be more clear. See if I understood correctly: Suppose there is a given individual A in a population with a very adaptive trait T. Presumably this individual would generate more descendants, and its descendants would also reproduce at a higher rate, so that in the long run a significant fraction of the population would acquire trait T. But this seems to imply that a significant fraction of the population would descend from A and therefore a lower genetic variation.. Is this your question? If so I suggest looking for genetic drift and related things

Yes, in neutral theory of evolution this is called fixation - when all the alleles (for a given locus) become identical. Note that it may happen, even if the gene does not have a striong selective advantage - due to the random effects.
If you are looking for the basic background in population genetics, Gellespie's book is a good starting point.


text:
Is there any animal known to produce structures of both keratin and chitin?
I began with thinking about the similarities between keratin in its hardest form (fingernails, horn sheaths) and the chitin that composes the exoskeletons of some few beetles I've seen in my life. To my eye the two materials seem to have comparable properties. Then I found out that tarantula hair is also made out of chitin, so in more aspects than one it seems that chitin and keratin have convergently evolved.
I understand that chitin is a carbohydrate while keratin is a protein, so there's no commonality regarding the origin of the two, but I am curious as to whether an animal has ever been demonstrated to produce both compounds in some capacity?

Some fish and some salamanders are capable of making chitin.


text:
I hit an area of my elbow and had a burning sensation throughout my hand
I happened to bump the side of my right-hand elbow on a corner and suddenly felt a burning sensation on the right side of the hand elbow-up. Any theories that could describe what I recite?

While this sounds like you hit your ulnar nerve, it also sounds like a question about personal medical health which are generally considered off-topic on this site.

Ulnar nerve supplies sensory innervation to medial 1.5/5 of the hand(i e. Medial 1.5 digits). So when you hit your elbow, ulnar nerve is involved (it runs over medial epicondyle of humerus). So there is a kind of burning sensation felt.

It's often referred to as hitting your funny bone:
Heres one reference on the subject:
https://www.huffpost.com/entry/hitting-your-funny-bone-i_b_12201698
and here is another:
https://www.mentalfloss.com/article/21474/what-funny-bone-and-why-does-hitting-it-hurt-so-much#:~:text=When%20you%20hit%20your%20funny,the%20ring%20and%20pinky%20fingers.
The ulnar nerve is exposed near the bones of the elbow, especially if the elbow is bent. You can probably locate it with your index. If you hit the ulnar nerve near the elbow, it can be felt in the little finger and one side of the hand.


text:
Growing Penicillium Digitatum Mold
I left a cup of tea with Lemmon on my desk and after a while green mold start growing on the water. From my understating this is Penicillium digitatum. I gave it some sugar and after one day black spots appeared. I read that it can be little bit dangerous to inhale mold so I wrapped the cup with saran wrap and make some holes in it in order to give the mold oxygen.

What do I need to do in order to give the mold better condition to grow?
Can it be dangerous growing it?

What's your goal with this project? You don't really know what you've got in that tea-cup, and DIY dirty dish biology doesn't sound like a great idea in general...

What makes you think it's specifically P. digitatum? Penicillium molds are very widespread in the environment, and can be almost impossible to differentiate based on visual appearances alone. That being said, I echo @jakebeal - what is your ultimate purpose in this experiment?

You could place part of the mould into a cut in a piece of citrus fruit to continue its growth. Citrus can also host P. italicum, the below website is one mentioning how to differentiate between them.
http://www.pestnet.org/fact_sheets/citrus_storage_moulds_197.html
Hazards.
Aspergillosis: (fungal spores growing in the lungs) which is uncommon.
Asthma: penicillium spores have been associated with increased chance of onset of asthma, and problems with breathing in people with asthma.
There may be other hazards.
I just cite one paper below, but a search using terms of penicillium and asthma shows lots more.
"Household airborne Penicillium associated with peak expiratory flow variability in asthmatic children"
published in :
Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology
by:
Kemp W. Bundy, MD, MBA, Janneane F. Gent, PhD, [...], and Brian P. Leaderer, PhD
doi: 10.1016/S1081-1206(10)60139-1

thanks. It seems too dangerous to keep growing it. Should I worry that it was in my room for a few days?

@ziv as long as you're not immune compromised and you haven't been purposely inhaling the fungus, you should be fine.


text:
How come the role of the Apis mellifera is determined by nutrition rather than chromosomes?
Prior to making my question I browsed on similiar question such as this one but it doesn't specifically addressed my doubt in the sense that it is related with a different species and on a concept not mentioned in that question. More specifically on whether does nutrition may influence genetics on the sex determination or not?.
My doubt arises as I'm learning about Partheneogenesis and genetic determination of the sex. Upon reading this entry in Wikipedia, it explains that a queen bee of the Apis mellifera is determined during the development of the larva. The article doesn't state anything about the chromosomes of the larva. It just states that the queen will develop into that by feeding it from royal jelly, from which I believe it has some sort of protein that may influence the development of such larva giving it their characteristics.
But this topic is letting me confused. Does this means that for example a male bee can become into the queen?.
This article explains that some insects produce haploid males from unfertilized eggs by I believe Partheneogenesis. But if the bee doesn't mate, how is the sex determined?. I believe that it will produce only females (as his genetic sex determining chromosome is ZW?) and as such will yield only females, but if the queen does successfuly mate with a male may produce males which in turn can also lay eggs (by Partheneogenesis) and those eggs will all be males?.
From this I'm getting the conclusion that it can occur that some individuals may be all females or all males?.
How come is it possible for an haploid organism get into full develpment isn't it necessary to be diploid?. Do they become into diploid at some moment?.
Can someone help me to clear out this doubt?. This topic has left me confused, so an answer which would help me the most is some sort of explanation on the concepts of partheneogenesis and sex determination in the bees.

Where did you read that bees have ZW sex determination system?

The Biology.SE community has agreed that questions that show little or no prior research effort are off-topic on this site unless you have shown your attempt at an answer. Please [edit] your question and tell us where you've looked for answers, what you do know about the topic, and where exactly you still have questions. Unresearched questions may be subject to down-voting and closure. ——— Searching for "sex determination in bees" leads to multiple pages such that should help you.

@BagiM I concluded this from reading at the wikipedia page on Partheneogenesis but of course I could be wrong, hence the necessity of an answer which could clear this doubt.

@tyersome I'm sorry but I disagree. If you read with attention I started my question by saying that I made an initial effort into looking for answers in Wikipedia. Not only this but I also browsed for similar questions on this community, but yet I'm unable to understand. Thus I require some sort of answer which could address my doubts.

You say you made an effort, but I'm suggesting you can (and should) do more — e.g. by doing some reading based on the previous comments and correcting the mistakes in your post. ———— This is not a forum or tutorial service; it is a Q&A site where specific questions relating to biology get specific answers. Please take the [tour] and 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.

