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Who discovered that phage phiX174 has a single-stranded genome?
I have recently read that Erwin Chargaff has discovered that the genome of phage phiX174 (ϕχ174) is single-stranded. However I could not find the paper reporting this discovery.
Is there a link to the paper reporting this finding?
Thank you.

can you give the citation, quote, or other paper trail for us to follow? Finding old papers can be difficult, and it isn't clear even whether Chargaff made that finding or merely if his work informed the discovery. I cannot find any meaningful association of him to the phage, though I also can't find an obvious paper or reference on pubmed that points to the discovery. Knowing what your starting point is would help.

I think @MaximilianPress was close. Chargaff certainly did early work on DNA structure, but he was not the one to identify that the genome of φX174 was circular.  As far as I can tell, the actual peer reviewed publication was a pair of papers in Journal of Molecular Biology, written by R.L. Sinsheimer in 1959. I can access these articles through my institution, but I suspect that they are paywalled.
These two articles are in volume 1, issue 1 of the journal on pages 37-42 and 43-53 respectively. I've reproduced the citations with abstracts below. The first indicates some oddities in the DNA of the bacteriophage and the second confirms these oddities and provides the explanation (emphasis is mine to highlight the salient point).

Robert L. Sinsheimer,
Purification and properties of bacteriophage φX174,
Journal of Molecular Biology,
Volume 1, Issue 1,
1959,
Pages 37-IN5,
ISSN 0022-2836,
https://doi.org/10.1016/S0022-2836(59)80005-X.
(https://www.sciencedirect.com/science/article/pii/S002228365980005X)
Abstract: Procedures are described for the isolation in pure form of the bacterial virus φX174. This virus is shown to have a particle weight of 6·2 × 106 and to contain 25% by weight of DNA. At neutral pH, the purified virus forms a discrete aggregate, probably a tetra-mer. This aggregate dissociates either upon dilution or at alkaline pH. Lysates produced by φX174 contain a second particle, antigenically related to the virus, but not infective and of lower sedimentation rate and lesser DNA content. The DNA of φX174 appears to have an unusual structure in that it reacts with formaldehyde (even before extraction from the virus) and in that the atomic efficiency of inactivation of the virus by decay of incorporated phosphorus-32, calculated by combining our data and that of Tessman, is 1·0.

Robert L. Sinsheimer,
A single-stranded deoxyribonucleic acid from bacteriophage φX174,
Journal of Molecular Biology,
Volume 1, Issue 1,
1959,
Pages 43-IN6,
ISSN 0022-2836,
https://doi.org/10.1016/S0022-2836(59)80006-1.
(https://www.sciencedirect.com/science/article/pii/S0022283659800061)
Abstract: The deoxyribonucleic acid (DNA) of bacteriophage φX174 can be extracted by phenolic denaturation of the virus protein. The DNA thus obtained has a molecular weight of 1·7 × 106, indicating that there is one molecule per virus particle. This φX DNA does not have a complementary nucleotide composition. The ultraviolet absorption of this DNA is strongly dependent upon temperature in the range 20° to 60°C, and upon NaCl concentration in the range 10−3 to 10° M. This DNA reacts with formaldehyde at 37°C and is precipitated by plumbous ions. This evidence is interpreted to mean that the purine and pyrimidine rings are not involved in a tightly hydrogen-bonded complementary structure. Light scattering studies indicate that this DNA is highly flexible and that its configuration is strongly dependent upon the ionic strength of the solution. Upon treatment with pancreatic deoxyribonuclease, the weight-average molecular weight decreases in accordance with the function expected for a single-stranded molecule. It is concluded that the DNA of bacteriophage φX174 is single-stranded.

well done! this definitely the right answer. Somehow I got the author/date right but clicked on the wrong article?

@MaximilianPress Thanks. Took a bit of digging to find them because they apparently aren't indexed on Pubmed - it only comes up with the symposium you found, which is odd as J Mol Biol isn't exactly an unknown journal with no publishing history.

yeah, that must be what happened to me! And then when I saw author-date matching in the reviews I assumed it was the same. I also think that the "cited by" PubMed feature got confused for similar reasons, and linked me out to the papers citing the right (JMB) paper by accident! What a tangled web we weave.

Thank you. Sorry but I did not have much quotes to report.

Update
please see @bob1's answer below.
Original answer
I suspect that this is the paper you are interested in but I can't find even an abstract of it due to the obscurity/loss of the journal.
In a different review paper, this 1959 Sinsheimer paper is described as such:

The first DNA molecule purified to homogeneity was the genome of bacteriophage ϕX174, reported by Sinsheimer in 1959 (12). Equilibrium buoyant density centrifugation of the ϕX virion yielded pure preparations from which the DNA could be easily isolated by phenol extraction. ϕX DNA turned out to be a single-stranded circular molecule that was estimated to be ∼5000 nt in length.

It’s not a journal but a symposium volume. Most big university libraries would have it secreted in the bowels of their archives. I’ll see if ours has it, just for fun.

@David thank you! that would be wonderful.

I've found it in Google Books at https://books.google.co.uk/books?id=6vm1eM7-zJYC&pg=PA1&source=gbs_toc_r&cad=2#v=onepage&q&f=false  If anyone has difficulty with this link I've taken screenshots and can mount a pdf on one of my websites. Chargaff wasn't present at that symposium, according to the list of participants at the end. I think the poster has probably got hold of the wrong end of the stick. Chargaff was interested in this because its base composition violated the so-called Chargaff Rule. However we now know that this reflects the base-pairing in dsDNA. I can post an answer if useful.


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Genetic entropy
One day my internet acquaintance told me, that genetic entropy is evidence for intelligent design and he also provides me this waiting time problem and this simulating evolution by gene duplication.
I took a dim view of that point, but because I'm not geneticist I can't answer this question and I don't know much about genetic entropy either. I'm not an internet troll, but I don't like when religion breaks into science, so help me to understand how can we explain it using our knowledge and logic.
Thanks.

What is your question? I can't see any interrogation point!

Also, your post might be a possible duplicate of this one.

I'm afraid this list doesn't exist to help users rebut arguments from third parties that they are unable to formulate themselves. I have never heard of genetic entropy, and acceptable questions do not require me to go elsewhere to read about it. I am therefore voting to close this question as unclear.

I'm new to this idea but did a bit of searching.  The origin of this idea of "genetic entropy" appears to be a guy named John Sanford. He is also the author of the "waiting time problem" you reference. The principal author of the other reference you cite is Michael Behe. Both of these guys are ardent creationists. This means they have an agenda. Good science is the product of good questions, it does not result from attempts to support preconceived notions. This especially applies to religious ideas since they are generally strongly held.
Further research into the "genetic entropy" idea suggests that Sanford has basically repackaged an older idea but with a decidely creationist slant. That original idea is termed Muller's ratchet. https://en.wikipedia.org/wiki/Muller%27s_ratchet
The conclusion of Hermann Muller, inherient in Muller's ratchet, is that his concept supports the rise and importance of sexual reproduction. I find no mention of creationism, this seems to be Sanford's addition to bolster his agenda.
If you really want to delve deeper into the flaws in the arguments of these two creationists:https://letterstocreationists.wordpress.com/stan-4/ This site contains an extensive list of links to rebuttals to the claims of these two men.

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When is the second polar body extruded from the egg nucleus?
When does the second polar body gets expelled from the egg nucleus during oogenesis ? I know that it occurs after the entry of the sperm into the secondary oocyte but does it occur before the fertilization or in the period between the entry of the sperm and fertilization ?

