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Is there evolution in humans since the first homo sapiens sapiens
Has the human species changed since first defined as homo sapiens sapiens?
I'm asking this question partly because I'm wondering how we might evolve next.

Do you mean in genetic sense or physiological sense or both? and what do you consider as change i.e. to what extent does evolution have to occur before it amounts to a change in your definition. Evolution depends on genetic and environmental factors so it is highly dependent on many factors and this question can have a highly speculative and subjective responses!

Highly Related: 1) How is evolution possible in contemporary humans? 2) Human Evolution in Modern Times 3) Are humans done changing?

We continue to evolve all the time: http://www.npr.org/2013/09/27/226837803/modern-humans-still-evolving-and-faster-than-ever

For those who think the forces of natural selection no longer apply to modern humans, paleoanthropologist John Hawks would urge you to reconsider. In recent times — that's 10 to 20 thousand years, for a paleoanthropologist — Hawks says we've picked up genetic variations in skin color, and other traits that allow us to break down starch and digest cheese.

Homo sapiens sapiens is over 100,000 years old and we have changed in many ways since then, as noted in the above NPR article!
I'm not sure we can say there is a "first" homo sapiens sapiens -- the change from one species to another is gradual.  You may know that mixing red and blue gives purple, but at what points do we officially have red, purple, or blue when mixing different levels of red and blue?

An additional question is, are we evolving in a positive or negative way stronger vs weaker.

Well, it doesn't matter to evolution as long as we reproduce more. Hence Idiocracy. As to whether there's a "first" homo sapiens sapiens -- it depends on your view of our evolutionary history. If you agree with Out of Africa, probably a group of them. If not, then you likely think Homo erectus slowly changed into Homo sapiens through propagation of traits.

Oh my god that movie. It's really shocking how just having more children can change the allelic frequencies in a population

There is certainly some evolution.
Take, for example, lactose tolerance. It's a relatively new mutation that happened less than 8000 years ago. Yes, basically all humans in the stone age were lactose intolerant. The change started to be common after humans defeloped argriculture on a big scale and is still less common in some groups than in others even today.
As another example, our jaws have become smaller and now we get trouble with the amount of teeth that hasn't changed since the first modern humans developed. Some people don't have wisdom teeth, that is part of the evolutionary answer to that.
Also people have become bigger since the early days.
I can't assure how humans will develop in the future, but even smaller jaws, weaker limbs (due to more dependence on technology and less use of personal strength) and longer fingers (because presicion is more important nowadays than raw power) might be some factors. Also with the increase of modern globalization, humans might become less diverse in appearance.

Hi Welcome to Bio.SE. We ask that answers on this site include citations or references. Please update your answer with reputable sources that substantiate your claims. Even though something might seem trivial and obvious, other users will benefit from having legitimate sources to continue researching. Thanks!

I second that - With references and sources you would get the upvotes you deserve +1

An additional question is, are we evolving in a positive or negative
  way stronger vs weaker.

That would depend on what you consider week or strong. All evolution really cares about is how many babies do you successful raise to adulthood.
You may be the strongest, smartest and most handsome man in the world. But at the end of the day, if you do not have children you are a failure.
So are we evolving better... here is something to think about. The BRCA mutation that causes breast cancer in women... also causes increase fertility in women. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4457526/  So is that good or bad? Bad for the individual.... but good for evolution. More children.
Or how about muscle strength... humans muscle strength per body weight is terrible compared to every other ape. The average chimp is half the weight of a man and 6 times stronger. So humans are weak.... well we can pick up and sewing needle and tread that needle but a chimp can't. In human evolution we have sacrificed strength for dexterity. So is this good or bad. Strong or week?
Answering the first question. Yes we have. Human evolved in africa. The most ancient population are in africa. All those strange looking non-africans are the produces of evolution in the past 60,000 years. Those moving northwards became paler. And developed longer hair. Mutations resulted in lost of eye pigments 5000yr ago resulting in green then later blue eyes. (Terrible in the savannah of africa but meh in Europe)
Also some evolution occurred in receptors targeted by viruses. So better immunity. Think the black plague 60% death in Europe and Smallpox in Americas, 90-95% death rate.


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Neuroscience book recommendations
I'm looking for a textbook in neuroscience for a rigorous introduction to the topic as an autodidact. I have no prior exposure to the field.
In particular, I'm interested in the chemical mechanisms of enzyme modulation, ideally something similar to Lehninger's Principles of Biochemistry where specific Protein Databank ID's are given, so I can load an enzyme in PyMOL and view where the inhibitors/activators bind, in conjunction with an explanation of the actual pathways involved from a molecular level.
I've read Wade: Organic Chemistry, and a good part of Clayden's Organic Chemistry, before self-studying biochemistry for 6 months, to give a little background of my knowledge.
I'm leaning towards Kandel's Principles of Neuroscience after reading some other suggestions here, but this seems like a gigantic text, and I'm unsure how detailed the biochemistry side of things is (which is my main interest)? Could anyone share some thoughts regarding that, or recommend an alternative smaller text with a specific focus on biochemistry?
I'm also concerned that a large amount of data and publications in the field of neuroscience fail replication (something as high as 60% I believe), so the book would need to contain only factual, widely accepted information and not cutting-edge speculative studies that haven't been replicated and widely accepted. Also, as little pharmaceutical-industry influenced as possible.
Ultimately, my interest lies in understanding how different medications and drugs cause different mental states, their exact pathways and mechanisms, and how they form tolerance. I'd like to one day conduct research in how to minimize said tolerance, eg: reverse receptor desensitization. Which book should I begin with to head towards this goal?
Thanks!

My friend recommended this book Neuroscience by Purves, et al. :)

I realize this was a year and a half ago, but since this question was brought back up: as a (college-taught) neuroscience and biology student, I'm concerned about some of the opinions you mention. Where did you learn that neuroscience data was failing replication? The discussion of how scientific research and theory becomes treated as "factual" can be left for another time, but I'll leave it at this: in a field as new as neuroscience, most studies are, in fact, cutting-edge, and eliminating those will absolutely be detrimental to your understanding of the subject.

I don't have enough rep yet to comment on your question, but I have read the whole of Kandel's Principles of Neural Science in 2nd year of med school (last year) and I thoroughly enjoyed all of it!
I would recommend Part II: Cell and Molecular Biology of the Neuron to you, as this is where most detailed discussion about the molecolular structure of membrane proteins etc. is happening. And that's only about 110 pages. It probably doesn't go as far as what you are looking for, but I found it a very good introduction to the field of ion channels and how they work. The rest of the book is very interesting if you are keen to get a thorough overview of the whole field of neural science, but you won't find too much detail on the biochemical level there. Part III: Synaptic Transmission with about 150 pages is also a very good read.
For a specific focus on biochemistry you'll have to look for another book, but quite likely you'll find good candidates in the Selected Readings at the end of each chapter, here is one example of those lists from chapter 7:

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Why are the positions of simple sequence repeats at the gene and related transcript sequences different?
I'm working on the simple sequence repeat (SSR). I found just one region (about 21 bp) with an SSR motif in a given gene. This gene has multiple transcripts, with the same SSR motif located in various positions of different transcripts. Could you please help me understand how this happened?

Because of Alternative Splicing, suppose an exon occurs neither the first nor the last, then the same exon will come at various positions in different transcripts of the same gene. Thus, if your SSR of interest exists in that exon, you will find the same SSR located in the various positions of different transcripts.

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At which step should I apply a detection filter when preprocessing microarray data? (Before/After normalization, batch effects removal)
What is the best practice when preprocessing microarray data using a detection filter (on scanner p-value)?
Suppose I have a microarray dataset that I have to normalize with Loess and correct with ComBat. When should I apply a detection filter, relative to the other steps in the process?
In my experimental design, I have two pipelines to test:

Normalize per sample between 0 - 1
ComBat
Loess normalization between samples

and

Loess normalization between samples
ComBat

Is there any best practice for the timing of applying a detection filter?

Why not try applying before and after for all pipes and see which gives you more believable answers?

@virtualxtc how do you decide if an answer is more "believable"? You will get a result eventually.

My guess is that both methods will work equally well, just plot the data and validate by eye. The first rule of biostats (according to Ethan Meyers) is just plot everything & don't add extra thought to it unless l something is broken. That said, I use interquartile normalization (due to the fixed lower bound at 0) then hit call.

did you find an answer to your question? If you did, it would be great if you could post it here for people having similar questions in future

you might also want to ask the bioinformatics.stackexchange.com

My comment above still stands; provided your detection filter doesn't rely on your data being normalized, your detection filter can exist anywhere.
However, since it seems you know that you want to run a PCA, and know all the normalization's you'd like to try already, it is simplest to run all of your normalization first, rather than having to filter out high scoring vectors that appear to be caused by inter-sample variation.

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What does it mean "specialized populations of neurons"?
I'm reading now the Campbell biology book (10th), and on page 1063 is written:

In all but the simplest animals, specialized populations of
  neurons handle each stage of information processing.

What does it mean "specialized populations of neurons"? I always knew that there is a population in biological hierarchy of creatures rather than the cells which assemble the creatures.

As in the occipital lobe handling vision processing, the prefrontal lobe intiating motor activities, etc...

I'm voting to close this question as off-topic because it is about English language usage, not biological terminology.

It's just a specialized group of neurons. You can call a group of cells a population of cells. They are specialized because those particular neurons carry out a specific function.


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What is the meaning of the verb "lines" in this context?
What is the meaning of the verb "lines" in this context?