I have found that when learning about a new area starting with a relatively accessible and reliable source like Khan Academy is very helpful. Wikipedia is also generally a good starting point and you can then check their references. Online platforms called MOOCs offer free (or very low cost) courses on a wide variety of subjects — two I am familiar with are Coursera and edX. Finally, textbooks with a good level of detail are also freely available online e.g. from NCBI.

So you have read the sentence: "Among species with the haplo-diploid sex-determination system, such as hymenopterans (ants, bees and wasps) and thysanopterans (thrips), haploid males are produced from unfertilized eggs." And you concluded the sex determination system in bees is ZW???


text:
Is there any plausible biological mechanism for "universally protective vaccines" via "MHC allotype-independent immune effector memory cells"?
Geert Vanden Bossche, who has recently gained some fame for dissing all current Covid-19 vaccines (and who is also asking the WHO to meet him so they can  be infused with his wisdom), has had the same poster at a couple of conferences/expos in 2015-2017. Quoting one of these (only the title seems to differ):

Universally protective vaccines: A revolution in modern vaccinology
Geert Vanden Bossche (University Leuven, Belgium; Univac NV, Belgium)
To eliminate safety risks related to infectivity, inactivated pathogens and more suitably, well-characterized pathogen-derived
antigens (Ags) have increasingly been used as immunogens in modern vaccines. The selection of these Ags is usually based on
their capacity to induce immune responses that correlate with natural protection. These Ags, however, are known to be antigenically
variable or conformation-dependent (e.g., B cell epitopes) and/or subject to immunogenetic restriction (e.g., linear, T-cell epitopes). In
addition, the immunogenicity of good vaccinal Ags is largely dependent on memory CD4+ T helper cells. However, activation of the
latter upon natural infection or foreign Ag exposure of genetically predisposed subjects can occasionally lead to immune pathology.
Priming of CD4+ T helper cells by adjuvanted vaccines is, therefore, increasingly raising safety concerns. On the other hand, Ags
that are highly conserved and vulnerable because of their exposure on the surface of infected or pathologically altered host cells are
either not immunogenic or subvert the host immune system. Hence, they are not used as vaccinal Ags in contemporary vaccines.
We consider that new technologies enabling immune targeting of these Ags by natural, MHC allotype-independent immune effector
memory cells is the new Holy Grail in modern vaccinology.

Basically, is this complete nonsense or is there any plausible biological basis for "universally protective vaccines"?
In his Covid-19 talk, he basically says that natural IgM is better than anything else, which actually seems dangerous crackpottery in the context of Covid-19 because patients with numerous but low potency antibodies are often among the dead.
But in his Covid talk he never mentions "MHC allotype-independent immune effector memory cells" which showed up as his punch line in these older posters that I'm asking about. So is this (older) concept (of his) phantasmagoric, or does it have any biological corresponded? I've looked through a review on memory T cells, which describes the effector memory as a rather problematic subset because it's apparently made of only seemingly connected further sub-types, but I can't tell if any of these could possibly have anything to do with what Bossche is saying. In particular, how would any effector memory cells be the basis for a universal vaccine?

I'd appreciate some comment(s) as to what is wrong with this q, to go along with the DVs.

"Universally protective" is the epitome of hokum; why spend energy reading any further?


text:
Does the two-state gene expression model apply to constitutive genes?
Wikipedia defines constitutive genes as

a gene that is transcribed continually as opposed to a facultative gene, which is only transcribed when needed.

I don't have a strong theoretical background biology/molecular biology, and I am currently studying gene expression analytically, specifically the two-state model of gene expression, where a gene can be on the 'ON' or 'OFF' state.
From this definition I get the understanding that constitutive genes are always in the 'ON' state, although I am not sure if that is the case since other sources describe constitutive genes as genes that are expressed at a relatively constant level, which could still be a gene fluctuating between 'ON/OFF' states.

This question cannot be answered as it solely depends on the definition of OFF and ON states. I.e. is it defined by a certain protein-assembly that would attract the RNA-pol? Or does it mean that the genes is currently being transcribed? Does it depend on the DNA-accessibility? I guess your model is NOT biologically defined and instead just wants to fit some data. In this case, this question makes no sense. It's just a model and does not have to be compared to any biological 'reality'. If it fits the data, it's good!

@KaPy3141I think it very much can be answered, and your comment is the beginning of such an answer.


text:
Do de-husked seeds germinate?
As simple as that, lentils beans and other legumes are sold both with and without husk, and often I make beans with the husk germinate in a jar.
Do those without husk germinate as well? Or are they simply dead?
I'm asking this because my girlfriend told me she's using de-husked legumes, but that they take longer and less of them actually do sprout.

De-husking and industrial storage reduces the germ's longevity quite a lot, although quite a lot of germs will still be viable if the humidity and microbial conditions are very stable, perhaps even a year.
De-husking will accelerate this graph:

The husk is designed to keep the germule in peak condition in the wild until whichever season it is supposed to germ, through droughts, rains, cold weather, changes in humidity, predation, infection.
If the germ is de-husked and left in natural conditions, it rapidly loses vitality and deteriorates. In storage it's kept in conditions made to discourage microbes, so it will last longer, but it will absorb ambient humidity changes and deteriorate much faster than with a husk.


text:
why dead mouse doesn't bleed when we cut their skin?
When we are pricked by a needle, we bleed nevertheless it's so small wound.
But when we do mouse anatomy, it doesn't bleed even if we cut their whole abdominal skin.
Other student asked about that, professor didn't know exactly but just guessed that mouse skin has no blood vessel. But I think it's wrong. that makes no sense.
As my guessing it's because mouse is dead when we do anatomy so there is no enough blood pressure.
Mouse have to bleed like ourselve. is this wrong?

You are talking about dead mice?

'because mouse is dead when we do anatomy '. Yes he is.

By the way, Blood-pressure can be negative (smaller that atmospheric) dependent on where you measure it (due to Bernoulli principle).

So, you should rather emphasize on blood flow, not blood-pressure.

the fact the mouse is dead is important dead humans don't bleed either. blood starts to coagulate after only a few hours.

@John: There are two stages to this.  Live animals, whether mice or men, bleed because the blood is under pressure.  (Considerable pressure, if you've ever had to deal with an arterial wound.)  After death, there can be some blood drainage from wounds, under the influence of gravity &c.  That stops when the blood coagulates.  See e.g. "livor mortis".