As stated in the answer by @CDB, these polar bodies don't last too long, and the second polar body which forms as the result of meiosis II, extrude only after fertilisation. The secondary oocyte is arrested in metaphase II until it becomes fertilised, so meiosis II can only by completed after ovulation and fertilisation (see e.g. UNSW Embryology: Meiosis at https://embryology.med.unsw.edu.au). This means that meiosis II, which actually forms the second polar body, occurs as a result of fertilisation. The secondary oocyte becomes a mature oocyte (ovum) by the expulsion of second polar body into perivitelline space.
The metaphase arrest is caused by the presence of two types of cytoplasmic activity
1. MPF - maturation promoting factor
2. CSF - Cytostatic factor that inhibits APC/C

Only when MPF is present, stabilized by CSF, and active will the M phase persist. However, this complex is very sensitive to calcium, such that a rise in calcium tilts the equilibrium away from complex synthesis towards destruction.

Capcitated spermatozoa that have undergone an acrosome reaction is capable of fusion and Calcium mediated calmodulin is required for this process. When fusion happens spermatozoon ceases to move and the nuclear with parts of mid piece and tail passes to the ooplasm. So sperm initiate Calcium release at fertilisation this helps in the completion of the 2nd meiotic division.
For further detail on these processes you could read the article Penetration, Adhesion, and Fusion in Mammalian Sperm-Egg Interaction
Increased Calcium activated Calpain (calcium dependent cysteine protease which causes CSF to disappear thereby activating APC/C which in turn causes dissociation of MPF. This results in completion of 2nd meiotic division.
For further details I recommend you to read Johnson and Everitts Essential Reproduction (6th edition), cell cycle chapter in The cell by Bruce Albert (5th edition)

During oocyte–sperm fusion and second polar body expulsion, the cytoplasmic contents of the sperm cell membrane (now fused with the oocyte membrane) pass into the oocyte cytoplasm. Between 4 and 7h after fusion, the two sets of haploid chromosomes each become surrounded by distinct mem- branes and are now known as pronuclei (see Fig. d). The male is usually the larger of the two. Both pronuclei contain several nucleoli. During the next few hours, each pronucleus gradually moves from its subcortical position to a more central and adjacent cytoplasmic position. During this period, the haploid chromosomes synthesize DNA in preparation for the first mitotic division, which occursabout 18–24h after gamete fusion. The pronuclear membranes around the reduplicated sets of parental chromo- somes break down (see Fig. e), the mitotic metaphase spindle forms and the chromosomes assume their positions at its equator. The final phase of fertilization has been achieved: syngamy (or coming together of the gametic chromosomes) has occurred. Immediately the first mitotic anaphase and telophase are completed, the cleavage furrow forms, and the one-cell zygote becomes a two-cell conceptus.

Polar bodies will usually undergo apoptosis in about 17 to 24 hours after the egg forms (the final stages of telophase II (cytokinesis)) because they have relatively little cytoplasm and shunted organelle development (Schmerler & Wessel, 2011).

A secondary oocyte contains n/2C genome and a sperm fuses with a cell with n/C genome (matured ovum). Therefore a secondary oocyte must divide and eject a polar body and that happens due to fertilisation.
so the answer is after fertilisation and before entry of sperm.

Hi Shoaib. Welcome to [biology.se]. Can you please add a reference to support your answer? Good references include books, peer-reviewed articles and verified websites of academic/scientific organizations.

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Detailed mechanism of the cause of diabetes mellitus type 1?
I have read in some texts that diabetes mellitus type 1 is caused by degeneration of beta cells due to our body's own immune reaction.Is it true? Can you explain further how are such types of immune reactions are induced? And are there any other causative factors known?

It can be true of diabetes mellitus type I

Diabetes mellitus is divided into four  type 1, type 2, gestational diabetes, and specific type of diabetes. Type 1 diabetes is commonly called as Juvenile diabetes or Brittle diabetes.
It is also called as "Insulin-dependent diabetes mellitus (IDDM)". For our bad-luck the causes of Type 1 diabetes remains obscure, and scientists believes its mostly related to genetics and other environmental factors like mutations or virus attacks. I found some articles that may help.

But it
  is believed that genetic and environmental factors (possibly viruses)
  may be involved. The aetiology ('cause') of type 1 diabetes is
  unknown, but a good deal is known about its pathogenesis (the way in
  which it develops). As with other complex diseases, the outcome is
  determined by the interplay of multiple genes and (most likely)
  multiple environmental determinants, together with an element of
  happenstance. The risk of developing diabetes is strongly influenced
  by genes affecting immune function, particularly the HLA system,
  but other factors are involved. The best evidence for this comes from
  the study of identical twins: if one twin develops diabetes in
  childhood, the other (who has identical genes) has no more than a one
  in three chance of developing the disease. Prospective studies in
  human populations reveal that circulating auto antibodies directed
  against the islets typically appear in the first 5 years of life, and
  may be present for many years (sometimes 20 years or more) before the
  disease develops. A similar latent period is seen with coeliac
  disease, and implies that some sort of regulatory balance has been
  achieved within the immune system, and subsequently lost. This opens
  the door to the possibility of 're-education' of the immune system by
  various forms of immune intervention.
  Reference
The pathogenesis of Diabetes mellitus type 1 shows a strong tendency towards genetic related factors,

Reference


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What mechanisms exist for the excision of specific sequences from DNA?
I already know about recombinases (specifically excisionases), but was wondering if there were other mechanisms present.

Welcome to Biology S.E.! If you need additional assistance, please visit The Help Center.

The absolute standard way has to be PCR. http://en.wikipedia.org/wiki/Polymerase_chain_reaction
Design primers for each end of a known sequence, provide DNA containing that sequence, and (hey presto!) amplify the length between the primers.

If you're asking about how sequences are excised in nature, an interesting case is the CRISPR-Cas viral defence system of bacteria, where sequences adjacent to a particular "handle" or "signal" in the viral genome are excised and added to an array in the bacterial genome which acts as a memory for immunity. I don't know how the mechanism works!

What about endonucleases?

I know about the Cas9 mechanism as well.  I guess my question was more oriented towards the "cutting out" of a sequence of DNA and then a religation of the two flanking ends.  Cas9 does the first part, but not the second part, while recombinases do both.

Genome editing techniques like CRISPR-Cas and TALEN use non-specific recombinases coupled to a DNA-recognizing part that can be designed to be specific for any stretch of sequence, as it is constructed out of single zinc-finger 'modules' that each specifically bind a couple of nucleotides (one nucleotide each in the case of TALEN).


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How to set threshold in ImageJ for quantifying relative fluorescence?
I have taken images from two different samples that have uptaken EdU during DNA synthesis (S-phase). The experiment setup is to find which condition had uptaken more EdU. Therefore I am detecting EdU with fluorescent to be able to quantify them in two conditions and compare them. The images are taken under same exposure. However in ImageJ when I want to adjust threshold I am not sure if I need to have the same threshold for both images or they can be different? Any tips are appreciated and let me know if I need to provide more info.
cheers!

Presumably your image is either a blot, or of cells. You're going to use some software to measure the density of the blots or cells - what software? You can use ImageJ if you haven't another way. Either way you need to have the original images in a lossless format for the quantification. I think if you adjust levels and click 'apply', you stand to change pixel values.
I've used an old program called OptiQuant to get numbers, and separately adjusted the images for ease of viewing.

I'm voting to close this question as off-topic because questions regarding software use are off topic on BioSE. I understand the need of bio researchers for protocols, but your question is still off topic

@Raoul you have a good point but image j framework is very specific to biology. I think seeing these sorts of questions here is within scope.