"Epithelial tissue covers body surfaces, lines body cavities and
  form glands"

I searched in the dictionary but I found a lot of results and I'm not sure which one is matched.

(transitive) To cover the inner surface of (something), originally especially with linen.

I'm voting to close this question as off-topic because   it's english language, not specific biology terminology

You've already had another question closed for this exact reason. Please use one of the English sites you're already a member of to ask basic English grammatical questions.

Lines in that context is the verb form of the noun lining which is a surface that forms an inner boundary of an object. Here's a dictionary entry.


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Real unipolar neurons do indeed exist in human?
I studied that the unipolar neuron in human body are not really unipolar but they're pseoudounipolar neurons. On the other hand according to what I understood from wikipedia (neuron) there are real unipolar neuron.
In fact, I'm confused (if unipolar cell does exist in human body or doesn't) and I would like get you help about it.


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Gland defined based on morphology or hormone secretion?
Is a gland defined by a visible morphology, or is anything that secretes a hormone a gland?
The answer does matter for the definition of histamine. Based on the answer I can conclude whether it's an hormone or not.

Thank you for your notes. Maybe I didn't explain myself well, so it would be better to see the place that the question came from... (kindly, look at "Wnt" things) https://en.wikipedia.org/wiki/Wikipedia:Reference_desk/Science#Histamine_is_considered_as_hormone_or_not.3F


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The difference between the two ways of glycine represntation
I'm confused because I see now two different way to represent the glycine amino acid. while I understand the first way of the representation the second one I don't understand at all. I believe that both represent the same amino acid but I see that some of the componenets are absent in the second way (no COOH and no carbon). I would like to know the explanation.
This is the first (and the simplest way):

and this is the form that I don't understand:

This is a chemistry question. In organic chemistry, the skeletal representation of molecules does not explicitly label the carbon atom. Line endings, angles and vertices denote a carbon atom. Likewise hydrogens are also not labelled because carbon is by default assumed to be attached to hydrogens if not labelled otherwise.

@WYSIWYG, isn't it _bio_chemistry. I don't think the hold is appropriate, there is overlap with chemistry SE but biochemistry is central to the study of biology as well.

@Michael_A This does not specifically concern Biology. It is primarily about organic chemistry and how organic molecules are represented on paper. If you really think this is an on-topic question then vote to reopen. Let's see what others think about it.

The skeletal diagram omits labels of carbon atoms. This lewis structure of glycine includes carbon atoms and makes the structure of NH2 and COOH a bit clearer as well;

Thank you for your answer, but I didn't understand where are the hydrogen atoms in the 2nd diagram that I showed (skeletal form).

The first method of representation is the regular way, where all groups, including carbon and hydrogen are shown.
The second method is the "skeletal form", where every bend in the line means a carbon group, and the hydrogen atoms attached to the carbons are implied. It does seem a little tricky to visualise, but it is easier and faster when you come to larger groups.
Check this out.

Thank you for your answer, but I didn't understand where are the hydrogen atoms in the 2nd diagram that I showed (skeletal form).

@Industrious like Malhar Khushu explained, hydrogen atoms attached to carbon atoms are implied in the skeletal form, which means they are not showed.

See, @Industrious, carbon atoms, in organic compounds have 4 bonds. If, in a skeletal form, a carbon atom isn't showing 4 bonds, then there are hydrogen atoms attached there.


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Do bile salts enter into enterocytes?
Wikipedia says :

The contents of these micelles (but not the bile salts) enter the enterocytes (epithelial cells lining the small intestine) .....

So, where do the bile salts go? Additionally, what prevents them from being absorbed by the plasma membrane?

The fatty acids within micelles are taken up by enterocytes in the upper/middle part of the small intestine (duodenum/jejunum) through selective transporters in their plasma membrane, which do not accept bile acids. The SLC27A4 protein is thought to be the principal transporter for fatty acids in enterocytes, although there has been some controversy about this.
As a result of this selective uptake of fatty acids in this part of the intestine, the bile acids are left behind in the micelles, as they are emptied of fatty acids. They travel down the small intestine until they reach the ileum, where enterocytes express a bile acid transporter, SLC10A2, which performs active uptake of the bile acids. The bile acids are then secreted on the opposite (basolateral) side of these enterocytes; enter the portal vein; and travel back to the liver, where they are reused. This is known as the enterohepatic circulation. A review of these mechanisms is found here.
So the uptake of fatty acids and bile acids differs by location in the intestine. First the emulsified fatty acids are extracted, then the bile acids are recovered in the ileum. There is also some passive transport (diffusion) of bile acids into enterocytes throughout the intestine, but this is considered a minor mechanism.


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Phylogenetic tree with tagging
I'm working for a software company. For one of our projects, we need software to cluster nodes in a phylogenetic tree by a certain kind of similarity and give them a user-defined tag. Preferably, the tag would consist of two different values: a unique ID and a human-readable name. It would also be nice to set multiple tags for one or several nodes.
Some more in depth information:
We get sequenced data from a laboratory. The first thing the software has to do is an alignment. Based on the aligned data we need a phylogenetic tree. The software then has to give us the possibility to set one or more tags on one or more nodes. After the tagging, the data has to be exported from the software, so that we can give our clients enriched data.
Phylogenetic tree:

                                       ________ M.HpyFI.dna
                                      |
                                      |_______________ M2.HpyFXIII.dna
                                      |
                                      |___________ M.HpyFII.dna
                                      |
                                      |        ___ M.HpyFIII.dna
                                      |_______|
                                      |       |__________ M.HpyFIV.dna
                                      |
                                      |  ________________ M.HpyFVII.dna
                                      |_|
                                      | |__________ M.HpyFXII.dna
______________________________________|
                                      |____________ M.HpyFIX.dna
                                      |
                                      |    ________ M.HpyFVI.dna
                                      |___|
                                      |   |_________ M.HpyFVIII.dna
                                      |
                                      |_____________ M.HpyFORFX.dna
                                      |
                                      |   _________ M.HpyFV.dna
                                      |__|
                                      |  |____________ M.HpyFXI.dna
                                      |
                                      |____ M1.HpyFXIII.dna

Phylogenetic tree with tags:
This graphic shows what we want to achieve. Every node should get a tag. In the shown case, it could also be possible that all nodes would get a second tag of Citrobacter.

                     ________ M.HpyFI.dna
                    |
                    |_______________ M2.HpyFXIII.dna
                    |
                    |___________ M.HpyFII.dna
                    |
                    |        ___ M.HpyFIII.dna
                    |_______|
                    |       |__________ M.HpyFIV.dna
                    |
                    |  ________________ M.HpyFVII.dna
                    |_|
                    | |__________ M.HpyFXII.dna
____________________|
                    |____________ M.HpyFIX.dna
                    |
                    |    ________ M.HpyFVI.dna (Citrobacter koseri)
                    |___|
                    |   |_________ M.HpyFVIII.dna (Citrobacter koseri)
                    |
                    |_____________ M.HpyFORFX.dna (Citrobacter koseri)
                    |
                    |   _________ M.HpyFV.dna (Citrobacter freundii)
                    |__|
                    |  |____________ M.HpyFXI.dna (Citrobacter freundii)
                    |
                    |____ M1.HpyFXIII.dna (Citrobacter freundii)

Our company has already developed a software which fits our needs for the alignment and the phylogenetic tree, using the Biopython package.
The question is: is there already a software (preferably open source) which does everything that we want — align imported data and create a phylogenetic tree and tag and export data? Or do we need to improve our own software by adding the ability to tag?
I hope it is clear what we want to achieve and what we are searching for.
Edit:
The text above mainly explains what we have. How we implemented everything with Biopython isn't relevant to this question. I only posted it to show our workflow.
At the moment, our software is not able to place user-defined tags, as shown in the second phylogenetic tree. It is no problem for us to improve our software so that it can do the tagging. But, if a software which can align data, create a phylogenetic tree, add user-defined tags, and export the data, we would prefer to use this software instead of modifying our own.
As a possible hint, the software MEGA (http://www.megasoftware.net/) can align data and create a phylogenetic tree, but it doesn't allow for editing/adding tags.
I hope this question is now clearer.
In case you want to know, the algorithm we used to create the phylogenetic tree was Maximum Likelihood

It's not clear what you're searching for. Please clearly lay out what Biopython doesn't do that you still want to do. Please also be aware that questions regarding analytical methods, such as those related to bioinformatics or biological simulation, that do not ask explicitly about the underlying biology are considered off-topic. Please [edit] your post to address only your question relating to biology or delete it and visit another Stack Exchange site such as [so] for programming, [stats.se] for statistics, etc. You may also find Biostars helpful.

In case you might be interested, here are some python-based tools that include tree manipulation functions:
http://etetoolkit.org/
http://p4.nhm.ac.uk/


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Multiple transcripts matching same gene in de novo assembled RNA-seq data, but FPKM values vary?
I have a data set of de novo assembled RNA-seq datasets across different sample types.
When BLASTing, many of the matches of the individual transcripts match to the same gene on the reference genome. However, each individual transcript has its own unique FPKM value.
I'm confused, firstly, as to how you can have multiple sequences from the same gene with different FPKM values — and of course, I'm also wondering what would be a suitable approach for the subsequent analysis. Should I just add the FPKM values together for the sequences with the same matches?

If the quantification is done at the transcript level, each identified transcript of a given gene will have a different number of reads attributed to it, hence a different RPKM value.
For the subsequent analysis, you can continue at the transcript level.
I think you cannot sum the FPKM values directly, because they are inversely proportional to the transcript lengths ("K" stands for "by kilobase"). If you want to do the subsequent analysis at the gene level and use FPKM values, you would have to multiply the FPKM values of the transcripts by the corresponding transcript lengths before summing. Then you will have to divide this sum by the gene length, or something like that.