From personal experience, extracting organs/tissues of over 1000 mice I can give some hints:
Mice blood coagulates quite fast after death. If you need to extract blood, you are under time-pressure and many scientists extract the blood directly after death from the heart using a syringe. If you are not fast, you miss the chance of drawing blood as this can't be done after coagulation. Others cut up the thorax (post mortem) and then directly draw blood with a syringe. I personally never tried this technique but I spectated that mice bleed a bit, directly after death, when opening the thorax, however it's not much.
After drawing all blood from the heart, mice don't bleed, no matter where you cut, potentially because of low blood content remaining. (Un-?) Fortunately, I never had to cut mice that were alive.. so I cannot tell you what would happen if they were alive.
Edit: Also, in theory, the smaller an animal is, the higher becomes the diffusion/volume ratio and surface-tension/volume ratio. This means smaller animals need less active blood circulation and and their blood vessels might have a small diameter, so that most blood would be kept inside by surface tension if these vessels were cut.
Edit due to comment:
The extractable blood from mice is around 1.5 ml, and I have seen opening of the thorax within seconds post mortem with minor bleeding. Afterwards, the majority of blood (1.5 ml) was extracted directly from heart with a syringe. As this was post motrem, I cannot exclude the possibility that coagulation of blood in small peripheral vesicles already affected the observation or how heart beating would affect it. I cannot say what would happen in live mice and I am happy that I don't have this knowledge.

Live mice certainly do bleed, though their total blood volume is only on the order of 2mL.

I know it's around 1.5 ml, and I have seen opening of the thorax within seconds post mortem with minor bleeding. Afterwards, the majority of blood (1.5 ml) was extracted directly from heart with a syringe.

thank you! this did help!


text:
What is this little (3mm) spotted insect in Northern Italy?
Every now and then I find one or two of these tiny bugs in my kitchen. They are about 3-4 mm long and seem to be very static on hard surfaces (furniture or walls). They rarely, if ever, more.
The one in the picture was found dead on the floor so I was able to take close-up pictures. The insect seems to have a very regular pattern of spots and presumably wings.
I tried to look online for Italian websites of "household bugs" but I could not find it.
Is it problematic, i.e. does it ruin food or something?
Location: Northern Italy, province of Vicenza


text:
Is there a favoured mathematical model of bacterial growth?
One of the most regularly measured phenotypes in bacterial synthetic biology is growth. Anyone who does wet lab microbiology or synthetic biology will have performed a growth curve measurement. However, it is quite rare in synthetic biology papers for growth to be characterised using a mathematical model - even though growth curves are regularly shown in supplementary materials.
There are a plethora of growth models around - from basic logistic growth to the more biologically grounded Monod growth. I recently discovered the Richard's model which seems to be a more general form encompassing logistic, Gompertz etc. Is there a favoured model for the microbiology and/or synthetic biology community? Is there something holding the synthetic biology community back from regularly reporting growth characteristics of their cells?

A few rather general remarks: Models are usually designed to describe specific situations using the minimal number of parameters. So the models that you listed are not necessarily mutually exclusive. One could design a more general model, but it would necessarily have more parameters and less statistical power. From statistics point of view it is also necessary to keep in mind that all these are parametric models, which can only approximate the growth curve.

Some clarifications:
Commonly used models for bacterial isothermal growth curves (which represent the growth curve directly) are for example:

Exponential

Logistic

Generalized logistic

The Monod equation expresses how the growth rate changes with the availability of substrate see a related question here.
The Monod equation can be incorporated into an exponential growth model (differential equation) like this:
$$
\frac{dX}{dt}=\mu X
$$
with
$$
\mu = \mu_{max} \frac{[S]}{K_M+[S]}
$$
where $X$ is the biomass concentration and $[S]$ is the substrate concentration. Or into a logistic growth model:
$$
\frac{dX}{dt}=\mu X \left(1 - \frac{X}{X_{max}} \right)
$$
with
$$
\mu = \mu_{max} \frac{[S]}{K_M+[S]}
$$
where $X_{max}$ is the carrying capacity.
Other growth-substrate relations like Haldane which takes into account growth inhibition by the substrate can be used instead of Monod one.
Regarding this:

Is there something holding the synthetic biology community back from regularly reporting growth characteristics of their cells?

It depends on what branch of synthetic biology you are looking into. Model-based design engineering biology interpretation of synthetic biology goes around the DBTL cycle. In the DBTL cycle, there are always (at least) models of both growth and gene expression.

the more biologically grounded Monod growth

Why is the Monod model more biologically grounded? It is empiric and NOT based on biological considerations! I only know this equation from enzyme kinetics, not for cell-growth, where the identical Michaelis–Menten equation assumes a random collusion model. So according to this model, your cells would grow more, the more substrate (glucose?) collides against the walls!
It seems quite logical to model enzyme-kinetics or chemical reactions with random collusion models. However, the only relevant biological facts I see are the following:

Cells divide, which naturally suggest exponential growth.
Cell-cycles and circadian cycles exist, which naturally suggests a
constant generation time. (within the limits that everyone knows)

So, if everyone learns about growth curves and logistic fits in their wet-lab courses, where logistic fits work perfectly fine to predict growth within the log-phase, then why would there be a need to use other - more complicated - models, while the logistic model is conceptually indicated? (Also note that the Monod model still fails to predict the lag phase and death phase.)
This leads to the final answer to the question:

Is there something holding the synthetic biology community back from
regularly reporting growth characteristics of their cells?

Practical use!

In daily routine, the typical wet-lab scientist is merely
interested in knowing the expected time until a certain optical
density (OD) of the cell-culture is reached. Practically, this is
done with as few measurements as possible, based on experience and a guess of a generic generation-time.
Exact predictions are needed in large-scale biotechnological
production. In such a context all parameters must be accurately predicted and validated. Given your exact microorganisms and your production plan, small-batch trails will be performed and up-scaled. Everything must be known and planned in detail and quite often, the whole production facility is designed and built to achieve a single task! Everything, including the generated heat, O2, CO2, Glucose, (end-) concentration of the yield.. is monitored and legally binding deviation-limits must be set before-hand and met at all times. Small deviations can cause losses of millions of dollars and companies don't rely on simple models like "Monod", but stress-test every aspect and monitor and react in automated systems. There is vast knowledge regarding growth-curves and models, just you are not aware of it, as it is kept company-internal, or written in expensive bioprocess-technology books.

Yes, that is true! Good addition!

I've been appreciating your answers, and I think you'd be a good contributor to the more interdisciplinary SynBio StackExchange we're trying to launch. Want to support the proposal? https://area51.stackexchange.com/proposals/125068/synthetic-biology?referrer=MzNjZmVjYzI0NDg3NzNmMmI1Y2YzZTlmNDk3ZGIyOWU1ZWZmNGQ0YTBjZmFhODA2ZWQ4OWJkOTgwN2M3YTM0NPwIycDDlI9PcBruZ0as_SrnCeYJMauTp-s2V857fCra0


text:
Why am I finding peculiar B cell population when pbmcs are cultured for 3 days with CD40L?
While performing intracellular cytokine assay on B cells, I am finding a peculiar population.
I use 2*10^6 cells for studying each functional marker. The pbmcs are cultured for 72 hours, with CD40L dose being given in 0 hour after plating and BFA in the 48th hour. When analysed, I am getting two CD19+ populations from the lymphocytes. Can anyone enlighten me about what actually is happening?