You definitely need to have the same threshold for both images because you want to make comparison between them. Do you have a control condition (the condition which is not supposed to uptake EdU)? if yes, then use it to set your threshold and keep the same threshold for the tests conditions. If not, you can either make a experiment control, or select a region of interest (ROI) in one of your 2 tests where there is no coloration (no uptaking of EdU) and set the threshold in this ROI.
Cheers

You need to normalize both images to the background. This can be done in many softwares including photoshop.
When I was learning this starting to do it with something more simple like SDS page protein bands helped me a lot. The principles are the same you are still subtracting background. Look at this tutorial:
http://m.youtube.com/watch?v=JlR5v-DsTds
However, when analyzing intensity values in fluorescent microscopy the most important parameter is area of your analysis. This needs to be an objectively applied as much as possible, and that can be by increasing the number of replicates whose area you analyze. Your going to look at pixel intensities for many many cells and average those intensities. Using the imagej cell counter plug-in is helpful to see how to determine cell area.


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What percentage of the fitness variance is explained by the 'n'- most important loci?
Introduction
Standard models in population genetics look up at the evolution of few loci which impact fitness. The variance in fitness is determined by the genetic variance and the environmental variance (and the co-variance between environment and genetics). In this question I am interested only about genetic variance and about what percentage of the total (additive or not) genetic variance in fitness do 'n' loci explain.
Question
In general, in natural populations, what percentage of the total genetic variance is explained by the 'n'- most important loci?
Here, by "most important loci" I mean loci which variance explain much of the total genetic variance.
In other words, the subquestions are of the kind:

how much of the fitness variance does the most important locus explain?
How much of the fitness variance do the 3 most important loci explain?
How much of the fitness variance do the 100 most important loci explain?

Of course, the answer depends on the population under consideration. Factors that might influence the answers are for example

species
population size
environment stability
…

Beside this question, I also welcome some insights concerning how different factors are likely to influence the answer.

Do you have at least one example of an empirical study of the type you are looking for ? It may be a helpful starting point for us in finding other ones.

No, unfortunately I don't know any empirical study that investigates my question.

And do you have any study, which measures percentual increase in fitness, regardless of the cause ?

Could you phrase this in terms of just one question?

@Atticus29 Thanks for your comment. I updated my post in order to have one clearly stated question. Does my question makes sense to you?

I think its exceptionally rare for the most important loci to collectively explain more than a small percentage of the total genetic variance, it's a fundamental problem with QTL - looking for something of large effect when by definition we expect most or all effects to be tiny. I'm looking forward to seeing an answer to this one! It's going on my favorites

I don't think there's a great answer to this one, partly because fitness is a tough trait to measure. I think more is known for other traits like height, but even there, if we want accurate estimates of the variance associated with 100 alleles, we're limited to humans at best.

I agree with Daniel. Maybe you should open your question to other polygenic trait. A lot of money is being invested in genomic selection and most of the time the target is yield. here we have hundred of markers with effect lower than 1%.  Fitness seems to be quite integrative and therefore very polygenic and environment dependent. Do you have study showing heritability of this trait? Another factor that could influence your variance is allele frequency. See GWAS model. Are you interested in study doing that on other trait? I may answer in that case!

This should be taken less as a holistic answer than as a case study describing an extreme example of very strong selection in a particular environmental context, yielding a particular natural experiment. I suspect that this question may be very difficult to answer in a general case without more work!!
This answer should not be taken to show any general case or reflect anything about the distribution of variant fitness effects of a relatively stable population.
I hope that posting this very partial and contextual answer might inspire other answers to this very interesting question.
In sticklebacks, armor morphology is mostly controlled by a single large-effect variant locus at the Ectodysplasin (Eda) gene, ~85% of phenotypic variance is associated with this locus. It is known that there is a strong fitness relevance of armoring according to environment, wherein freshwater fish are under selection for low armor (due to metabolic cost), and saltwater fish are under selection for high armor (due to predation pressure).
This pattern is highly repeatable across events of colonization by saltwater fish of new freshwater habitats, wherein populations are swept by the low-armored allele of Eda as soon as they become resident freshwater populations.
Recently, Dolph Schluter and colleagues set out to directly quantify the fitness effects of this variant in a newly colonized population of sticklebacks that was undergoing the microevolutionary shift from high to low armor. In this population, the selection coefficient for the lower-armor allele was extremely large ($s = 0.5$).
Schluter and colleagues mapped QTLs for female reproductive fitness in an F2 cross, unsurprisingly yielding the Eda locus. They detected no other loci, though this should not be taken to mean that there are no other loci, due to power issues. They found that Eda explained 8% of the variation in fitness across their F2 panel.
In summary, in this particular case of very strong selection and quite high fitness variation of the population, one locus explains 8% of the fitness variation in an F2 cross (which is likely not completely representative of the population). No other loci have any detectable fitness effects compared to this.
It would be very interesting to see how this is repeated in other case studies, more stable populations, more polygenic cases, or measured at the whole-population (GWAS) level rather than the F2 intercross case.


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Is there something amounting to "check sums" in genetic code?
Humans use checksums for many different applications in informational processes.
Genetic code is used as a "program" to synthesize proteins, so it could (I'm a layman when it comes to biology!) make sense that its integrity is protected in some way. And since there are just so many cells in a human body a few "retries" could be attempted when encountering bad strands in one source during DNA replication or protein biosynthesis.
Because minute mutations can have a big effect, I was wondering if there is any mechanism that amounts to check sums in genetic code? And if (no) such thing has been discovered as of yet, is there any theory as to why (not)?

I would suggest reading more about error correction in DNA replication, homology-directed repair (https://en.wikipedia.org/wiki/Homology_directed_repair), polymerase proof-reading (https://en.wikipedia.org/wiki/Proofreading_(biology)#:~:text=In%20bacteria%2C%20all%20three%20DNA,and%20excises%20the%20mismatched%20base.), translational proofreading (https://www.pnas.org/content/113/48/13744). I doubt that there is any mechanism that amounts to checksums. I think that there are many cases in which an error-checking/correction procedure has something kind of like checksums.

You should also consider the balance between costs and benefits from such a system. Would evolution be possible with such a system? Biological check sums could only be maintained if preventing all change is beneficial over evolutionary timescales ...

@tyersome yeah, actually it should be. Because if the same "check" fails on the same segment of RNA/DNA the "error correction" could give up.

@MaximilianPress thanks for those links. It'll take some time for me to read through all of that. Feel free to write up an answer around those. Again, as a layman I know too little so perhaps my analogy was "off" and so even if these mechanisms may strictly not amount to being check sums, these links appear to be in line with my question (from my perspective).


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Can I use grayscale images when working with ImageJ?
I am using ImageJ to analyze Western Blots. I have scanned films in as grayscale images because this is how we did it in my old lab. People in my current lab are not satisfied with that explanation and think I should consider using color images. I've been searching for protocols but they all seem to address how to use the program once you have some films scanned.
Can anyone help me figure out what considerations go into choosing how I scan my films?

You are using film, so the resulting image is black-white anyway, right? ImageJ can of course also deal with grayscale images.

I've never used films in imageJ, but I have done fluorescent microscopy images, which come as black and white images, 1 image per channel. Then I have to go and set each image to a particular color channel, red, green, blue, etc, to create the final colored image. I don't know how to get colored images of western blots since most gel imaging cameras I've used have a black and white camera with multiple filters, creating a situation similar to the fluorescent microscopy images I've worked with. Of course I have no clue how film and scanners would work with this.