Indeed you can't sum FPKMs, and nowadays you should probably try to void using them in the first place (they have some bias, but are still widely used). But even if you get the raw counts per transcript, you should not directly sum them to get counts per genes.
If you got your counts using Kallisto or Salmon, the easiest way is to either use sleuth to work directly on transcripts, or tximport to sum counts and input them into DESeq, edgeR or another program.


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What are the possible reasons to get extra unrecognized band in agarose gel electrophoresis?
I ran 0.7% agarose gel electrophoresis of my plasmid DNA sample consisting of GFP vector, using NheI and HindIII restriction enzyme.
I used two types of plasmids, i.e., isolated by miniprep-alkali method, and another isolated by midi prep system (pure) of the same source E. coli.
The 4 and 5 lines show cut and uncut plasmid, respectively, isolated by midi prep system.
The 1, 2, and 3 lines show the 500 bp marker, cut, and uncut of miniprep isolated plasmid signal, respectively. In the attached image, we found an extra band in the plasmids isolated by alkali method (line 2 and 3), but in the pure samples (line 4 and 5) no such extra bands were found.
What are the possible reasons behind the result? How may I interpret this result? If anyone has experienced similar results, please share.

Not sure what it is, but I noticed this today as well on a gel. It was only present in plasmids (digested) that were grown in DH5alpha (and absent in the XL1 blue). Could be coincidence though.

Looks like genomic DNA contamination to me.
More importantly, does it really matter? I certainly appreciate the curiosity but, if your objective is cloning, I would just keep going and then do some diagnostic cuts of your plasmid after transformation. You can clearly see your vector or insert in the gel.

If it was gDNA contamination I would expect to see many more bands...

@JoeHealey I would too but, to me, it's the most plausible explanation for such a large fragment.

Especially given that it is absent in the so-called "pure" fractions, which are presumably cleaner.

Could be several things...just off the top of my head. Without your vector map and expected sizes it will be almost impossible to say for sure.
You'll probably also have to give us more information about your incubation conditions etc.

Your original culture you prepped from might not be as homogenous as you think:

You've ended up with a mutant (perhaps in your restriction site in that particular clone)
Your original culture is contaminated, perhaps with a second E coli bearing a different plasmid.

This is probably unlikely, assuming your molecular/microbiology technique is decent, but does happen from time to time.

Incomplete digestion. Something in the eluate of your first extraction method has possibly inhibited your enzymes, that isn't happening in the other extraction mechanism, or you didn't leave the digest for long enough.
You missed something out of the reaction mix for one of the samples (I usually blame myself first when things go wrong so I usually just repeat it to be sure!)

Uncut plasmid can run at all sorts of lengths. If it's supercoiled, it will run further than it 'should' for its size. If it's circular but not supercoiled, it will run slower than it 'should' vs if it was a single linear fragment as it doesn't move easily through the gel.


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Why are the walls of the bronchioles folded?

The bronchiole shown in the section above has folded epithelium, why is this so?

I think most of the answers here are wrong. The smooth muscle around the bronchiole can expand and contract, so the epithelium has to have a morphology that allows this. I'm not too familiar with bronchiole histology so I'll keep this as just a comment rather than a full answer, but I wouldn't be surprised if fixation/processing also led to an atypical "constriction" of the bronchioles beyond their normal state in a healthy animal/human.

Those foldings are called as mucosal folds, formed by the contraction of smooth muscles , are also present in trachea, and in many other organs such as gallbladder etc.
Physiologically: This folding causes an increase in area for better action of mucus which protects the body from entry of dirt, pathogens and loosing the moisture.
Anaomically: as @Bryan pointed out that the folding permits the  contraction and relaxation of smooth muscles around the bronchioles.
Source 1
Source 2

This is the best answer so far, but it would be much improved if you can find some references to support what you say to make it clear that this is the correct answer.


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Why can't we half-close our eyes?
Can we half-close our eyes such that they don't vibrate?
If not, then why we are unable to half-close our eyes properly?
Alternatively, why isn't it possible to keep the upper eyelid close to the lower eyelid without it vibrating?

The motion of the eyelid is driven by the levator palpebrae superioris, i.e. elevating muscle of upper eyelid, and it can be positioned to the intermediate, half-closed positions. At least I can do it.
Yes, this muscle tends to shake or oscillate simply because it's a very weak muscle. It's similar with the muscles controlling the motion of the little finger (or ring finger). Vibration and "noise" is present in all muscles but the stronger muscle you have, the more accurately the random motion is averaged out.
If you connected $N$ eyelid muscles so that they move in unison, the noisy vibrations would be reduced by the factor of $\frac{1}{\sqrt{N}}$. This is the well-known scaling of the statistical errors in physics etc.
I would think that this question was totally appropriate at the Physics Stack Exchange.

What is the number N in this context? A muscle, even a small one as that of the eyelid, contains countless number of muscle fibers, and even more myofibrils ...

Roland, it isn't supposed to matter how much $N$ is. You may take $N$ to be the number of fibers. The point is that what matters is the ratio $N_1/N_2$ between two situations. The eyelid muscle is a lot thinner ($N_1/N_2$ is large) than the biceps so the relative oscillations are square root of lot times more pronounced in eyelids. The oscillations only appear in the middle because the eyelids are "supported" in both extreme positions. When a person with Parkinson's pushes his hand on the table, it cannot vibrate up and down...

That doesn't sound quite right to me. For very large N1, the statistical error (and therefore muscle tremor) should vanish, and then it's irrelevant if some other N2 is even larger than N1. So the 1/root(N) law should be important only when N is quite small. I would guess that the key factor is how many neurons innervate the muscle; very small muscles have few motor neurons, which makes for a small N. Can you elaborate and provide references?

Dear Roland, the number of neurons innervating an elementary muscle fiber was assumed to be the same while comparing the quivers of $N_1$ and $N_2$ nerves. It's plausible that the source of the oscillations is the small number of neurons around the muscles, not the thin mechanical part of the muscle. In that case, $N$ in my answer should be interpreted as the thickness of the nerves innervating the muscle. From a broader viewpoint, it's a detail. No, I don't have references, this was being answered as a physics problem which can be done even if no one else was solving it before.

I think this is not the cause, the muscle is already very much larger in terms of number of myosin bridges compared to the scale at which you'd expect oscillations of noticeable amplitude. And also, the motion is controlled by 2 muscles for the upper eyelid, and 1 for the lower but at a different angle than the levator.

Can you bring in some data on the expected amplitude of such oscillations?

The upper eyelid position is governed by two muscles (tarsus sup and  levator palpebrae sup) working against one another, but they are at a 90 degree angle:

See Wikipedia on tarsus.
When you are closing your eyelid, it is the tarsus that contracts and reduces its length. If you try to maintain the upper lid in a half-closed position, you need to counteract with the levator muscle. But because of the nearly 90 degree angle, a little force of the levator needs to be counterbalanced with a strong levator force, simply because of trigonometry:

You see above (upside down compared to eyelid muscles) that for a constant force of the levator (F, down), the force of the tarsus to the left and right need to be doubled when you go from 30 to 20 degree angle of the "eyelid". These variations grow even larger when the angle goes flatter, in fact, it is a $1/\tan \alpha$ singularity [EDIT]as $\alpha$ goes to zero[/EDIT]. Tough maths problem, and also tough control problem for your nerves!
And definitely, this question is very much physics!

Very interesting elaboration, thanks. But could you please be a little bit more specific which singularity appears near 30 or 20 degrees in tangent etc.? You surely don't dispute that tangent of 30 degrees is regular, finite, and of order one, do you?

@LubošMotl If $|F|=1$, then $|F_L|=|F_R|=1/(2 \tan \alpha)$. It is $1/\tan$ which is singular, as you well know.

Sorry, $\tan\alpha$ is singular for $\alpha=\pi/2$ or 90 degrees. None of your angles is 90 agrees, is it? Similarly, $1/\tan\alpha$ diverges for $\alpha=0$ but your $\alpha$ isn't zero. So there's nothing singular. Are you playing a shell game trying to sell an argument that obviously doesn't work or am I overlooking something?

OK, maybe this was unclear: we are looking for nearly closed eye, so nearly straight polyline joining $F_R$ and $F_L$, hence $\alpha$ small. I realise you have taken the angles in the diagrams as the only values considered, they are examples.


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Lysis step during DNA purification
I am currently studying DNA extraction from various bio-originated samples. I am new to this field, and have learned how commercial DNA extraction kits work for bacteria.
I understand that the very first step is called 'lysis', and that this is supposed to break cells to pull out all the stuff inside them, including DNA.
I am studying cell-free DNA extraction procedure from human blood, and I don't understand why the lysis step is necessary in this context.
If lysis is to break cells, and cell-free DNA is already out of the cell and freely circulating, such a step seems unnecessary.
Is my understanding about lysis right? Then, why is the lysis step necessary during cfDNA isolation?

You want to isolate the cfDNA, and leave anything else in the plasma out of your analysis — essentially, the lysis step is part of the purification.
(See here)
(I'll elaborate with edits shortly)
Edit:
Actually, it looks like lysis is not a good idea in cfDNA isolation — lysing cells in your sample will result in contamination by genomic DNA, as discussed here. It would be better to stabilize/fix cells to prevent them from lysing, to avoid this risk.
In other words, your initial instincts were correct!