Have you phenotyped the populations further, other than using CD19 after presumably gating on CD3-? How are you detecting the two populations of CD19+? Are you plotting CD19 vs another marker, or is it simply CD19 intensity? Can you share your plots and gating strategy, comparing untreated vs treated? Also, what is BFA - brefeldin A?


text:
Why is electroporation not the prefered choice transforming for Mammalian Cells (HEK)?
I see a lot of folks using different techniques for transforming mammalian cell (specifically HEK) instead of doing electroporation like I see with E.Coli (bacteria). Is there a reason for this ?

Viral methods are just more efficient and give you a higher viability in the end. Electroporation works but you'll have a low yield of viable cells after. Here's a nice paper looking at the effects of buffer composition on cell viability/transfection efficiency: https://www.nature.com/articles/s41598-020-59790-x with the general take away being, if electroporation is working well enough to transfect the cells, it will also kill a fair percentage as well.
Hek cells in particular are pretty easy to transfect through viral methods for stable integration of your plasmid or Fugene/lipofectamine for transient expression.

The reason mild electroporation has low transformational efficiency in eukaryotic cells is because they  sequester their DNA behind a nuclear membrane, right?

I'm pretty sure that all transfection techniques like electroporation/CaCl2/Lipofectamine are designed just to break the hurdle of getting it into the cytoplasm not the nucleus. The nucleus is a barrier to transfection but the prior mentioned methods aren't responsible for getting it there. Another shout out to retroviral based methods which will bring it to the DNA for you and integrate it into the genome

@yp66t89 I guess my followup question would be: "Why don't people use the retroviral methods for bacteria ?" Is there something that makes it not work, or is it just that electroporation would just be cheaper.

I'd assume bacteria tend to be more efficient at both integrating plasmids than mammalian cells, no one cares if most of your E.coli die as long as one bacterium survives with your plasmid, and I don't actually know if you can use virus on bacteria, I think you'd need a bacteriophage

@yp66t89 A bacterialphage is a virus --- that's the name for a virus that infects bacteria.

@jakebeal thanks for the clarification on my wording. Most people who work in mammalian cell culture refer to lentivirus and AAV as virus as a generic term and its easy to forget it can be confusing for others

By the way, @yp66t89: you seem to have some good synthetic biology knowledge: would you like to join the SynBio SE site proposal?


text:
Garden weed identification
I'd like to identify this weed found in a garden in northern England at this time of year (March).
It reproduces using underground roots rather than flowers - so if you dig it up and leave any behind it grows again.
EDIT: here's a photo with the bulb cleaned a bit.

if the leaves are cylindrical, with pointed tips, maybe Juncus spp. If you want info on how to grow (or get rid of) then ask to have the question moved to Gardening (or move yourself).

This certainly looks like a graminoid, but my guess would be a species of Poa. Very common for lawn grass, and when it doesn't get mowed they can get tall like this.

Is it possible to clean the roots in water to see the "bulb"?


text:
How does PCR mutagenesis add restriction site near the gene of interest?
I have been learning about PCR mutagenesis to add restriction site right next to the gene of interest using a primer that's attached with single stranded restriction site (first image). I have drawn my own diagram (second image) to better understand how this works, but I am stuck at the last step in question mark. How does DNA Polymerase 'insert' the green sequence (restriction site) so I would end up with the gene shown in the bottom?
Thanks for anticipiated response.

[![enter image description here][3]][3]

This diagram would be easier for you to conceptualize if you instead used the actual nucleotides in the restriction sites and green GGAGAA region along with your gene of interest (GOI). I recommend working with the DNA sequences when learning about primer design for various applications. I believe it has led you to be slightly confused with what is the restriction site and what is not in this diagram so I'll walk through it.
At the first step shown, you have your annealing region of the forward and reverse primers binding to the GOI. The overhanging region on each primer contain your restriction sites, which are flanked by the GGAGAA region for these restriction enzymes to have a sequence to "grab on" when you perform a restriction enzyme digest. Note that the annealing region of your primer anneals to the GOI because it has homology to the DNA sequence. Your restriction sites and green "clamping" region do not have homology to your DNA template so they are considered the overhanging regions. It is important to have your annealing regions of both primers of similar annealing temperatures when designing this or you may not have an efficient PCR reaction. I typically use this tool from NEB to design annealing regions of my primers. https://tmcalculator.neb.com/#!/main
Moving forward, these primers are both going to be used in one PCR reaction, not separate. Thus, when the reaction begins, the double stranded DNA template will denature, giving your forward and reverse primers the opportunity to anneal during the annealing phase of a PCR reaction. During the elongation phase, your DNA Polymerase will add complementary nucleotides in the 3' direction of your primers. Now after the first cycle, you have two different products. The forward primer's product has the GOI with a single stranded BamHI overhang on the 5' end, while the reverse primer's product has the GOI with a single stranded NotI overhang on the 5' end.
During the second cycle, after denaturation, the reverse primer with a NotI overhang anneals to the forward primer's previous product with a BamHI overhang. The DNA polymerase then adds nucleotides in the 3' direction of the primer, eventually adding complementary bases to the BamHI overhang. The same is done vice versa with the forward primer and the reverse primer's previous product.
Now after the second cycle, you have the desired products which will be amplified exponentially. Your GOI flanked by NotI and BamHI restriction sites with the GGAGAA region on both sides. This product is ready for a restriction enzyme digest.

Thank you for your thorough explanation. So after every round of PCR, I would have a complementary strand in the overhang region, right? I found this image quite similar to your explanation, and want to check if it's a correct diagram I could refer to. https://ars.els-cdn.com/content/image/3-s2.0-B978012385544200003X-f03-02-9780123855442.jpg

I like your hand-drawn figure. I will do a pictorial explanation starting from that. You are correct in the primer binding and first stage of PCR step. But PCR1 and PCR2 and the final product is wrong.
This is the way you think about it - In each step the primers bind to products extended in the previous steps (+ original template DNA, which is miniscule in comparison after a few cycles). The tails of the primers, that don't bind to the original template DNA are incorporated during extension from the other primer.


text:
Brain centers vs areas (and how they relate to nuclei)
I'm looking for a reputable source that can provide succinct definitions differentiating the following terms in the central nervous system (CNS; particularly in the brain):

Area

Center

Nucleus

Examples include Wernicke's area, piriform area, deglutition center,  olivary nuclei, vestibular nuclei, etc.
Really, I'm trying to corroborate my experiences having seen many examples of each but never having seen official definitions of either centers or areas. I know well that a nucleus is a cluster of cell bodies in the CNS [ex: source]. I also feel as though areas are regions with functionally-related roles, and that they tend to be associated with the cerebral cortex. Centers seem to be deeper functional regions.
What I'm not clear on is what the official differences between an area and a center are, whether (or to what degree) either term is inclusive vs exclusive of nuclei, and to what degree the relationship of all three words overlap either structurally or functionally.

I do know that Tortora & Derrickson (15th ed, 2017) indicate explicitly that certain centers are nuclei, but I'm not sure whether this more broadly describes all centers or is simply indicates a narrow example of a center.

Examples of nuclei in the medulla ...include the cardiovascular center and medullary rhythmicity center.