There is no evidence that one is better than the other, most likely because it differs from case to case. Neither you, nor your critics, are right. There is a tiny bit of science in a paper on digitizing blots, generalizing from blots of a specific protein (PMID: 19517440), and they use grayscale for no given reason. Come to think, that is the best paper in the field of immunoblot quantification., and it still lacks evidence.
Immunoblot is semiquantitative, meaning it may sort and order bands (and protein amounts), but it fails often at estimating differences and ratios, and may even fail to see differences. Just try your best to find a difference, in the knowledge that if there is no difference in protein amounts, any fiddling with contrast won't create a difference in bands quantitation.
There is almost no difference between color and black-and-white digitized images of an immunoblot. The parts of the blot that are black will still appear in the computer as White = 0, even though a tri-color image file will detail it to Red = 0, Green = 0, Blue = 0. The parts that are nearly black will still be very close to zero.
The only thing that changes a lot between RGB and color is the background.  The background may change, for example, from White = 200, to Red = 190, Green = 190, Blue = 220. There is one consequence of such switching between values for background. (These changes may be induced by switching between grayscale and RGB, but also by altering exposure time etc.) When you use a method where the background gets too close to the blots, the "amplitude" of the blots, the height of the peaks in ImageJ, will be reduced. This loss of contrast should wash out some of the differences between blot bands and lessen support for differences between bands (i.e., for the alternative hypothesis), making you miss a genuine protein difference.
Again, if your blot bands are different enough so that your percent increase / decrease is huge, and your p value is small, you are all set, regardless of the method you chose. Ask your critics to explain your observed differences other than by differences in protein. But if your quantification fails the p test, I think it will be a honest effort, to change the color from grayscale to RGB, or the other way around, just in case your first choice had been the one that dampens contrast.


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Does the human abdominal cavity use pressure to maintain posture?
Several of my PT friends have referenced a physical therapist p who has studied breathing named Mary Massery. In her articles, she has referenced the idea of "intra-abdominal pressure"
http://www.masserypt.com/images/pdfs/Massery.%20Seating%20Symposium.%20Vancouver%202010.pdf
See page 2
If I am understanding her correctly, she is basically saying that

an unopened soda can is sealed and hard because of the pressure inside the canister
the human trunk tries to support itself upright. In this sense it is rigid. Therefore, it too must be using an internal pressure to create the rigidify necessary for uprightness. This is what she calls "intra-abdominal pressure."

My Question
Given what is known about the mechanics of human breathing, do the pressures of the abdominal cavity actually behave this way? Does the abdominal cavity rigidity itself using some sort of pressure? If so, how does this pressure mechanism relate to the mechanisms used during respiration?
If I am understanding her model correctly, I am extremely skeptical. A soda can is really not similar at all physically to the abdominal cavity.

Given our chat, I am confused whether this question is on posture (ref. question title) or on respiration (ref. body question). What exactly is your question?

I was previously trying to understand respiration in an attempt to understand how pressure is utilized in the body during breathing. My logic was if I can better understand how pressure is utilized during inhale, I would have enough info to answer this postural question myself. Nathan's answer wasn't sufficient. It didn't actually address the levels of pressure in the abdominal cavity itself and how that works with respiration. My ultimate goal was understanding this issue. But I got the sense the respiration approach seemed to not be specific enough, so I am presenting a different viewpoint

@AliceD Massery's claim is that posture is dependent on respiration in a sense. She seems to be making some claim about how pressure in the abdomen affects posture. At least, I think that is what she is saying.

Great, thanks for explaining. I took a quick look at the cited abstract and it seems that the author is simply saying that bad posture impairs breathing, but I just took a quick glance.

Haha I would argue my answer was sufficient to the question, which had no words like "intra-abdominal pressure" or even posture in it.  Hope you find what you're looking for, though intuitively a meaningful relationship between the two sounds bogus to me.

I found this review which can help to clarify this notion of intra-abdominal pressure : Intensive Care Med. 2009 Jun;35(6):969-76.
What is normal intra-abdominal pressure and how is it affected by positioning, body mass and positive end-expiratory pressure?
De Keulenaer BL1, De Waele JJ, Powell B, Malbrain ML.
The authors mention that there is indeed a positive pressure in the normal subject. This IAP is contributed by gravity, uniform compression (abdominal contraction, diaphragmatic contraction, mechanical ventilation, rib cage excursions) and shear deformation, this last one depending on the intrinsic stabilty of the tissue.
The authors conclude that "the abdomen behaves as a hydraulic system with normal IAP of about 5–7 mmHg..". Kind of a can of soda, without the bubbles...
Pathologies affecting this pressure are named "abdominal compartment syndrome) and result from multiple etiologies (obesity, trauma...,).

This addresses the IAP issue, but not the actual question about posture.

@kmm. Right, but I would say that this amount of pressure is not enough by itself to maintain a rigid posture. As a comparison a tyre normally filled at 2 bars is at 1500 mm Hg.


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How many ancestors' DNA do we have per generation?
DNA can be recombined and it's pretty random which ancestor will donate how much DNA other than your parents which is an almost perfect 50/50 split. For example, my family have had DNA tests done and I have significantly more DNA in common with my maternal grandfather than my maternal grandmother (something like a 60/40 split). When you go back a certain number of generations you will find that some ancestors no longer donate any DNA to you. For instance I have ancestors from Cornwall but no detectable Cornish DNA. I imagine that this number will asymptote to a particular value. Each generation going back will double the potential number of remaining donors, but probably half of them will be eliminated from consideration.
So, potentially, if you go back 10 generations you will have 1024 ancestors but maybe only have DNA from 100 of them. Maybe 11 generations gives 110 ancestors, 12 gives 113, etc. and 125 is the limit (on average).
Is there a calculation or some research for the number of ancestors per generation you have identifiable DNA in common with?

Out of curiosity, since DNA is such a young science - what proportion of the Cornish were tested to give a baseline of what constitutes Cornishness? How far back in time/generations? We'd also need to qualify what the percentages mean in terms of base-pairs, or is it some sort of selective sample of key sequences that was being tested for rather than the whole genome being sequenced?

@JiminyCricket not many are really needed. It's possible to identify Cornwall and Devon specific clusters using ~70 samples from each as long as their grandparents are local source.

@CJ this should at least give you a clue about the answer https://gcbias.org/2017/12/19/1628/

https://en.wikipedia.org/wiki/Coalescent_theory

A paper just came out from Elizabeth Thompson that I think answers this about as well as it's going to get answered. Here is the pertinent section of the abstract that may give you an intuition for the answer:

Our ancestors are many and, in an unbounded population, increase exponentially in number. Our genetic ancestors are few, bounded by the number of ancestral genome segments which increases linearly over past generations. First we show that the major loss of potential ancestral lineages is at 8-11 generations, and that thereafter the number of genetic ancestors increases approximately linearly, but does not approach the upper bound.

It's a long paper with a lot of math, but Figure 21 is instructive:
It shows the simulated number of (genetic) ancestors for ideal panmictic stable populations of different effective sizes (values of $M$). So a crucial question is what the size of the population some people are drawn from is. It shows the number to increase somewhat over generations, but at a rate much lower than the maximum possible.