Thanks, you gave me a piece of confidence to solve this problem. Then is it okay to say that the lysis step for cfDNA is to clean or degrade other stuff in serum such as protein?

Let me know if this answers your question!

Yes absolutely it does! I never knew there could be WBC in serum... Then lysis step might cause a mess in my sample. Thank you very much :)

@Kidan My pleasure! Please do mark the answer as accepted if it helped you :)


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What would happen to a body in an astronaut suit over time if floating free?
I'm not sure if this is best in Biology or Physics, but on Earth we decay to skeletons and then eventually to dust.  What would happen in space in a space suit?

You are probably going to need to be more specific.  If the body is floating free for an extended period of time then it must be either in orbit around something or really far away from any gravity well.  If it's in sunlight, it will get really hot, if it's not it will get really cold.  How long will the suit stay pressurized? How much oxygen is available until then?  I'm not an expert on this site, but I doubt you'll get anything decent with this question as it stands.

@AdamPhelps. I agree. It heavily depends on where, as close to the sun the answer is very different than in a cold environment far from any heat source. Also the how matters, as the space suit characteristics also matters in terms of heat and radiation that may affect the body

Closed Duplicate. Answer here : http://biology.stackexchange.com/a/20958/8804

That's not a duplicate, though it is very close.  To answer your question Adam, by "floating free" I mean you are ejected from a spaceship between galaxies.  You're lightyears from anything.  Would a suit stay pressurized for 100 years?  Would the oxygen run out?  I don't know, that's part of the question.

@Raoul the moon has little atmosphere and gravity which is not the same as space

@CRags, thanks for that, but I think given the answers to those questions, the more important part is that it is very close to a sun, which apparently makes a huge difference.


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Are all genes capable of being switched on or off?
Are all genes capable of being switched on or off or only some genes? Are there some genes that permanently do not have the functionality that enables them to be switched on or off?
Everything I have found in response to this question seems to assume that ALL genes are capable of being switched on or off.
When I have searched for the answer to this question all I find are explanations about how things like epigenetics, gene regulation and expression work. I understand at the basic level how these things work and that there are different ways by which they are accomplished.
I realize the answer may be "as far as we know" or "we don't know" or "it's complicated" and that's fine and definitely understandable.

Welcome to SE Biology. This is a question and answer site where we hope the Q&A will be of general benefit. For that reason we try to ensure that questions are unambiguous, editing if necessary. Hence two requests for clarification. 1. Are you taking about bacterial or eukaryotic cells? 2. By “switching off” do you mean specifically prevent transcription of a gene, excluding general effects of starvation of metabolites?

Eukaryotic. I expect "prevent transcription" is the appropriate clarification but preventing something is different than lacking the functionality for something. With regards to my question either would have the same effective result - a gene where regulation is not possible.

I cannot think of a mechanism that would entirely prevent a gene from being regulated. For example, consider mechanisms like histone modification: there is very little about the sequence of a single underlying gene that can itself cause or prevent histone modification, yet those changes regulate the expression of associated genes. However, you can really only provide evidence in science for things that happen; providing evidence that things do not happen is often questionable. If you have some example gene and you'd like to say "this gene is not regulated", the best you can ever get to is "I haven't yet found a circumstance in which this gene is regulated by any manipulation I know of".
In practice, there are some genes that are not typically "switched on/off" and always expressed at fairly constant rates, we call these housekeeping genes. For many of these, the consequence of 'switching them off' would be death of the cell. However, I would not consider that these genes are "not capable" of being regulated, rather, I would say that they are specifically regulated to be always active, and that there is very strong evolutionary pressure for this to occur. To show that I mean by this, consider some quoted lines from Wikipedia:

The housekeeping gene expression levels are fine-tuned to meet the metabolic requirements in various tissues. Biochemical studies on transcription initiation of the housekeeping gene promoters have been difficult, partly due to the less-characterized promoter motifs and transcription initiation process.

Little is known about how the dispersed transcription initiation of housekeeping gene is established. There are transcription factors that are specifically enriched on and regulate housekeeping gene promoters.[12][13] Furthermore, housekeeping promoters are regulated by housekeeping enhancers but not developmentally regulated enhancers.[14]

In summary, steady activity is carefully controlled, and difficult to study. Comparatively, if a gene has very different expression in different environments, you can follow an iterative process to look at cells in each environment and see what is different: if you find another protein is phosphorylated or otherwise modified, or has also changed expression, you might be looking at a transcription factor involved in your gene of interest. On the other hand, if something never changes, where do you start? Trickier problem for an experimentalist.

Thank you very much for your comprehensive answer. I do appreciate you taking the time to provide links, quotes and your thoughts.

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


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What is the difference between growth hormone and growth factor
What is the difference between growth factor and growth hormone?
I am aware of the fact that hormones are directly poured into the blood stream and that the growth factors can be released by non endocrine organs.
But how else do they vary from each other ?
And are they functionally different and if yes how?

Welcome to the site. What research have you done on your own to answer this question? 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. Our goal is not simply to be an answer site, but rather a site that promotes self-learning with some expert help along the way.

Plugging your exact question title into Google yields many helpful resources.


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Why would GREML in GCTA treat SNP effects as random effects?
I've read many papers, but none of them gave clear answer to my question.
For example,
https://www.nature.com/articles/s41576-019-0137-z#Sec5

The univariate GREML approach can model multiple random effects and
hence estimate multiple genetic variances using multiple GRMs, each
built with SNPs selected on different annotations.

https://www.nature.com/articles/ng.608

The effects of the SNPs are treated statistically as random, and the
variance explained by all the SNPs together is estimated.

I've also read that random effect refers to random grouping (site) effects. Why should SNP be considered groups?

Linear mixed models are used in genetic association studies because if you try and fit SNP effects using a straight forward fixed effects linear model and ordinary least squares, there is a tendency to overfit the $p$ (where $p$ is a large number of SNP densely located SNPS in some kind of LD) model parameters, as SNPs are often in strong linkage disequilibrium with one another (i.e. the SNPs effects are non-independent). Instead, if you treat SNP effects as random effects, you can restrict the SNP effect parameter values to a joint 'variance parameter' which is estimated from the data. In other words, we want to estimate a single 'shared' variance parameter value rather than many parameters for all $p$ SNPs to avoid overfitting the model.

Thanks for your answer. Do you know if there is a model that can take continuous variables as random effect? https://stats.stackexchange.com/questions/605703/is-there-any-regression-allowing-correlated-values-other-than-lmm


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Can a less fit strain of a virus impose over a fitter one?
According to this link, the Dominant Delta Variant may mutate itself into destruction.

The Delta variant in Japan was highly transmissible and keeping other
variants out.
But as the mutations piled up, we believe it eventually became a
faulty virus and it was unable to make copies of itself.

I was told that evolution was about survival of the fittest, and that in the case of virus strains, a more contagious strain would likely increase in frequency relative to a less contagious one. So how can a mutation of the strain Delta which can't replicate or replicate less, increase in frequency relative to the original Delta strain?
Can a less fit strain of a virus impose over a fitter one?

Could you clarify what you mean by impose?

the original coronavirus strain was displaced worldwide by other strains called alpha, delta, etc. The delta, alpha, etc. imposed over the original coronavirus strain

How are you quantifying 'displaced'? The original strain still exists, presumably, but the other variants are found at higher frequencies. Are you interested in whether it's possible for a less fit strain to reach a higher frequency than another? 'Imposed' doesn't seem to be the correct biological term. I think 'outcompete' is better to use. Sorry if I sound pedantic, but having the correct terminology often is the best way to understand something.

If I can simplify the question: “Why would a ‘faulty’ mutated strain of the delta variant increase in prevalence relative to the wild type delta variant?” The answer is probably “it’s complicated” and “more information is needed.”

That's a discusion of semantics, not biology. Displaced can also be used to the Situation you describe. If you partially mover someone from a position you can use the word displaced

Btw, there are a Lot of researchs using the word displacement to describe the displacement of alpha by beta

Also note that the term “fitness” has a specific meaning in biology. For a given genotype, relative fitness is the proportion of that genotype in the population gene pool of the next generation. So, by definition, a “less fit” strain cannot overtake the wild type.

correction, I meant "there are a lot of researchs using the word displacement to describe the displacement of alpha by delta*". typo or corrector

@acvill "Why would a ‘faulty’ mutated strain of the delta variant increase in prevalence relative to the wild type delta variant?” Even though the question arised with sars-cov-2, I would like to know if there was ever a known case with any virus where a less contagious strain of the same virus could overtake a more contagious one. Because if there wasnt, that means this is also impossible for sars-cov-2

If one strain of a virus displaces another, or even becomes more prevalent, isn't that strain the fitter one, BY DEFINITION?

@jamesqf  the question is, how can a strain that's faulty to replicate to the point is going to disappear (cleary not the fitter) impose over another. If a strain replicates little, or not at all, the hosts are going to be taken over by other strains. But the japanese man claims (indirectly) that a faulty to replicate strain took over the non faulty ones.

@Pablo a less fit strain may outrun a fitter one due to genetic drift, if the infected (sub)population is small... although in this case measuring fitness is problematic. It seems that the variant introduced in Japan, although classified as Delta, had actually low fitness (there is some genetic variation within each variant). Also, a fitter strain may simply become extinct by exterminating all its hosts - not the case of sars-cov-2, but not something unheard of.