Motivation: trying to find a reputable source to provide a simple definition for my students. I usually just run with broad explanations based on repeated exposure of each, but I think my students would appreciate a cited, specific definition of each term.

I think the answer is that ultimately there are no specific definitions of these terms, and likely some exception to any rule one can craft. That's a hard thing to cite, though. I'll hunt around and see what I find.

@Bryan I'm glad you said that. Because after teaching A&P for the last 10 years, I've never seen such formal definitions. Still, there must at least be some sort of first usage or something for guidance. Perhaps I'll explore this from a historical word usage perspective to see if I find anything more definitive

Anatomists are the enemies of formality. Thinking it over more, some things like "area" seem primarily used in neocortex, at least the examples I can think of, which probably denotes that those areas aren't discrete "nuclei" or anything but more of a vague region (given that aside from some subtle cytoarchitecture they're not histologically separate from other adjacent areas). "Center" may be the least well-defined of the group.

I am not aware of an official organization that handles neuroscientific terminology so I doubt you will get official answers. However, brain areas are defined based on some criterion, e.g. anatomical landmarks, cell density changes etc. Nuclei are usually clusters of neighbouring brain areas that often participate in a common brain function (e.g. auditory or visual thalamic nuclei). In my subfield of neuroscience, center is never used. I've heard it in cognitive neuroscience studies and is associated to me with an implication of functionality (e.g. the "fear" center).

If you want to provide your students with some explanation of what one of the terms means, perhaps you may consider the idea of discussing how and why they were proposed. The situation is relatively clear if you choose for example the Broadmann areas and you can find plenty of material. I have not seen any information on how/when/why the "nucleus" term was first used.

"Anatomists are the enemies of formality" One example about this are the basal ganglia, which are located in the CNS, so they should be called basal nuclei. The mistake is already settled down in the CNS nomenclature, although some people tried to name them basal nuclei (e.g. Haines, fundamental neuroscience)


text:
Blood samples in cell lysis
I will be joining a team of field biologists on a trip to some uninhabited islands in the tropics. We will be collecting bird blood samples for some genetic research. We will be out there for two weeks. Will blood samples in lysis buffer last for two weeks with out refrigeration or freezing them? Or should we do our sampling closer to the day we leave so they have less time in tropical heat?

The exact answer to this greatly depends on the lysis buffer used, what you are lysing the cells for (DNA/RNA isolation, protein analysis, etc.) and how you intend to quantify your samples.
https://www.sigmaaldrich.com/content/dam/sigma-aldrich/docs/Roche/Bulletin/1/11814389001bul.pdf
This is a link to a standard red blood cell lysis buffer and handling recommendations. Note the following:

Lysis buffer must be stored at low temps prior to use
Use blood stored in EDTA, citrate or heparin anticoagulants
To obtain RNA use fresh blood only
For best results in DNA applications, use fresh blood or blood stored for less than 3 days.

Here is another paper describing the effects on DNA/RNA extracted from blood in ranging temperatures and storage methods
https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0184692


text:
Does anyone have a tutorial or some guide to get started with Rosetta protein modeling and design tool? (I am a Mac user)
I have been trying to get started with Rosetta protein modeling and design software bundle. I searched online but the tutorials in the Rosetta website are difficult follow. I have the binaries already downloaded.
I would highly appreciate if someone could help me out with this.
My initial goal is to model a few proteins structures and to design basic backbone structures.
Thanks in advance

I don't think this is really the place for this kind if question. You might be better off going to   biostars or reddit bioinformatics if you have a specific question. Good luck.

You give no link to the software you are enquiring about, so we cannot check what sort of support they provide, but you should certainly check yourself. If there is no such support, I suggest SE Bioinformatics would be a better bet.

Welcome to Bio stackexchange! I edited your question to make it more specific, and detailed. I found through a youtube search that meiler lab has some nice tutorials for rosetta, like this video on protein design

You're not going to like my answer.
Rosetta is not intended to be accessible to the general public. the complexity of the codebase and of the biophysics means that it is typically learned through mentorship and academic training.
If you are really interested in pursuing it, check the faculty list on the Rosetta Commons website, and start emailing professors asking to volunteer as an early career scientist.
You will have so. many. questions. at every step. it's just... you'll be so much more successful if you have mentors to guide you.
You may be interested in foldit standalone. It's the more options version of foldit. With foldit, you can work on real biological problems in a training setting. You might be annoyed by this because you want to program, but getting intuition for the structural biophysics is step 1. foldit was explicitly designed as a training tool for people (like you) who do not know about rosetta. Using foldit will teach you about the score function, for example.
Everyone starts with foldit. I started with foldit.
Getting good at foldit will increase your chances of a Rosetta professor agreeing to mentor you.
If you are an undergrad, there is a Rosetta Commons mentorship program about to become active - please join the Rosetta Commons forum and inquire there for info.
If you're being asked to do this for some school thing, it's absolutely ridiculous for someone to think you could do it without at least several class days about it.
In summary - I strongly encourage you to reach out to the Rosetta Commons faculty and mentorship program if you would like to seriously pursue Rosetta.


text:
Why do the COVID vaccines contain the cationic lipids they do?
Why did Moderna & Pfizer specifically pick their SM-102 and ALC-0315 cationic lipids with tertiary amines, branched tails, long linker chains, and small hydroxyl head groups? Are the large tails and packing parameter to keep the lipid from leaking out of the liposomal membrane? Why not use any other large hydrophobic groups? Thanks!

Are those vaccine's lipids very similar to our cell wall? I was told a while ago that due to the similarity, those lipid balls could just "merge" with cell walls and bring the content in the lipid balls inside the cell. I was pretty satisfied with that answer as I wasn't even aware of the amount of nuances that existed in the lipid itself.


text:
Can restriction enzymes (Type II) displace single-stranded binding proteins (SSB)?
Many type II restriction enzymes have been shown to be able to cut ssDNA.
If single-stranded binding proteins are bound to single-stranded DNA (ssDNA), does this prevent restriction enzymes which cut ssDNA from scanning the ssDNA and interacting with the target cut site?
The NEB website says that using SSB's improve restriction enzyme digestion, so it doesn't seem to be the case that SSBs inhibit target site recognition. But it is unclear to me how a restriction enzyme could recognize the target sequence unless it can also displace SSB's while scanning.
edit: specified REs that cut ssDNA

I'm curious as to why you are trying to add SSBs to ssDNA endonuclease digestions, is this some in house protocol you are trying?

I was thinking about how ssDNA endonucleases would work in vivo, where there are other proteins like SSB that could potentially interact with the ssDNA and interfere with cutting.

Please update your question to indicate why you think type II restriction enzymes (that cut  double-stranded DNA) would need to displace a single-stranded DNA binding protein.

I was thinking about type II restriction enzymes that were capable of cutting ssDNA.

Do you have some reason to think that this is a normal activity of type II REs? If so, please [edit] your post to include a summary of that evidence with supporting references. In the absence of that evidence your question doesn't appear to make sense.