I have no idea how good the following population size estimates are, but some estimates of effective population sizes of different human populations are given in this paper, ranging from a few hundred to a few thousand. (Note that effective population size is much less than census population size!!!) A slightly older paper finds similar or slightly higher values.
So if we say that you're in a population of ~2000 people and you go back 10 generations as you say. Eyeballing, it looks like you might have on the order of 200-300 coalescent ancestors, compared to your 1024 maximum possible. If you have a smaller population it will obviously be lower, if higher, it will clearly be higher. However, there is a fundamental limit to how many genetic ancestors you can have that is much lower than potential ancestors, based on the extinction proportion of the population.
I'd highly recommend reading the paper in more detail.


text:
MTT assay data pre-processing
I was handed MTT assay data, consisting of drug doses and raw OD scores. The drug treatments were performed three separate times, each followed by MTT assay.
I applied some non-linear mixed-level dose-response modeling (log-logistic model) to the data and generated dose-response curves, ED50, etc.
I got the feedback that I first needed to subtract mean blank values of each plate from each OD on a plate, then divide the blank-subtracted values by the mean blank-subtracted value for dose = 0, again on each plate. THEN the PI wanted me to "propagate error" for the modeling.
What is the function of the division-by-zero-dose mean OD? Will that suppress plate-to-plate variation, which  means any aggregate model will be less trustworthy? I was told that all that pre-processing was the standard procedure "in the field". Is this the case? If so, why is it "standard procedure"?
If one assigns random effects to each plate, one can account for plate-to-plate variation without suppressing it, after all.

I’m not sure the poster is expecting an answer to this question, so why it has been edited escapes me. He would have been well advised to define MTT, as “mean transit time” seems hardly appropriate, but it’s too late now, I imagine.


text:
Book about RNA structure
I am looking for book recommendations about the structure of RNA molecules (in particular, functional non-coding RNAs, such as ribosomal RNA, riboswitches, rybozymes, etc.)
I really liked "Introduction to Protein Structure" by Carl Branden and John Tooze. Is there some book out there doing for RNA what Branden & Tooze did for proteins?

Have you tried yet to find anything in particular? For example what does a book have that a review paper like this doesn't?

@MaximilianPress That's not talking much about RNA structure? No mention of riboswitches, for instance. Seems the emphasis is on coding RNA.

That article is entitled "structure and function of nucleic acids"- it seems that you are not actually looking for a general purpose RNA structure reference, but rather one that is specifically concerned with catalytic RNA. You might consider making that clearer, because most people will jump right to backbone structure and mRNAs. have you done any research on your own already? If you have then it might be helpful to see it and to understand why it isn't what you want.

@MaximilianPress In my question I mention specifically non-coding RNAs (so, not mRNAs). Some examples are catalytic RNAs like rybozymes, but also riboswitches (which are not catalytic), ribosomal, and others. I have read mostly about riboswitches, and more general things like https://www.cambridge.org/core/journals/rna/article/abs/geometric-nomenclature-and-classification-of-rna-base-pairs/0D16AEB8C228306F9003E43276B91AAC (or anything by E. Westhof). Does that give a better idea?


text:
Do humans have enough biological differences to be grouped into races or subspecies?
After my online research on the subject, I learnt that, biologically speaking, many scientists believe that there is no such thing as a race. Homo sapiens as a species is only 200,000 years old, which has not allowed for any significant genetic diversification yet, and our DNA is 99.99% similar. I've read statements that there can be more genetic variation inside a racial group than between different racial groups, meaning that, for example, two individuals from the same "race" can have less in common with each other than with an individual from another "race".
Wikipedia on Race (human classification) quote:

Scientists consider biological essentialism obsolete, and generally discourage racial explanations for collective differentiation in both physical and behavioral traits

Q1: If Homo sapiens has no races (according to biologists), why are we so different morphologically? (hair/eyes/skin colour and even athletic performance seem to differ between human populations)
Q2: Is it common for other species too, when genetically close populations have very different morphological traits? Are there any other mammal or animal species that exhibit biological diversity comparable to human diversity, and how do taxonomists treat these species? (excluding intentionally bred domestic species to keep the comparison fair)

The question has been paraphrased to emphasize that it is the biological debate that is in question, not the sociopolitical. I.e., why is there no consensus in evidence and opinions of scientists?

Why did you remove "to the point that we cannot tell an individual of one racial background from another based on a DNA sample" from the question? This makes the first sentence in the answer obsolete.

You have to note that taxonomy is artificial

Here a recent paper that mixes philosophy and population genetics that is probably of interest. I haven't read it though.

See also Does it make sense to classify all humans in a single species?

Some random googling gives this article on the topic (more searching might give other articles with different conclusions; I haven't made any comprehensive effort) which finds that ...human races/continental groups or clusters have no natural meaning or objective biological reality.

Firstly, it's not true that you can't tell racial background from DNA. You most certainly can; it's quite possible to give fairly accurate phenotypic reconstruction of the features we choose as racial markers from DNA samples alone and also possible to identify real geographic ancestral populations from suitable markers.
The reason that human races aren't useful is that they're actually only looking at a couple of phenotypic markers and (a) these phenotypes don't map well to underlying genetics and (b) don't usefully model the underlying populations. The big thing that racial typing is based on is skin colour, but skin colour is controlled by only a small number of alleles. On the basis of skin colour you'd think the big division in human diversity is (and I simplify) between white Europeans and black Africans. However, there is vastly more genetic diversity within Africa than there is anywhere else. Two randomly chosen Africans will be, on average, more diverse from each other than two randomly chosen Europeans. What's more Europeans are no more genetically distinct overall from a randomly chosen African than two randomly chosen Africans are from each other.
This makes perfectly decent sense if you consider the deep roots of diversity within Africa (where humans originally evolved) to the more recent separation of Europeans from an African sub-population.
It's also worth noting that the phenotypic markers of race don't actually tell you much about underlying heredity; for example there's a famous photo of twin daughters one of whom is completely fair skinned, the other of whom is completely dark skinned; yet these two are sisters. This is, of course, an extreme example but it should tell you something about the usefulness of skin colour as a real genetic marker.

Yahoo answers say you can't tell race from DNA... that's why I mentioned it. I also never heard this in crime investigations or detective stories... are you sure we can? Just double-checking, by no means I imply that my sources are credible.
Regarding skin colour, we can also consider that the skin colour of a Caucasian can vary from pale-white to red to dark-brown at different levels of UV exposure. These changes are only in the phenotype, not in the genotype.
What about athletic performance though? It's something more than just skin tinge. It must be related to organ systems, muscles, etc.

It depends what you mean by race; because race isn't actually meaningful you obviously can't reconstruct it. However, given a DNA sample it is possible to make a good approximation of the appearance of the person the sample is from. I don't think such a reconstruction would be reliable enough for law enforcement purposes, but it's pretty good none-the-less.

@Herman Suppose that in some sport it is an advantage to be very tall. Then because all genetic variation of humans is in Africa, you would expect the tallest people of the world to be in Africa. But you would also expect the smallest people in the world to be an African people. Similarly, in Africa you would find those who can sprint fastest. But you would also find in Africa those which are the slowest runners. So expect all variation to be on that continent. Also remember that those Africans who were deported to the Americas as slaves, all came from a small area on the west coast of Africa.

does Europeans are no more genetically distinct overall from a randomly chosen African than two randomly chosen Europeans are from each other ?

@Qbik, yes, I believe it is, and I mentioned this information in the question too. I suggest you go to this part of Wikipeida's article on Fixation Index. There are also two links there to original studies, if you won't to go even further.

@Jack Aidley, how do "deep roots" of African populations and "more recent separation of Europeans" explain higher genetic diversity in Africa? Sorry, it doesn't make "perfectly decent sense" to me. Europeans inherited these deep roots too when separated, no?
From my ecology background I know that there are theories that claim that evolution occurs faster in the tropics, but I never thought about it in the context of human populations. That could explain your point, but I don't think that's what you meant.