@Pablo: But if a strain mutates in such a way that it can't replicate, or doesn't replicate as well, that mutation has made it less fit.  Conversely, a strain that replicates so well that it eliminates its hosts (perhaps by causing collateral damage), is likewise not fit.  The ideal would be for the virus to reproduce and spread without adversely affecting its host.  Or even benefitting the host, as many of the microorganisms in your microbiome do.

@jamesqf agree. That's why what that japanese researcher said doesnt make sense to me, and I came here to ask if there is an explanation for what he said.

@RogerVadim I'm not familiar with the concept of genetic drift, for what I read it would seem randomness play a role, but here we are talking about 10 millions viral particles per mililiter per infected person, so it's a population of trillions.

@Pablo we are not talking about competition within a single host, but about being transmitted to another host and successfully establishing a new infection. The number of people in the cited article is rather small.

"I find it incredibly difficult to believe that all Covid-19 in Japan has simultaneously and more-or-less in unison, evolved to be a dead end, that seems like a bizarre suggestion.  " I think this sentence means the first man believes all sars-cov-2 particles independently (not from the same parents) mutated in the same direction. Is this even possible?


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Why can't SARS-CoV2 antigen lateral flow tests be used for testing animals?
Real use case:
Two male neutered Felis catus individuals live in a household where up to three humans live of which all were infected with SARS-CoV2 at the same time, proven by antigen and PCR tests. All three humans were clearly symptomatic.
Funny sidenote: All three humans most likely contracted the infection at the same event, however two were diagnosed with omicron and one with delta by sequentiation.
After a week and with the symptoms of the humans already declined one of the cats developed symptoms with similarities to the humans in the following temporal order:

sneezing
coughing
repeated choking while feeding
sneezing with sputtering blood from the nostrils

After onset of symptoms and three days later an antigen lateral flow test designed for detection of SARS-CoV2 in humans was applied to the symptomatic cat. Sample was taken from the throat. Test kit was from brand Longsee. Both tests yielded a clear positive result. The cat was treated symptomatically and has recovered.
The results were reported to different veterinaries including the district veterinary office. All stated that the test result is void and most likely false positive, because tests designed for use on humans can't be used on other animals.
I want to discuss, which possible causes might lead to a false positive in this case.
I think it is very unlikely that we have a false positive here, my thoughts are

To my knowledge lateral flow tests for SARS-CoV2 detect either a spike protein or a capsid protein, so they react only on presence of parts of the virus.
The lateral flow tests are designed to be very specific to that virus. There are lots of corona viruses able to infect humans and provoke symptoms of a typical cold. So the tests should not react to other corona viruses.
There are corona viruses specific to other mammals (e.g. FCoV), however many of them have strong similarities to human corona viruses, so it is very likely that the tests are specific enough to rule out false positive

What aspects did I miss? Which effects you can think of preventing fairly good specificity of such tests when used in cats?
Maybe this question includes another question: What is the nature of false positives in lateral flow antigen tests for SARS-CoV2?

I had a look around the literature, and it seems that the tests are slightly less sensitive for some of the variants of concern on non-human saliva samples than they are for human1, but in general can be used to test for SARS-CoV-2 infection in animals. The linked study investigated bats, cats, ferrets, sheep, goats, cattle and pigs. RAT (Rapid Antigen Test, AKA LFA for Lateral Flow Assay) style tests have also been used successfully to test for SARS-CoV-2 in lions in Spain2
The tests largely detect nucleoprotein, as this is the most abundant protein in the virion.
to quote conclusion of the first linked article:

In summary, saliva of the species tested has no impact on the functionality and performance of SARS-CoV-2 RATs. Therefore, the use of RATs can be recommended as a point-of-care surveillance tool for SARS-CoV-2 infections in these species. However, the tests should be checked beforehand for their suitability to equally detect VOCs B.1.1.7 and B.1.351.

The only thing I would be concerned about is a false positive from the person sampling the animal contaminating the test.
However, I've also had a look around and the CDC and USDA do not currently recommend testing animals (admittedly, this is for farm-animals, not pets) unless all other causes of illness have been ruled out, and in consultation with state authorities, and it looks like the only authorized tests in the USDA regulated diagnostic labs are the PCR tests. Based on this, it is likely that your vet is being cautious and is following the guidelines published by your state/federal authorities on testing for SARS-CoV-2 in animals - which would mean a PCR test is needed for confirmation of symptomatic cases.

Hagag, I. T., Weber, S., Sadeghi, B., Groschup, M. H., & Keller, M. (2021). Impact of animal saliva on the performance of rapid antigen tests for detection of SARS-CoV-2 (wildtype and variants B.1.1.7 and B.1.351). Veterinary microbiology, 262, 109243. https://doi.org/10.1016/j.vetmic.2021.109243

Fernández-Bellon, H., Rodon, J., Fernández-Bastit, L., Almagro, V., Padilla-Solé, P., Lorca-Oró, C., Valle, R., Roca, N., Grazioli, S., Trogu, T., Bensaid, A., Carrillo, J., Izquierdo-Useros, N., Blanco, J., Parera, M., Noguera-Julián, M., Clotet, B., Moreno, A., Segalés, J., & Vergara-Alert, J. (2021). Monitoring Natural SARS-CoV-2 Infection in Lions (Panthera leo) at the Barcelona Zoo: Viral Dynamics and Host Responses. Viruses, 13(9), 1683. https://doi.org/10.3390/v13091683

Can you please define RAT?

@MattDMo - will do: Rapid Antigen Test. AKA LFA (Lateral Flow Assay).


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Transcription of Genes: Are Specific Transcription Factors + Enhancers Necessary?
I learned about transcription in my AP Biology class and we discussed how transcription occurs, but I was wondering whether transcription always requires the enhancers, activators (specific transcription factors), DNA-bending proteins, etc. to be present, or if this is only used for higher-level production of RNA transcripts?
Can transcription occur if only the RNA Polymerase (I, II, or III) and the General Transcription Factors are present?
Thanks!

enhancers, activators, silencers, repressors are necessary in controlling of the transcriptional process. Utilization of enhancers/silencers plays a part in differentiation of developmental processes (i.e. maturation, growth)
https://en.wikipedia.org/wiki/Enhancer_(genetics)


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Photoperiodism: Short-Day Plants
My Campbell's Biology textbook discusses photoperiodism of plants and introduces us to short-day and long-day plants. What I don't understand is why short day plants will not flower if they are exposed to a very brief flash of light during the night, even if that brief period + the actual day's length is still less than their critical day length? Or, put more concisely:
Length of Flash + Length of Day < Critical Period    <-- Why does the short-day plant not flower?
The following diagram is from Campbell's and makes no sense to me, because it also seems like a long-day plant which is exposed to a brief period of light during the dark will flower even if that period of brief light + its actual day's length is not greater than its critical period (i.e. it never fulfilled the pre-requisite for flowering).

I think you are looking at other the wrong way around. There is no critical light period, there is a critical dark period. That long-day flower is also a short-night flower. As long as there is never any period of darkness that exceeds the critical dark period, it will flower.
In that second picture at the bottom, exactly that is the case. The dark period is not long enough to prevent the flowering.
And in the bottom example of the first picture, there is no uninterrupted dark period longer than the critical dark period, so the plant never flowers.

What doesn't make sense for me is this: "As long as there is never any period of darkness that exceeds the critical dark period, it will flower." Take a look at part (b) of the diagram and the very bottom scenario. The period of darkness is longer than the critical night period, but the plant is a short-night flower and thus requires a night period that is shorter--not longer--than its critical period. Even with the added flash of light, the yellow bar does not exceed the black bar. Could you please explain that part? That's mostly what confuses me.

The thing to remember is to not add them up. It only counts if it's in one "piece". For those flowers it's not like our sleep, where being awake for 5 minutes between two 4 hour periods still feels like a good night's sleep. For the long day plants, it's only important that no continuous dark period is longer than x hours. Does that help?


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What percentage of our DNA is never transcribable? What percent is never actually transcribed into RNA unless researchers force it to in a lab?
From what I gather, the vast majority (but not all) of the DNA in our genomes will transcribe and create an RNA, if only under certain conditions in a lab (forcibly unwound, among other steps).
How much of our DNA can be transcribed but not translated?
How much actually does so on a regular basis in our cells, becoming useful RNA, but doesn't code a single amino acid?  (Non-coding functional RNA, or junk RNA?)

While, as you say, most of our DNA can be transcribed, you are right that it is not well accessible and/or lacks strong promoters. It's said that over 80% of DNA is transcribed but only <2% transcribes into mRNA, that will be translated [1]. It is not yet known what percentage of non-coding RNA (ncRNA) is junk (by identity) [2], but if weighted by mass or numbers, most of ncRNA is functional as ribosomes and tRNAs make up most of the cells dry mass:

(image source)

Minor detail: doesn‘t the left pie chart say that rRNAs make up most of a cell‘s dry mass and not tRNAs..?

I once read in a book „Numbers in Biology“, that ribosomes can make up to 80% of cells dry mass. The chart is not about dry mass but about RNA mass, ignoring not only water but also lipids, proteins etc.

Oh I meant together they make up most of the cells mass. Not tRNA alone.


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Evolution: Can the genotype frequencies change, but the allele frequencies remain constant?
If a population isn't evolving because it's in Hardy-Weinberg (HW) equilibrium, then I know that both genotype and allele frequencies must stay constant.
My question is, can evolution still not occur even if Hardy-Weinberg conditions aren't met? In all of my books, the conclusion seems to be that if HW conditions are met, then evolution doesn't occur. However, they don't clarify if HW conditions being met is both a necessary and sufficient condition for evolution to not occur (they only imply that it's sufficient).
Any thoughts?