Sorry, I just added a paper that supports the idea that there are some type II REs that can cut ssDNA.

That is talking about cleavage happening while the ssDNA forms dsDNA regions.  Why would you expect such regions to be bound by SSB proteins? Is there any evidence for this?

I did not read carefully, apologies. I did find a paper (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC432807/)  which describes the cutting of ssDNA by an endonuclease, but it is not a type II RE. I can either delete this question, or rephrase it.

Since you've got an answer, I would recommend rephrasing so that it fits the answer you got as well as possible. Thanks!

This is an interesting point. In the case of typical restriction enzyme digestion, it is double stranded DNA that is being digested. So in this case the SSBs are presumably binding to the sticky ends after digestion, so there is no competition with the restriction enzyme.
If you are interested in a specific case where you are digesting ssDNA, and have decided to add in single strand binding proteins, the binding strength (rate constants) of the SSB and restriction enzyme would influence how much the enzyme can displace the binding protein.
Here's a paragraph from the NEB/T4 gene 32 page indicating many similar applications involving reverse transcriptases, polymerase etc.

"Recently, it has been shown to improve restriction enzyme digestion
(6), improve the yield and efficiency of reverse transcription (RT)
reactions during RT-PCR (7-9), enhance T4 DNA polymerase activity
(10-11), as well as increase the yield of PCR products (12)."

EDIT: Although the reference (6) cited by NEB does not have any evidence that proves the enhancement of restriction digestion with single strand binding protein 32. This chapter might be helpful? - Kowalczykowski et al., "21 single-stranded DNA binding proteins." The enzymes. Vol. 14. Academic Press, 1981. 373-444.
From their abstract, it looks like the mechanism of enhancement could be through prevention of ssDNA hairpins so that the endunuclease can access it's recognition site (I haven't read the full chapter). Another fact supporting this is that ref(6) mentions that other interacting enzymes can work alongside SSBs only when SSB's are not saturating all the DNA in the in-vitro reaction. In an in-vivo context, the chapter abstract states that intracellular SSBs are sufficiently abundant to saturate all ssDNA intermediates formed inside cells (I presume they are talking about E. coli)
Below is the supporting text from reference (6) mentioned by NEB - bolding is mine, for emphasis : Bittner, M., R. L. Burke, and B. M. Alberts. "Purification of the T4 gene 32 protein free from detectable deoxyribonuclease activities." Journal of Biological Chemistry 254.19 (1979): 9565-9572.

Nuclease Assays-The presence of both exo- and endo- deoxyribonuclease contaminants in the 32 protein fractions has been monitored carefully throughout these purification schemes. The results of exonuclease assays are presented in Table III, and the results of sensitive endonuclease assays are presented in Table IV. Note that, when such assays are designed to detect nuclease activities on single-stranded DNA, it is important to test 32 protein at subsaturating, rather than only at saturating, protein to DNA ratios. Otherwise, an activity which hydrolyzes only free (non-32 protein-com- plexed) single-stranded DNA will escape detection.

Thanks for the response, that makes sense about dsDNA. I was mainly interested in the case of RE's cutting ssDNA, and how SSB's might interfere or not there. I looked at the paper  in that is referenced in your quotation, but don't see the data that would point to the same conclusion. I assume it must be something in Table IV?

Oh yes. I couldn't find anything relevant in that paper, NEB might have cited it in error. I edited my answer with another potential reference

I looked near both table III and IV

Please do not post text as images. Copy and paste the text into your post. Images are not searchable, and can not be interpreted by screen readers for those with visual impairments. Use the [edit] link to modify your answer. See this for more information. Thanks!

Ah, that makes sense. Thanks for pointing that out. I was lazy because it was an ancient PDF that wasn't copying well. I fixed it now :)


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Is there a DNA sequence that is true for all primates?
There are a total of 324 million known variants from sequenced human genomes. https://en.m.wikipedia.org/wiki/Human_genetic_variation
Is there an DNA sequence that is true for all primates?  Is this more acceptable on another site maybe?

It's not totally clear what you mean by the words "identifier" and "true". do you mean "is there a DNA sequence that exists in all primates?" if so, how long do you need it to be? does it need to be in a homologous location in all primate genomes? It is trivially true that the one-letter sequences A, G, C, and T exist in all primate genomes, but I doubt that is what you mean. why do you want this sequence?

Please rephrase your question. It is not clear what is meant with "324 million variants from..". Is this the total number of human genomes that have been sequences or are these the total number of alleles that have been found? Please also report your source. Please also specify what you mean with "identifier". Do you mean any sequence, that is common in all human genomes, but is expected not to occur in any other species? Then the answer - forced by stochastics- is yes, without any doubt whatsoever. Finally, what does your last sentence mean?

Ribosomal RNA sequences (rRNA) are present and highly conserved in nearly all organisms (excluding viruses) and serve as the basis for reconstructing the tree of life (archaea, bacteria and eukaryota). Such reconstruction obviously implies that there also differences between rRNA sequences, but they are smaller for a limited taxonomic groupings, such as primates. Still, even within primates there is some variation, although identical regions can be identified, see, e.g., here.

Thanks to your Wikipedia link, I was able to track what you meant with "324 M variants". These numbers refer to entries in the dbSNP (single nucleotide polymorphism database).
If you have a look at the submission guideline, it is not allowed to submit sequences over 50 nt: https://www.ncbi.nlm.nih.gov/snp/docs/submission/hts_launch_and_introductory_material/
This means your number doesn't necessarily refer to either the number of known alleles (might be longer) or the number of fully sequences humans (might give many SNPs per sequencing).
Anyways, if you compare this (incomplete) number to the size of the human genome (3.1 billion), you will see that the genome is roughly 10x bigger than the total count of known SNPs. Those heavily are enriched in SNP loci, meaning they overlap in location.
So from this data one may only say that >>90% of the genome consists of non-known SNP sites. So your question is answered with a yes, most of the genome is similar/"true", while this just reflects the current state of knowledge and most certainly, the number of known SNPs will increase over time.


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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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How to convert a genus name to a noun or adjective
Consider the crayfish family Cambaridae.  As I understand it, this familial name can be turned into an English noun or adjective by changing the first letter to lower case and dropping the "ae." An example use is "Responses of cambarid crayfish to predator odor" (adjective). Similar conversions from generic names are widely used as well.  For example, for the crayfish genus Procambarus, the english conversion "procambarid" is widely used, primarily as an adjective, but also as a noun. A google scholar search for this word turns up hundreds of uses.  A search for "id" conversions for other generics names for hermit crabs, and snake genera turn up uses of them as well. I cannot find any information that actually describes this conversion and it's rules.  Can someone point me to a reference, or otherwise help clarify the issue?

some resources note the capitalization but not the rules themselves: https://scientistseessquirrel.wordpress.com/2020/10/13/why-dont-we-capitalize-taxonomic-names-used-as-adjectives/ (i left a comment there asking)

I think that it boils down to taking a Latin name and removing the case ending to get an acceptable English adjective. Given that it might be a purely linguistic situation, it's possible another SE site would be better (English language?), but this topic is definitely relevant to biologists, as they're probably the ones who run into it most frequently.
We can look at IAPT article 60.10 and it suggests a systematic way to do this, albeit for an unrelated reason. I don't see that they directly address the anglicized Latin adjective form:

A noun or adjective in a non-final position appears as a compounding form generally obtained by
(a) removing the case ending of the genitive singular (Latin ‑ae, ‑i, ‑us, ‑is; transcribed Greek ‑ou, ‑os, ‑es, ‑as, ‑ous and its equivalent ‑eos) and
(b) before a consonant, adding a connecting vowel (‑i- for Latin elements, ‑o- for Greek elements).