@Jack Aidley, as to your first paragraph, have a look at this question. If you learn something new and change your opinion, you might want to edit your answer a little.

@Herman, from the answer to the question you link "So to sum up, DNA analysis can tell the gender, skin color, and eye color of the suspect, but very little about height and weight, and virtually nothing about age."

@Herman: Evolution follows a branching, hierarchical structure (broadly, it's more complicated than that) and Europeans group within the various African populations, i.e., they're essentially a subpopulation of a particular African population.

@JackAidley, do you mean the founder effect? A subset of the original African population that founded European nations did not represent the whole genetic pool of the original African population, is it right?

@Herman: No, although that can also be a factor. Have a look at this image - http://bit.ly/1iHOMss - and note how there is no clade that includes both Africans but not the Europeans. This is because the European population is a subpopulation of the African population. The two African populations shown are as different from each other as the European population can be from the first African population. In reality, there are many more distinct African populations than shown here.

let us continue this discussion in chat

I'm not sure skin color is a good example of characteristic that is used to classify people into race. In an ordinary life yes, race mostly equals skin color, but it seems that 20th century racial scientists relied more on skull measurements and facial features.

Well, that's just it, we don't actually have much phenotypic variation. For example, compare this:

to this:

or this:

Or this:

to this:

This is phenotypic variation:

So, as I hope is clear from the images above, phenotypic variation among humans is tiny compared to other species. We just notice small differences much more because, well, it's us so little differences are much more noticeable.

This ridiculously obvious illustration somehow put the issue in a totally different perspective for me. Quite an eye-opener. I think this is a brilliant answer, thank you for the effort.

Hmm... I'm not sure how useful comparing natural variation (human phenotypes) to artificial variation (dogs, cats and pigs) really is. Are you humans really less phenotypically variable than wild animal species? I guess ring species might make a good comparison?

@JackAidley birds of paradise are "natural" as far as that goes. In any case, the point is moot, whether the observed variation has been affected by humans or not, it is clear that the human species shows relatively little variation compared to what can be seen in others.

@terdon: The bird of paradise are not a species, as you note in your answer and I don't think it's clear - at all - that humans show relatively little phenotypic variation. I would say that humans are probably on the high side (likely due to the huge range that humans occupy).

@JackAidley the statement is one I remember from university. Anecdotal evidence like that presented in my answer seems to confirm it and I was tought it years ago. I'll see if I can find a proper reference but it certainly looks to me like we have far far less variation than other species.

Dogs are deliberately hybridized.

I also think it is misleading to compare human phenotypical variation and phenotypical variation that is the outcome of artificial breeding. To make this argument you would have to place human phenotypic variation within the range of phenotypic variation from a large number of "natural/wild" species. And comparing variation in birds of paradise (family Paradisaeidae) would only be valid if compared to Hominidae, i.e. including chimps, orangutans, extinct Hominini etc (still ignoring that taxonomic families cannot really be considered equal).

"excluding intentionally bred species to keep the comparison fair"

@Rodrigo yes, that was added after I posted this answer.

Maybe it's just me, but I'm having a hard time estimating any objective scalar value of the variation here. Nevertheless, it seems like humans still are on the top of the league regarding phenotypic variation. Look at the western jackdaw for example, four different subspecies identified mostly on the base of some slight colouring variations.

@Alex I'm normally a stickler for quantification, but I think the point is made quite well qualitatively. Your rebuttal is neat -- the jackdaw has similar variation to us. But that itself is justification for ignoring the subspecies divisions in jackdaws as much as imposing subspecies labels in humans! @bshane offered a great summary of subspecies here that demonstrates how arbitrary a term "subspecies" is.

All pictures exhibit some degree of phenotypic variation, and if you see all these people in person and close up, you'll notice yet more variation than with isolated faces. Even the smell is different (but how have we lost our smell senses recently!). So your answer is considered good because you used beautiful pictures, though your reason is completely subjective.

@Rodrigo of course there's some phenotypic variation. And of course you, as a human whose eyes and entire social structure are centered around the necessity of differentiating between the different members of your tribe, would see variation. That, however, does not mean that humans exhibit a lot of phenotypic variation. That said, no, this isn't a very good answer and yes, of course you'd need some hard, quantitative data to be able to answer correctly.

You say: What is race? "a lot of phenotypic variation". Seeing 29 upvotes in this answer reminds me of the fact that Homo spp are about 80% vision, but much less reason.

@Rodrigo what? I never said that race is a lot pf phenotypic variation. This answer is just pointing out that humans have far less phenotypic variation than other species. In any case, I'd appreciate it if you'd stop now. You first commented on this question in 2014, so just downvote it and walk away.

By the way, races of dog are really races? To me they seem only a few genetic loci that can control a limited range of morphological and behavioral traits. They're probably not the kind of "general genetic diversity" that some have been proposing for us humans.

Your example cannot show how less phenotypic variation, actually. The pathways between genes and morphology are far from linear. And we should not walk away from questions that bother us, should we?

@Rodrigo this isn't a discussion forum. If you disagree with an answer, you can downvote and you can leave a comment explaining, if you like. But engaging in long discussions in the comments is against the rules. I also have no interest in defending this answer from your accusations given that I dont' make the claims you think I'm making. So if you insist on badgering me, at least take it to [chat] where it belongs. Ideally, just downvote, express your disagreement and leave me alone though.

Sorry, but I think this is of relevance to anybody following this page. If we need to go to chat, the message appears automatically, like "Please avoid extended discussions in comments. Would you like to automatically move this discussion to chat?"

Let us continue this discussion in chat.

Human Fst is comparable to cats' Fst: https://emilkirkegaard.dk/en/?p=7753

I decided to summarize a competing hypothesis to make our answers more balanced. I also tried to address the question about the degree of human morphological diversity compared to other animals.

According to Woodley (2010), it is plausible that H. sapiens does not belong to one species and subspecies (i.e. is polytypic). Some of the data he uses to support this hypothesis could be useful for answering our question. He claims that H. sapiens, which is often considered monotypic, posses higher levels of morphological diversity, genetic heterozygosity and differentiation than many animal species which are considered polytypic.
Woodley cites a study by Sarich and Miele, who claimed that morphological differences between humans, on average, are equal to the differences among species within other mammalian genera (excluding species bred for domestic purposes), and are typically more strongly marked than in other animals.
However, morphological differences are known to be caused by little genetic differences too, like in the case of domestic dogs, which are still considered to be one species. Therefore, Woodley presented further evidence that looked on these inconsistencies in classification using allele frequencies and genetic diversity.
He presented data from a wide range of studies, which compares genetic diversity of various mammalian species based on heterozygosity (H), which is a common indicator for genetic diversity, and describes whether both alleles are the same or not on a studied locus. According to this data (which you can find in the linked paper):

Chimpanzees exhibited H of 0.63-0.73, which is very similar to H found in humans (0.588 - 0.807), however, chimpanzees are divided into four subspecies.
Some species like the grey wolf even exhibited a lower H (corresponding to lower genetic diversity) than humans (0.528 vs 0.588 - 0.807), while the grey wolf has been divided into as many as 37 subspecies.

This data suggests that humans are more diverse both morphologically and genetically than some of the other mammalian species that have been divided into subspecies.
References:
Woodley, M. A. (2010). Is Homo sapiens polytypic? Human taxonomic diversity and its implications, Medical Hypotheses, 74, 195-201. doi:10.1016/j.mehy.2009.07.046 (full-text PDF)

It's a political question. They think (or pretend?) they're fighting racism denying human races. At the same time, a country with more species and subspecies receive more funds for conservational programs (see my answer).