Could you clarify what specially you mean by 'evolution'? Are you referring to the evolution of a morphological trait, molecular evolution, evolution as a general response to selection? I'm also a little bit confused as to how this relates to the title of the post.

That’s important because by definition, if HWE assumptions are all met then there can’t be any selection occurring.

At the risk of further confusing the issue (there are already 2 answers focusing on different aspects!!), I am going to focus on a somewhat different aspect of this question that I think we need to nail down before it can be addressed.
Going mostly off your question title, it would help to know what you mean by genotype vs. allele frequencies. These are quite different, and it's not clear how you are trying to employ them. Speaking strictly, we use alleles to talk about genetic variation within a locus, and genotype variation to also mean variation across loci as well (how alleles across loci are sorted into individuals; this is sometimes also called "gamete frequency"). Of course, people generally talk about HWE in the context of only a single locus, which means that it is easy to get tripped up here.
It is possible for us to have non-equilibrium genotypes while also having equilibrium allele frequencies, in direct response to your question title. A trivial example of this is linkage: when two loci are very close to each other on a chromosome, their alleles will be more closely correlated than genes on different chromosomes. This yields the phenomenon with the unfortunate name linkage disequilibrium (LD), which implies nothing about evolution or HWE but rather about a non-equilibrium mixing of alleles into genotypes.
For context, it is quite common to apply tests of HWE locus-by-locus in genomics, as a sort of quality control or preprocessing step. It is also common to measure LD for relevant pairs of loci, but there is not much biological relationship between these measures (even though LD can be thought of as an extension of Hardy-Weinberg to a multilocus case, for historical perspective see here.). In any realistic case, global linkage equilibrium across the genome is very unlikely, whereas HWE for most loci is very likely.
As a thought experiment, imagine that a (neutral) inversion arises, and then starts segregating. All of the alleles remain at HWE, but suddenly you have new LD (genotypic disequilibrium) that wasn't there before.
With all that out of the way, I see no reason why evolution could not happen at the level of overall genotypes even in the case that HWE is maintained statistically. This can be achieved by the evolution of e.g. sign epistasis, I am sure there are other examples as well that would yield apparent HWE while trait evolution is technically still going on.
I think that it might be fair to say that monogenic evolution isn't happening with apparent HWE, I don't think that you can say the same thing for polygenic evolution.
I'll finish by just saying that I refer specifically to the statistical phenomenon of HWE, and not to the assumptions themselves (which would be tautological; "can evolution happen if you assume there's no evolution?" as commenters point out). After all, You can violate most of the assumptions of HWE and still end up with allele frequencies that look like HWE:

Although statistical deviation from Hardy-Weinberg expectations generally indicates violation of the assumptions of the theorem, the converse is not necessarily true. Some forms of natural selection (e.g., balancing selection, which maintains multiple alleles in a population) can generate genotypic frequency distributions that conform to Hardy-Weinberg expectations. It may also be true that migration or mutation is occurring, but at such low rates as to be undetectable using available statistical methods. And, of course, all real populations are finite and thus susceptible to at least some evolution via genetic drift.

Where do you get that populations aren't evolving?
A population might be in HWE for a particular trait if there is no selection on that trait, but that doesn't mean that there is no selection or drift happening on any trait!

True but that wasn't the main purpose of my question. The more important part is regarding whether HW is necessary not just sufficient

@Ally Maybe an example of what you are thinking of would be helpful. As-is, to me this question just raises my eyebrows. I think you might have confusion somewhere but I'm having trouble pinpointing where that is.

If a trait is under selection, by definition it's not in HWE.

Yeah so reiterating the question in an if..then format might make it more clear. Right now, I'm getting that "if HW, then no evolution", which also implies "if evolution (aka if a trait is under selection), then no HW". However, from the original premise it does not necessarily follow that "if no evolution, then HW". So my question was basically asking if there was no evolution occurring, would that necessitate the population being in HW or if there was some other mechanism / set of conditions that would allow no evolution to occur

Stop talking about "evolution". It's too broad, and the idea that evolution "stops" because you try to apply some equations to a single trait is silly.  Evolution is pretty much always occurring, even if the proportions of some individual traits are stay steady.

The HW principle is not a mechanism.  They are equations that build a rather simplistic model that sometimes is applicable and useful in real life.

Let me focus on the necessary and sufficient part: such a language is suitable in mathematics, but does not really have much meaning in evolutionary/statistical context. Instead we talk about rejecting the null hypothesis, which does not mean accepting the alternative hypothesis. Equally, a failure to reject the null hypothesis does not mean that this hypothesis is true.
Hardy-Weinberg is a null model of evolution with about a dozen of assumptions. It is not a model of "no evolution", but rather a model of how evolution happens all the time (but it seems like "no evolution" in the sense that not much interesting is happening). Rejecting this null model/hypothesis means that some of its assumptions are violated. However, if the genotype frequencies do satisfy HWE, it doesn't automatically mean that the assumptions of this model are satisfied.


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How do plants prevent infection from retroviruses?
Why are plants not affected by animal viruses such as retroviruses? What prevents them from being infected?

I think your question is answered in my answer to: Can an infectious diseases come from a plant?. I also have an answer to another question in this area: https://biology.stackexchange.com/questions/90174/is-there-any-disease-in-common-between-human-and-insects/90493#90493

I think you have the question backwards.  Viruses tend to be pretty specific in what they attack: not only animals, but particular species of animals, and often only particular cell types.  So why would you expect a virus to attack such different things as animals & plants?

Plants do are not affected for the same reason that linux virus cannot infect windows computer: viruses work like a lock and key for specific infiltration methods in different hosts.

Virus are extremely host-dependent because they need to enter the host, move inside of it, use its replication mechanisms and codon usage. There are virus that cross the family boundry (ToMV for example) but crossing the kingdom boundry is less probable.  For example, animal cells don't have a cell wall, which is a major change and requires a change in strategy for entrance to plant cells.
For retrovirus, they simply are virus that can integrate into the host genome.  Several articles [1, 2, 3] describe retroelements that have been classified as retrovirus, retrovirus-like particles, and retroelements encoding coat proteins. This can lead to the conclusion that there are retrovirus in plants.
It is worth noticing that virus are not the major pathogens of plants (fungi are) and resistance to virus can be acquired even without understanding the mechanism.   This leads to a lower level of interest, funds, and researchers in the area, which leads to a lower rate of discovery of new virus.
In conclusion, we have not found a virus that crosses the kingdom barrier but have families of virus that contain both plant and animal virus.


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What does allelomorph mean?
Is there any difference between allele and allelomorph since most websites call them the same.
If they are same then why two different term?

Welcome to Biology.SE! Thank you for taking the [tour], but please also go through the [help] pages starting with [Ask] questions effectively on this site. In particular asking why synonyms exist is about language not biology. Also note that for "homework" questions, you are required to use the "homework" tag. (Note that "homework" can apply to questions even if they are not assigned as homework — in this case you question "addresses a basic biology concept that may seem trivial to biology professionals".) Thanks!

Ok , thanks would consider your points

Allele, allelomorphs - the common word in both is "Allele" - When Multiple genes code for a contrasting or similar traits/ or multiple genes in the same locus on homologous chromosomes can be qualified as an allele.
Now let's look at second word "Morph" - Adjective MORPHOLOGICAL meaning that - relating to the form or structure of things. Now I'm going to mix this word MORPH with another word POLY which gives "Polymorphic" (Meaning Many Shapes/Forms) - Polymorphism is the ability of an object to take on many forms. This is the same behavior that we could see in an allele. Let me put this polymorphism more specific to our topic.
Gene-Polymorphism -

A gene is said to be polymorphic if more than one allele of a gene exists within a population.

In addition to having more than one allele at a specific locus, each allele must also occur in the population at a rate of at least 1% to generally be considered polymorphic. - Wiki definition

Now comparing the definition of allele with this second point of Gene Polymorphism, we get Allelomorphs - Meaning that a single Allele taking different forms/ multiple occurrences within a given population.
Here is an example for easier understanding,
Eye Color is a Trait,
Let us say that eye color is controlled by a single gene, for simplicity (this is generally not true in nature).

Blue Eye gene variant is an Allele,
Red Eye gene variant is an Allele,
Yellow Eye gene variant is an Allele,

Your eye color is then controlled by which of these alleles you have for the eye color gene.
Here eye color allele takes different forms. Thus making it polymorphic, Putting all these forms together we get Allelomorph(s) (plural), each individual one is as an allele/allelomorph (singular)

I edited to remove some unclear statements and make it easier to understand. (I think that this is a case where diagrams would really help.)


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Can ants distinguish individual ants in the colony?
I am aware that ants have the ability to distinguish which female is the queen and which ones aren't. However, can ants also uniquely distinguish other individual ants in the colony? Is the differentiation between the classes only (worker-ant, queen, non-queen) or is it within the classes as well like hey its bob?

I edited for clarity and conciseness, but please check to make sure I have preserved your intent. Also note that we expect you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). Starting with wikipedia is often a good bet. ——— Please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. Thanks!

@tyersome, thanks for the edit. Yes, the intent is preserved and I shall add references later. +1


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How do we determine the common ancestor of a species?
I have seen a lot of articles about common ancestors. But I didn't find any perfect articles that said about the evidence of common ancestor.

https://www.khanacademy.org/science/high-school-biology/hs-evolution/hs-phylogeny/a/phylogenetic-trees

What do you define perfect? Are you speaking about making phylogenetic trees or about the theory of evolution in general? If about the later, it is a theory (so no definitive proof) but with a lot of supporting data and biological value. As far as I remember this site does not try to convince about that theory, there is enough material online

What is your actual question? If you have read up on the subject what specifically do you not understand?