I think that we want to apply step (A) but not step (B) here, as their goal is the formation of compound names, and step A alone will get us -id, which is an anglicized adjectival ending (-idus --> -id).
Taking your examples:

Cambaridae --> remove Latin genitive suffix -ae --> cambarid.
Procambarus --> make Latin noun into the adjective procambaridus --> remove suffix -us --> procambarid.

Unfortunately, it looks like there are a ton of possible Latin adjectival endings- the -id examples seem pretty straightforward because you can get an English adjectival ending directly, but other taxonomic names don't resolve so neatly. For example, if I want to use "Lachnospiraceae" as an adjective, I could imagine the following (applying only step A above doesn't seem to work well: "lachnospirace"):

lachnospiraceid
lachnospiraceal
lachnospiraceous

and I don't really know how to pick among them!
I have left a comment on a blog post from Stephen Heard on a related subject (comment above), perhaps he'll see fit to weigh in here.


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What can you learn about someone's mother and father by examining their DNA?
Disclaimer: I ask this question from the position of having paid absolutely no attention throughout school/highschool science classes. I am incredibly ignorant, but I don't know how to find the answer to this question using google, and would rather consult actual live minds via this stackexchange.
My question is (I think) fairly straightforward: By examining someone's DNA, how much can you learn about their mother and father? Is it perhaps possible to analyse the DNA and do the equivalent of a "fast fourier transform" to extract and reconstruct the respective DNAs of their mother and father?

I have found that when learning about a new area starting with a relatively accessible and reliable source like Khan Academy is very helpful. Wikipedia is also generally a good starting point and you can then check their references. Online platforms called MOOCs offer free (or very low cost) courses on a wide variety of subjects — two I am familiar with are Coursera and edX. Finally, textbooks with a good level of detail are also freely available online e.g. from NCBI.

In principle, you can reconstruct 1/2 the genome of each parent.
Each of these halves is still a "complete" genome, in the sense that it (usually) contains 23 full chromosomes (there are 23 human chromosomes). Every person has two copies of their genome, one of which is inherited from each parent. I strongly recommend reading about meiosis to learn more about this.
Each of these single genome copies is called a haplotype, and is an outcome of recombination between their own two genome copies. So neither copy looks exactly like a parent, but is rather a mixed-up version of that parent's genome.
There are a lot of genomic methods out there that try do exactly this task (reconstructing parental haplotypes) by various means. It is somewhat complicated and expensive, but possible in principle:

One method is trio-binning, which involves also collecting data from the parents, but focusing most effort on the child. This is not very convenient of course if you don't have samples from the parents.

Other methods use only information from the child, but rely on various genome technologies to reconstruct haplotypes inherited from each parent. Here is an early example, and here is a very recent example. These methods however do this mostly on a chromosome-by-chromosome basis, so it is not always obvious how to group the 46 total chromosomes into 2 parental haplotypes of 23 each.

This is a very active area of methods development, so we can expect these references to be quickly outdated.
I do not think that any method will be able to use only the DNA of the child to reconstruct the full genomes of the parents. Maybe if you have a large database of other genomes you can do some imputation of the missing haplotypes, but I doubt that that would work very well.


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How large an expression boost is typical from codon optimization?
There are lots of different codon optimization approaches out there, and a lot of different qualitative reasons to want optimization (e.g., organism codon bias, GC content, avoiding secondary structure).
One may also want to avoid optimization, however, in order to increase reusability of a component, comparability with prior results, or opportunities for error.
I'd like to know how much I'm likely giving up if I decide not to codon optimize. For example, in my typical work giving up 10% is likely to be lost in the noise, but giving up 2x is worth thinking carefully about, and giving up 10x means it's a must-have.
I know "it depends", and there's a lot of qualitative information out there, but is there any way to get a good rough-order-of-magnitude estimate of the typical expression boost from codon optimization?

The "it depends" might hint toward a nice opportunity for a bioinformatics tool as prior data should allow to make an informed prediction. Maybe biostars.org or https://bioinformatics.stackexchange.com would be able to help on a related question, whether there already is a tool to predict boost based on custom sequences and/or expression host.

I think that there is a problem with how well current codon optimization algorithms actually "optimize" protein expression. I am not aware of any algorithms that work beyond a heuristic level and so for an arbitrary protein, one cannot predict the expression boost that optimization will provide - sometimes yield is significantly decreased. This review covers some of the complexities of optimization really nicely https://doi.org/10.1016/j.molcel.2020.09.014.


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Do slime mold expand or multiply?
After reading about slime mold I was wondering, do slime mold simply expand outwards or multiply?
e.g. if I put 100 grams of slime mold in 1 location, will it expand to say, 2 locations, and have the 1st location with 80 grams left, and 2nd location with 20 grams (i.e total 100 grams), or is it that they multiply; 1st location still 100 grams, and 2nd location with 20 grams?

It is difficult to understand your question expressed in grams and locations. I suggest a question about multiplication would be better expressed in number of cells in the first instance, with the size of the cells a second parameter.

The answer is that they will do either or both, depending on conditions: this is one of the things that has caused complex systems scientists to be so interested in things like using slime molds in modeling optimization problems.
In good nutritional conditions, the cells will happily multiply. At the same time, they will flow and reshape themselves to spread and migrate in search of food when nutrients are not uniform.

Thanks a lot! Any idea about the growth rate (e.g. multiplications)? I was trying to find it but couldn't. If you are familiar with any paper/sources that would be great!

I haven't personally worked with it, just heard about it from colleagues who wanted to do slime-mold computing.


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Do penguins "test the ice"?
Do penguins have a way to test the ice that they stand on to ensure that the ice will not break? In other words, do penguins make sure that they will not fall into the ice before stepping onto it?
I have conducted research but have come up short, which made me assume that penguins don't test the ice. However, I wanted to make sure before I just made an assumption.

What would happen to a penguin if the ice did break under their weight?

@BryanKrause They would fall into the water; they would be startled, but if the conditions are right, then they will be able to swim under the water, correct?