How would that translate into multiple species? From my uninformed perspective it looks like a species with a high but uniform heterozygosity is possible, so that there would be absolutely no clear cluster or even that any attempt to build clusters based on this would lead to weird effects such as people ending up into a different species than their siblings.

It seems to me that many answers to this question suffer from the nasty habit of "political correctness". As a zoologist, I never heard of somebody sequencing the whole DNA of any species to decide when to use or not the term "race". If a group of animals comes from a side of a river, and the other comes from the other side, and they have one or a few distinctive features (color of chest pelage, tuffs of hair in the sides of head, etc), that's enough to call them both different races (or even subspecies). Of course some geographical isolation has taken place, although it hasn't been long enough to divide the two (or more) populations into full species. The same logic should be used to humans, right? Maybe some folks believe that, pretending there are no human races, then the question of racism is "solved"? Bad logic, to me.
Look at http://www.worldbirdnames.org: they cite 10,518 extant species of birds and 20,976 subspecies. About 2 subspecies per species. How do they do that? (No DNA for most of them.) Subspecies/races are usually from different regions (like human races), their vocalizations are usually different (like human races) and their colors sometimes vary (not as much as in human races). My point is: there is NO SCIENTIFIC REASON to say there are no human races, if we're using zoological reasoning. (Unless we are not animals anymore!)
For mammals, http://www.catalogueoflife.org/col/browse/classification/kingdom/Animalia/phylum/Chordata/class/Mammalia/match/1 cite: 4,843 species, 2,998 infraspecific taxa. Again, if someone show me they did complex DNA analysis for most of those infraspecific taxa, and those analysis showed that variation inside races is smaller than between races, THEN I will be forced to agree with them.

Maybe, but the "why?" question is beyond our scope here, I asked the "is it?" question, which is purely biological. If you improved your answer by expanding on your experience as a zoologist when it comes to defining subspecies and removed the "why?" question of your own -- I, personally, would like your answer much more :-)

I just inverted your question: "If human populations have several distinct phenotypes, why (they say) there are no human races?" Or, from other point of view, I questioned your first "If" in the title. It's not just a biological question, to me it seems much more a political one. How many biological races have been described? Or subspecies? Take a look at IUCN Redlist, for instance, or Zoological Records in many universities. Do you really think they scanned their DNA in depth? There's no biological reason for a different approach on human beings. As I said, it's just politics.

I think you make a fair point... I might paraphrase my question. Why paraphrasing? Although intuitively I agree with you that it might have something to do with politics, it's not really something that I wanted to discuss, and it's probably not even allowed to be discussed on Biology SE. If we do, someone will ask: "Well, how do you know that it's all just politics", and here we go, it becomes a debate with no science behind it, just opinions.

Rodrigo, ok, most of subspecies and "races" in zoology don't have DNA analyzed but are still considered to be separate. However, in the case of humans it is analyzed, so it would make sense to apply this information if it indicates that humans cannot be grouped in races, wouldn't it? (whether that's what our DNA indicates or not is another, not mentioned by you, question)

What is the definition of race? Is it the same as subspecies or semispecies? http://www.ucl.ac.uk/taxome/jim/Sp/Sub-semi.pdf By this article, what human DNA says is that human races are not human semispecies nor subspecies. According to Mayr definition (http://en.wikipedia.org/wiki/Race_%28biology%29), "races" is a concept that requires less genetic divergence than subspecies.

@Rodrigo However, generally, I would argue that when classifying non-human animals into races we either know or imply a very low level of gene flow between races/subspecies. We know that this is not the case for humans.

While I see your point about there being races, I very much doubt you'll be able to support the use of the term as it tends to be used today. With the criteria you state, the Scots and the English would be different races, for example. If we take variations in vocalizations and geography as indications of race, each country will represent a race of its own. So while your argument does indeed support the existence of human races, it does not support the idea that those races are defined by color alone.

Well, all this should be properly studied. I just don't agree with the "findings" that "there are no human races".

Couldn't you also phrase this as "genetic diversity of most animal species is probably overstated, because morphological differences which aren't sufficient to establish the existence of subspecies in humans are used to claim the existence of subspecies in other animals" -- or in other words "look at how there aren't human races -- therefore there probably aren't  as many animal races in most cases where we assume that there are animal races". I don't understand how your answer shows that there are human races, in other words. It just seems to show that zoological reasoning is bad.

@Will Actually I'm asking: What is the present definition of race? Is it the same definition we used 30 years ago?

Oh OK that makes sense

You claimed that vocalizations & hair/skin coloration are evidence of substantial genetic differences between races; but this is flawed. Fair-skinned individuals, if exposed to UV radiation develop darker skin. While this isn't permanent for them, the fact that the change can happen within an individual's lifetime indicates that it is not a dramatic difference in genetic / evolutionary terms.
Human vocalization is dependent on the environment. If you adopted an infant of another race and raised it, it would speak in your language & accent; not that of its biological parents.

@Kent.Green people who lived in cold climates for millennia developed a white skin, and those who lived in warm climates for millennia developed a dark skin. Both are well adapted to their environments. That's the biological definition of race, not the amount of DNA involved in the adaptation.

That's exactly my point, while superficially races appear very different; the amount of DNA involved in the distinction is relatively small, which is the reason that "race" does not make sense as a classification on the level of species or subspecies. Moreover, you still haven't addressed the differences in "vocalizations" which are even more contingent on environmental conditions than skin pigmentation.

@Kent.Green Races are indeed less "discrete" entities than subspecies. I just want to know how much DNA divergence people want to use as part of their definition, since I've not seen such "objective" definition anywhere, just a systematic denial of the existence of human races (motivated by some kind of "political correctness" it seems). About human vocalization, you're right, it's not the best trait, but it does show that human populations remained isolated for long periods. That's the general definition of "geographic races" used in zoology, or I've been learning it wrong for so many years?

Here is a source that might be what you're looking for: "The biological definition of race is a geographically isolated breeding population that shares certain characteristics in higher frequencies than other populations of that species, but has not become reproductively isolated from other populations of the same species."

http://www.biologyreference.com/Ar-Bi/Biology-of-Race.html#ixzz4dVXjcmSb

Not objective at all. Skin color, hair type, nose format... those already are "certain characteristics". By this definition there are human races.

This is a bad answer, opinion-based and apparently driven by some kind of political views, and proposes an incorrect definition of 'race' or 'subspecies. People in the past didn't use genetics to identify subspecies, but they do now, and for good reason. Take a read of this paper to educate yourself.

@user438383 Thanks for the link. Dog races are called dog subspecies?

Bias
When you say phenotype you mostly mean "skin color", "size of the nose", "hair color", "shape of the eyes", "height", and some others. All these traits that we manage to find to explain population structure among humans. But you forget all the rest of the phenotypic diversity. If you would choose 1000 randomly chosen traits (external morphology and other stuff) and make a PCA. Will the main axes explain much of the inter-subpopulation (or inter-racial) diversity? I am not sure about that. One cannot use one subset of the total phenotypic or genetic variance and use it in order to define several species within what was previously thought to be one. It is not because two genes are associated with the same population structure that one can define two different species.
scientific observations vs biased intuitions
You say:

[..] is it reasonable to use a genetic approach to races and claim that biological races do not exist, while it seems to be a poor indicator, when it comes to comparison of phenotypes of human populations.