The most definitive conclusions about the common ancestor are made by comparing genetic sequences of the organisms, for which well developed mathematical/computational methods exist, see, e.g., Inferring Phylogenies or An introduction to molecular evolution and phylogenetics.
For distant species the genomes are rarely directly comparable, so that some ambiguities can exist. Therefore the existing tree of life and species classification are based on comparison of the ribosomal RNA, which is believed to be rather conserved:
rRNA is one of only a few gene products present in all cells. For this reason,
genes that encode the rRNA (rDNA) are sequenced to identify an organism's
taxonomic group, calculate related groups, and estimate rates of species
divergence. As a result, many thousands of rRNA sequences are known and stored in
specialized databases such as RDP-II and SILVA.

Note that this still leaves out the viruses, which are acellular and therefore do not have theor own rRNA.

Thank you so much.


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How many plant species would have existed immediately after the K-PG extinction?
Specifically, what is the best estimate for the minimum number of plant species during the aftermath and recovery period following the K-PG extinction event?
Do we have any idea how low that number got?

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Good question.
The fossil record post Cretaceous-Paleogene boundary is much less clear than the animal fossil record. It's basically impossible to give a true value, since there's no way to determine the number of plant species either side of the event, due to the sporadic nature of plant fossilisation.
In contrast to the wide-scale extinctions that occurred in the animal Kingdom, no major plant groups became extinct across the boundary, and the damage primarily occurred at the species level. However, there is a very strong bias towards sites in North America as these are the ones which are the most well preserved.
This is a cross sectional map of the palynological diversity across the K-PG boundary from North Dakota (source).

The average extinction proportion of miospore taxa in North America is
around 30% (Nichols, 2002, Nichols and Johnson, 2008) and this is
synchronous with a significant drop in gross palynological diversity
(Fig. 5). An additional 20–30% of the miospore taxa underwent a
statistically significant decline in abundanceThe extinction magnitude
was apparently lower within New Zealand assemblages where 15% of
pollen and spores species disappeared


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How can "position" be measure by bp unit?
In "[Genomics: A Very Short Introduction]" by John Archibald, the author discusses the CNV:

Whole-genome re-sequencing is fast becoming the norm in the field of human comparative genomics. It is sufficient for the accurate detection of single-nucleotide polymorphisms or SNPs (i.e. variations in a single nucleotide position in the genome in members of a population). To a lesser extent it can also identify short insertions and deletions in non-repetitive DNA, as well as reveal copy number variations (CNVs) between target and reference genomes. CNVs are increasingly recognized as being important in human biology and disease; in genomic data, they manifest themselves as differences in the depth of sequence coverage obtained for a specific gene or stretch of DNA. Genomic regions showing a large increase or decrease in the number of individual reads mapping to the reference genome are indicative of changes in copy number in the organism of interest (see Figure 8).

I don't have enough knowledge about this topic, and I don't know how "position" could be measured by "bp" unit, which is mainly a unit of length in similar contexts!

@user438383 So, does "chromosome position" refer to "the position of the chromosome itself" or "position of a specific thing within it"?

The latter - the position within a chromosome.

‘Position’ (or genomic coordinate) in genetics is just a 1-dimensional measurement, as the genome is basically a 1-dimensional object (in most contexts - the genome actually has a 3d structure but that’s usually ignored for simplicity in a majority of case).
‘Chromosom(al) position’ will therefore almost always refer to the position of something like a gene within a chromosome.
Perhaps this is confusing if you assume ‘position’ refers to at least a 2-dimensional coordinate like it does on a map or something.


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What does ‘per DNA fragment’ mean?
In "[Genomics: A Very Short Introduction]" by John Archibald, the author discusses the DNA sequencing:

In living cells, DNA rarely exists in isolation; it is typically bound tightly to proteins (see Figure 2), proteins that serve to compact it and to regulate the process of gene expression. Consequently, the act of purifying (or ‘extracting’) DNA from the multitude of proteins, lipids, and other macromolecules inside the cell requires the use of harsh chemicals and subjects it to physical damage. While it is possible to estimate the size of intact chromosomes in the lab, modern DNA sequencing instruments typically collect at most 1,000 base pairs of nucleotide sequence per DNA fragment.

What does this sentence mean?

They are referring to sequencing strategies where you chop a longer stretch of DNA into fragments, sequence each of these, and stitch the sequences back together.
The sentence is explaining that the lengths of DNA actually sequenced from these fragments are relatively short, up to 1000 base pairs per fragment.

Are you sure? If this the case why don’t they just say so without reference to the sequencing machines. Without knowing any more about it, I would interpret the sentence to mean that regardless of the fragment length, the machines become inaccurate after 1000 nt.

I agree with David. Depending on the method of fragmentation (restriction enzyme, sonication/shearing, etc.) you can sometimes end up with fragments that are a lot longer (or a lot shorter) than 1000bp. I think the sentence is talking about the maximum usable length of a read, not the fragment size itself.

@MattDMo Updated to clarify that this is the sequenced length from a fragment, not the size of the fragment itself.


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What does "run" mean in DNA sequencing?
In "[Genomics: A Very Short Introduction]" by John Archibald, the author discusses the DNA sequencing:

In reality, most nuclear genomes are a mixture of unique sequences and short and long repeats of various kinds, and researchers have developed ways of dealing with the issue. One approach is to obtain sequences from both ends of the randomly selected DNA fragments (see Figure 6), and to have the algorithm keep track of these so-called ‘paired ends’ and the distance between them (which is known because the genomic DNA was size-selected prior to library construction and sequencing). This improves the chances of being able to anchor the sequence data from each DNA fragment onto the genome. It is also common to perform multiple sequencing runs using DNA that has been sheared to different sizes (e.g. 2, 10, and 50 Kbp); this makes paired-end data even more effective in overcoming the problems associated with repetitive DNA.

I don't have enough knowledge about this topic, and I'm not sure of the exact meaning of "run" in this context. Does it mean "performing the process of sequencing multiple times" or "generating multiple sequences"?

This is English not Biology. I suggest you abbreviate the question and transfer it to SE English Language Learners.

@david ‘run’ is a technical scientific term that’s used often, and asking about terminology is on topic here. Most importantly, this is likely to be useful to biologists, so I disagree with your suggestion.

@user438383 See Merriam-Webster Run noun "4 : a continuous period or series especially of things of identical or similar sort" with 7 examples, including ": a set of consecutive measurements, readings, or observations". The poster seems to be trying to use this site as a consultancy to help him reading a book, rather than asking questions about biology arising from it. I would encourage him to learn to save his own life.

It looks to me like that sentence should really read "It is common to prepare multiple sequencing libraries using DNA that has been sheared to different sizes". While you can run the same library over and over again, since one run is only a sampling of the library contents, it looks to me like the author is talking about combining information from libraries of different insert sizes as being more effective than resampling from one library with one target insert size.

Each run is simply each time a reaction/process is performed, though usually applied to something that is performed on a machine or device that does the "running" - so you could do quantitative PCR runs or run a gel.
Multiple runs would be repeated reactions/processes (in this case sequencing library preparation then run on the sequencing device).

DNA sequencing (e.g. Illumina dye sequencing) does not sequence all DNA available; it simply sequences a sample of what you provide, i.e. it "samples". Say you have a bag of 100 differently-colored ping pong balls, and you have a set procedure wherein you take out 50 balls at random and note down their color to understand the color distribution. You could do this "run" once, but you can get a better, more reliable look into your bag if you do a 50-ball-random-sampling multiple times! You do many "runs". That's why in research we use the phrase "multiple runs" when we have preset procedures.

^above is addendum to answer to help make it more intuitive, i make no comment on the actual answer, it's very good. +1


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Why do people get headaches after oversleeping?
I've tried a web search, but the results are mostly non-scientific advice on good sleep etc. One link provides some explanation, but I have not noticed them providing links to that referenced research:

Getting too much sleep is actually a common headache trigger.
Multiple explanations exist for why exactly this happens, but
scientists have dug into some research on this connection. Serotonin
disruption
Some research suggests that oversleeping has effects on
neurotransmitters in your brain — particularly on one (rather famous)
neurotransmitter called serotonin. ....

What is current status of scientific research for such phenomena? Please provide links to studies etc.

I don’t think the place for this question is Biology, but it may well be appropriate on SE Medical Sciences.

Maybe I better rephrase, but I am interested in biological underlying mechanism of pain from oversleep, AFAIK it is not considered a decease, so I posted here.

Doesn't happen to me, so I suspect one also needs to ask what genetics are involved too. It seems circadian rhythm disruptions are suspected as the cause in such cases.

More recent review https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6381824/

It may not be a disease, but headache is a medical condition. that I would consult a medic rather than a biologist about if it affected me. SE Medical Science considers the science underlying medical conditions.

Is there data to suggest that this is a common/universal phenomenon?

Headache (by any cause) is still a frustratingly not understood phenomenon from a neuroscience perspective.

Is it even possible to get too much sleep?  As opposed to the more common use of "oversleeping" as not getting up in time for work, school, or whatever - in which case your body probably needed the sleep.

@jamesqf, internet finds entries from search for headache from oversleeping - that is sleeping too much (as they say).


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Are there autoimmune disorders caused or mediated only by T cells?
I have frequently read that 'most' or 'the vast majority' of autoimmune disorders involving the adaptive immune system are caused by autoantibodies.
These comments imply that there are known disorders involving only rogue T- cells.
Does anyone know of specific examples?  Is there a list somewhere?