I could also envision a scenario that the ice reseals, thus trapping them under the ice -- perhaps a great distance from the next breathing hole. Seems like an interesting question to me. Please [edit] your post to explicitly indicate what type of research you've already done. (You say you've "come up short", but where did you specifically look and what have you learned along the way?)

This HIGHLY apocryphal blog post (https://thealchemistskitchen.blogspot.com/2013/02/how-penguins-do-it-testing-waters.html) suggests that some groups of penguins test water by pushing their leader off and seeing whether it's safe. However, I couldn't find any scholarly references that back that up (or otherwise suggest that penguins test water or ice). Regardless, I just wanted to caution against concluding that they don't just because it hasn't been specifically studied. A lack of research on the topic doesn't necessarily indicate that the phenomenon doesn't exist.


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Are there any species whose descendants can meet their ancestors from 100 generations back?
I.e. Humans can sometimes meet even their great-great-grandparents, but are there any species that can be alive at the same time as their great-great-……-great-grandparents? I imagine it would be those species with a long lifespan and an early age of first reproduction.

Do the species have to be animals?  Many trees would seem to qualify.  Then there's the Greenland shark: https://www.newscientist.com/article/2100823-worlds-oldest-vertebrate-is-a-shark-that-may-live-for-500-years/

I’m voting to close this question because it comes under the category of “idle amusement” rather than being a real problem in biology faced by the poster.

@David: Is it an official rule, that questions must relate to a "real problem in biology faced by the poster" ?

@KaPy3141 I quote from the [Tour] "Focus on questions about an actual problem you have faced. Include details about what you have tried and exactly what you are trying to do." And in the Help on  Asking Questions "are more than just mindless social fun"

I take it that questions must not be motivated by the reactions or interactions they cause. I think I get it!

Yes, cryopreservation works quite well for many species, including multicellular animals. So you can freeze the ancestor and wait until the descendant is there, then unfreeze them. A good recent example in the news would be the Siberian worms that woke up after being frozen in permafrost for a very long time.
Cryopreservation is routine in laboratories, to freeze ancestors and compare to descendants; see the Long Term Evolution Experiment. It doesn't work well for every organism of course. In principle it might work for humans.
Some bacteria will sporulate, and in spore form they can persist for thousands of years theoretically. They don't even need cryopreservation. There are other organisms that do something similar as well.


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Can animals speak like humans?
I know some animals don't have the required vocals. But, I do think that some like parrots, etc may have the capability to produce speech and talk just as we do.
My question is that if an animal is trained from birth, spending all the time around only humans, in the initial years of growth when their brains are much into learning everything, can they learn to talk just as we do?

Have you read about Alex the African Grey parrot? https://en.wikipedia.org/wiki/Alex_(parrot)  Or Washoe the chimpanzee? https://en.wikipedia.org/wiki/Washoe_(chimpanzee)

I think the smartest could understand sign language

It depends on what is understood by speaking.
Anatomy  If by speaking one means producing sounds similar to those produced by humans, than the ability to speak is largely determined by the anatomy of the speech organs - whether they can produce the same type of sound as human does. There are very few animals capable of this (I will find the reference), and this notably excludes some rather close human relatives, such as the great apes.
Neurology Language is a more complex phenomenon than speaking. The most notable difference between the animal and the human communication is that the former typically uses a set of signals with hard-coded meanings, whereas the humans can construct an infinite number of phrases coveying complex meaning. The study of language from this angle has been traditionally carried out by linguists and computer scientists rather than biologists, under the general name of universal grammar (but may also appear under such terms as transformational grammar, generative grammar, etc. ) However, these studies have a direct biological implication that humans possess a genetically coded set of rules for sentence/phrase structure, which is independent on their native language. This clearly requires certain degree of neural development, which the language-less animals do not necessarily possess.
Psychology  Finally, language requires significant psychological development - even in humans. Feral children often fail to acquire language competences. Similarly, the extensive studies on small chidlren in care homes (starting from the works by Anna Freud and Melanie Klein from more than a hundred years ago) demoinstrated that children deprieved of normal human contact have significantly diminished speaking abilities. Getting back to the OP - one can therefore question whether an animal could concievably be exposed to normal human environment to facilitae development of linguistic ability similar to that of a human.
See here and here for more background.


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Arthropod identification request (a spider with no legs?)
My mother sent me a picture of a creature she encountered and couldn't identify. It looks kind of a like a spider - a mostly black body, about 1cm in size, with white specks - except without any visible legs. Apparently it was hanging from a thread, descending to the ground, and still moving.
I don't know a lot about arthropods, and, perhaps unsurprisingly, searching for "spider without legs" gives no useful results, so I'm at a loss.
This is in Northern Germany, mid-March. (The background is a cork floor.)

Any info on what this could be - and whether it's dangerous or not - would definitely help put her at ease.

ID chances are much higher if you photo the top side. Perhaps fiip him with a piece of card, that looks like it's feigning to be dead, trying to look like a stone.

This appears to be the underside of a walnut orbweaver:

These orbweaver spiders are not medically significant.
Spiders often lose their legs in wasp attacks. Some spider wasps will remove the legs and then try to bring the spider to its nest for larvae to feed on. Sometimes they drop their spider victims accidentally.
Some will simply deposit eggs into the spider and leave it there, letting the larvae grow inside the spider and feeding on it from the inside.. these ones don't usually remove the legs - they usually just paralyze the spider.
Spiders can lose their legs through various attacks, but they can also lose their legs in molting accidents... particularly if they are in the middle of a molt and then are aggressively interrupted.

This is a great answer, so interesting and informative! +1 (more if I could). Where did you find out about the... unseemly... wasp behavior? Do they also decapitate their prey? I'd like to read more. Thanks!

Thanks! Here is a video of a wasp removing legs... it says 'spider' but it appears to be a harvestman ("daddy long legs"): https://www.youtube.com/watch?v=NwPuhVS2RhE
But that's not a spider wasp... that one is just using it for meat. Here is a spider wasp, which will be using the spider to grow a larvae:
https://www.youtube.com/watch?v=rs_Q7S3Rxkk
and:
https://www.youtube.com/watch?v=9tfblWSdEHs
and here's one with the act of removing legs:
https://www.youtube.com/watch?v=BKZAsxHAV7w

@anongoodnurse Found another video of the full process (the hunt, the attack, leg removal, and carry-away): https://www.youtube.com/watch?v=a592T6KmwmU

BTW - I'm not convinced this was the fate of the spider. The question poser said it was descending down a silk line. I think @aliential is correct that it was probably feigning a dead pose. It looks like you can see some of the legs against the body (the hind leg on the abdomen and the tarsus/foot slightly covering the ventral white mark)

Thanks for the reply. Those videos... omg. Nature is really red in tooth (or mandible) and claw.  Your comments led me to explore and learn. I hope you're right about this spider's fate. I like spiders, especially orbs and jumping spiders.

Thanks so much for your answer! I'm not sure about it being a wasp attack as it's not yet wasp season (though it's fascinating that that can happen), but the species looks to be a perfect match. :)