Can you provide a link for where you heard that from please?

There are several primarily T-cell driven autoimmune diseases like Rheumatoid arthritis, Type 1 diabetes, Inflammatory bowel disease, Multiple sclerosis [PMID: 29123529, 32457742].


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Identify this extremely tiny white bug please!
I have noticed these extremely small, hard to notice with naked eye bug for about 3 nights now. Twice on my body in the kitchen and once on my thumb in my living room. I managed to catch one last night from my living room which has an area rug near a mattress, coffee table and couch. I managed to put it in a small 2 inch box with white lid. Today it seems little brownish and inspected it under a microscope.
First  picture is of the box size to put some real world perspective on the actual size.

Second pic is of the bug lying on the white lid, doesn't seem to be even 1.5 mm.

Third and fourth pic is from the microscope(150x), I had to move the bug so I might have squished it a bit.

We are getting bite marks and are almost convinced that this bug is the reason as we never had a bug problem ever. The only other thing we noticed is a silverfish in our living room but not sure if that can cause these bite marks.

Do you have birds or rodents in the home? Do you have birds nesting or spending a lot of time on any structure on the outside of your house?

Yes, we did have 2 bird nests in front of the main door on the roof, which we let since we didn't want to hurt the birds. But the birds left last week and we washed the nest afterwards on Monday10/5.

Thanks @perfectionist. We have not been to any grassy area recently. We did however have 2 bird nest on the adjoining wall (with a window) under the roof which we let it be as we were not aware of consequences :)

@theforestecologist - I know you linked the thread which talks about Ornithonyssus. Just wanted to check if you think this is the same specie I am dealing with. This is to see if we can eliminate Red Mite /Dermanyssus Gallinae from the equation) and considering we are in USA, its highly likely we don't have Ornithonyssus Bursa (tropical fowl mite) so we might be able to zero in on Ornithonyssus sylviarum(northern fowl mite). We are infested for for about 4 months now and I am not sure how to devise an eradication plan since each type requires some specialized steps as I found in my research.

@Anx sorry to hear :/. You'll need to include better pictures if you want anyone online to help determine your species. If you've narrowed down to a few species as possibilities, see if you can find a resource or 2 that tell you what to pay attention to in order to differentiate them -- Using that info, take really clear zoomed-in pictures of body regions that are important for telling species apart. If you update your post asking to differentiate these species specifically, include a few more detailed photos and link to some useful info you found already, I'll reopen your post as unique.

Also, you might also consider contacting a local exterminator for help. If you're concerned about price, some will help ID a species before providing a quote... ...

@theforestecologist Appreciate you responding so quickly on this. We did reach out to a number of pest control operators (total 62 so far), but Orkin was the only one who came back with Bird Mite identification however they were not aware of specie level information. Also, we no longer have any visible mites in our environment, we were lucky to catch that first one. We have already gotten the pest control spray done 11 times by now, but these mites are so hard to beat :(  My last resort is to try fumigation but I am worried about the unhatched eggs..(as people reported) resulting it useless.


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What is this tiny creature?
Is this a bed bug or book lice? They were crawling all around the furniture.
Found in North East Florida, USA.

Is that a wooden surface? It could also be a termite. Do you have any additional pics?

Yes it was wooden surface. They were really tiny and fast. The other pictures are kind off blurry,

Book lice in Florida: https://inaturalist.ca/observations?place_id=21&subview=grid&taxon_id=372873
Bed Bugs in Florida: https://inaturalist.ca/observations?place_id=21&subview=grid&taxon_id=53667
Termites in Florida: https://inaturalist.ca/observations?place_id=21&subview=grid&taxon_id=118903&view=species
Ghost Ants in Florida: https://inaturalist.ca/observations?place_id=21&subview=grid&taxon_id=69122

Welcome to Biology.SE! For identification questions your post should include the size and location (e.g. country and region — the more specific the better) where you observed this creature. These can be essential clues for identifications. (Please [edit] this in since essential information should not be put into comments as they are ephemeral and often overlooked.) ——— If possible clear, closeup photos of the creature from multiple angles would also be helpful. ——— Please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!

The picture is hard to see details, but it seems you might be dealing with ghost ants:

I'm guessing ghost ants over lice or termites or bed bugs because their light-coloured abdomen ends off in a pointed end, rather than a round bulbous end. The darker thorax and antenna are also a match. And the distribution/range of ghost ants seems to be heavily concentrated in Florida:

(Map source:
https://inaturalist.ca/observations?nelat=39.32226574471&nelng=-51.18647084246517&place_id=any&swlat=18.339761895743152&swlng=-117.94819281111599&taxon_id=69122 )
Apparently, they smell like rotten coconuts when crushed. (http://entnemdept.ufl.edu/creatures/urban/ants/ghost_ant.htm )
They eat any kind of food, and they are easily controlled by eliminating food sources (so if they are in your furniture, maybe look within cushions or cracks for old dried food and clean it out).


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Is the mRNA produced constant during time?
I am doing a statistical data analysis of a dataset of P. Furiosus cells exposed to gamma radiation.
For the samples exposed to gamma radiation, I have the values of mRNA produced over time. For the samples not exposed to gamma radiation (reference samples), I do not have the time at which the mRNA has been extracted.
Therefore, I was wondering: under normal conditions, generally, is the mRNA produced constant with respect to time? I thought that maybe the fact that is constant could be the reason for which there are not the values of time.

If your sample culture is asynchronous, meaning they're at all different stages of the cell cycle, then mRNA production should be consistent over time. However, if you use chemicals or environmental conditions to synchronize the culture, then release it, you'll see periodic production of mRNA for a while until the cells start to gradually slip out of synchrony. For your paper, I highly doubt they synchronized the cells, otherwise they would have clearly mentioned it.

thank you  @MattDMo but I do not really get the meaning of "consistent over time" ?


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Chiasmata and Adaptation
We know that during the crossing over of meiosis II, some portions of the paternal chromosome recombine with the maternal chromosome along the  chiasmata. And the number of chiasmata varies.
My question is this: If the crossing over is responsible for genetic variation, then does the number of chiasmata increase in the same chromosome in the same species for the sake of the species' survival? And if so, what factors contribute towards increasing that number?

Welcome to SE Biology! A note - selection virtually never occurs at the level of the species - it is almost always occurs at the level of an individual organism (or gene). So your question might be better framed if you ask about how crossing over might affect the fitness of an individual rather than how it might affect 'the survival of the species'.

The number of recombination events (chiasmata) varies dramatically from species to species.
It is also unlikely that this number has any universal relationship to selection, though for specific cases it has been shown that selection can change recombination frequency.
For some more information about the processes controlling this in present-day species and the inferred mechanisms driving among-species variation in recombination frequency, you might see this paper.


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Why are some organisms able to regenerate?
Why can sponges, cnidarian polyps and planaria regenerate if broken up, but other animals e.g. humans and phylum chordata cannot?

All organisms, including humans, have the ability to regenerate something in the body. But the process is much more developed in lower organisms such as plants, protists -- unicellular organisms such as bacteria, algae, and fungi  and many invertebrate animals such as earthworms and starfish. These organisms can grow new heads, tails, and other body parts when injured.
Scientists don't know why mammals don't have the same ability to grow new limbs. But they think it is because mammals have more complex biological structures; limb regeneration would require sophisticated controls to ensure that limbs and organs don't grow out of control. Humans, for example, are already equipped with safety mechanisms to ensure that individual cells don't grow uncontrollably. But these mechanisms wear down as a person ages and cancer is often the result.
Nevertheless, mammals do regenerate skin, muscle, and blood. Scientists are just beginning to learn about other types of cells, such as those in the brain and blood, that also regenerate. Further study of the phenomenon might lead to a way of growing replacement organs and limbs outside the body.
Not all organisms regenerate in the same way. In plants and organisms like hydra and jellyfish, missing parts are replaced by reorganizing neighboring tissues into whatever parts have been cut off. Animals with more complex bodies usually regenerate parts by producing a specialized bud, or blastema, at the site of amputation. The blastema supplies the tissue necessary for the regenerated part.
The regenerated body part is not always the same as what was lost. Many insects regenerate abnormally small legs from which some segments may be missing.
Tadpole tails, for example, typically grow back to about only half their original length. And regenerated parts often differ in details. A regenerated lizard tail, for example, contains a cartilaginous tube instead of the vertebrae in the original.

Nice answer but you should add some references. Alvadro labs work on S. mediterranea for example.


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What disease / parasite / fungi has affected the mango in the picture?

The mango is found to have some kind of fungi / worm on it's surface . This has affected a huge number of mangoes in the same tree . It can be described as white and fibrous / weblike structure near the top of the mango .

What about the inside of the mango, did the insect make tunnels? if so, photo of slice please. What region of the world are you in?

If you zoom in on your picture, you will see that the small orange blobs have legs. These are red spider mites (Tetranychus urticae), which is a very common pest species of plants world-wide. They are called spider mites as they may spin webs on the plants they are feeding off. You have quite the infestation in the picture. It will take quite a bit of pest control to get this under control. I suggest spraying with Neem oil.
The mites feed by puncturing the cells of the plant they are feeding off and sucking the cytoplasm out. This puncturing results in damage to the plant, which might cause invasion from a bacterium or fungus. In your case I would guess a fungus, probably a sooty mold. Sooty molds grow on sugary excretions from parasitic animals (like spider mites) or on secretions from the fruit itself.