Similarly, one could say

Bats look like birds. We consider them as being mammals just because that is what scientific observations (genetic data or in-depth observation of the phenotypic variance) says. Should we follow scientific explanations when my personal bias intuition tells me that these observations are poor indicators?

The answer is yes if you want to increase your knowledge and no if you just want to be comforted into what you think you already know.
I have to confess though that I don't know much about phenotypic or morphological variations among humans. And I'd be curious if someone could give some words about that and whether or not much of the phenotypic and morphological variance is explained by what we consider being racial groups. It might be possible that very little of the total phenotypic variance is explained by racial groups but quite a lot of the face morphological variance is explained by racial groups.
Concept of species
For species that can reproduce exclusively with sex, we tend to use the concept of reproduction isolation to define a species and I really don't think that there is a pair of racial groups are sexually incompatible (however you delimit the racial groups). Eventually, there might have some slight inbreeding depression but I am not sure.
You might want to have a look at this answer to understand the semantic difficulties behind the concept of species

I would be very, very surprised to find out that any two racial groups cannot reproduce: not only we are one species, we are also one subspecies, and we share over 99.9% of the same genome. The world would be a totally different place if this was true, from the sociopolitical perspective. It might happen one day though. I hope collectively we'll be much wiser when and if it does happen.

Yes, that would be immensely surprising indeed! But I don't think any study ever reviewed cases of reproduction between all "considered social groups".

On the other hand, it also means that no one has ever noticed any suspicious trends in child mortalities from cross-racial parents to think about such a survey.
I also believe that gentlemen from the Third Reich would be very interested in this question, and they conceivably could do some research, which wasn't published because the results were negative. It's just my guess though, and I'm no specialist in history.

Remi, sorry, I'm not familiar with PCA, and the Wikipedia page is intimidating. Was your first point that we share so much traits in common that the ones that distinguish us from each other are statistically non-significant?

"For species that can reproduce exclusively with sex, we tend to use the concept of reproduction isolation to define species and I really don't think that there is a pair of racial groups are sexually incompatible" But this reproductive isolation is not only due to genetic incapability, but to purely practical geographic isolation as well, right?

But other animal races are only defined genetically? Or is it (or has been for millennia) more a biogeographic concept? Or, for any species where there is no genetic data, we just can't say anything about races?

First you can take a look at this diagram:

You can make a google image search for "Cavalli Sforza" and get a lot of similar diagrams. This diagram is using a concept known as genetic distance by fixation index. This is a way to measure how different different ethnic groups are genetically.
Basically what you do is you compare how many differences there are on average between two humans from the same population and between two humans from two different populations. The same method can be applied to animals. There is no "threshold value" where you can say that two groups of people or animals have become different enough that they can be defined as "different races".
Traits such as skin colour are regulated by a very small handfull of genes so even if we have different skin colours that does not mean that we differ much genetically speaking.
Lions and Leopards can have fertile offspring and live basically in the same habitat in Africa. I do not know if crossbreeding is known to have occured in the wild. Probably a hybrid has lower fitness than the original species.

So, what's your point about human races?

I would say focus on the actual differences instead of the name. Differences as far as Fst, IQ etc. goes. "These are the differences between group A and group B". I like the term "ancestral group", nobody can really deny that they have an ancestry.


text:
background extraction in microscope analysis
I have taken microscope pictures for proteins in HeLa cells, in order to quantify the intensity (immunofluorescence). The proteins are both at the nuclear envelope, and in order to quantify the intensity I draw a line that goes across the whole cell,through the nucleus, and measure the intensity on that line (ImageJ). Which value should I use as background?

The area outside of the cell typically. Adjust contrast until the background black

and what about the cytoplasmic zone? (both proteins are nuclear) also, should I take an average of certain number of values?

It sounds to be in your best interest to set your analysis boundary around the cell but can you post a sample image so we can see your contrast issues

sorry but cannot upload any images. I consulted several people and I have been told to use outside cell as background as well. Thanks!


text:
Why do skinny people live for shorter than the norm even though calorie restriction extends life expectancy?
If I understand correctly, calorie restriction may extend life expectancy slightly (not proven exactly how much for human). But according to the statistics, skinny healthy people have even shorter life expectancy than healthy, slightly obese people. Could you explain why this is not considered as contradictory?
(Reference)

Could you include a link to these statistics?

The original source is written in Japanese, so I cited the following page written in English.
http://phys.org/news/2009-06-japanese-overweight-people-longest.html

Could be cultural differences. Young people die alot due to car deaths.

rate of ageing and age at death are influenced by many things, calorie intake is just one tiny factor.

Interesting point. Note that it is "calorific restriction" in the animal experiments, not fat vs skinny mice. Skinny people don't necessarily eat less than average, and I imagine smoking is a big factor (makes you skinny and sick). I wonder if the original study controlled for this.

"Slightly obese" means that they weight more than a standard reference weight for their height. If these people are more healthy than most this only means that the standard reference weight is wrong.

Well fed people are happier, and happy people live longer?

This is an interesting point you raise, and as the study you linked to states, "the link between physique and life expectancy is not clearly understood," which is certainly true at the moment. The relationship between BMI and lifespan in humans is a very different story to controlled dietary restriction in model organisms.
Dietary restriction is defined as "undernutrition without malnutrition" [1], and by definition model organisms live in controlled environments. In contrast, humans have confounding factors that may reduce weight and health (for instance smoking status, early-life diseases, malnutrition, etc) that are not modelled in these experiments.
In addition, the relationship between BMI and mortality is complicated in older humans, known as the 'obesity paradox'; overweight and obese elderly hospital patients have a lower mortality risk than low-normal weight patients [2]. There are a number of hypotheses regarding this, but the favoured one appears to be that the association is not actually paradoxial, but that higher BMI only appears protective because losing weight is associated with many diseases of ageing, so after accounting for many of these confounding factors (e.g. dementia, cancer, etc) high BMI no longer appears protective.
Therefore the study you found only appears to be contradictory to the dietary restriction experiments; in human populations the situation is much more complicated. Additionally, there is conflicting evidence as to whether dietary restriction even works in primates [3], let alone in humans (the largest effects are observed in worms and drosophila).

Weindruch et al. The retardation of aging in mice by dietary restriction: longevity, cancer, immunity and lifetime energy intake. (1986) J Nutrition; 116(4):641-54
Yamauchi et al. Paradoxical association between body mass index and in-hospital mortality in elderly patients with chronic obstructive pulmonary disease in Japan. (2014) Int J Chron Obstruct Pulmon Dis; 9:1337-46
Maxmen. Calorie restriction falters in the long run. (2012) Nature; 488, 569

I started writing my own answer and realised you hit each of my points better! Again I would point out that (healthy) skinny people don't necessarily eat more. Although we know that they're skinny, did the study in question confirm that they consumed less calories?


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How to remove bad lanes in ImageJ Westernblot analysis
I use ImageJ to do an analysis of a Westernblot Image.
If everything goes as wanted the workflow is fine. But if I do something wrong creating a lane there is no undo for a lane and also no way to remove all lanes that I can find.
How do I get back to my original image or undo a lane creation?
I'm using 1.49e on Mac OS

You question is slightly unclear! do you mean how to crop out a WB lane in an image or how to remove a lane from the middle of an image if it did not produce the results you were looking for?

So you chose a lane by accident which you don't want to include in your analysis?

Yeah I created a lane with the wrong size and I can't find a way to undo the creation to recreate the lane correctly.

ImageJ doesn't have a feature to remove individual lanes. But that shouldn't be a problem. All you have to do is draw the first lane correctly (I'm referring to size). Then press 1. Now, while the selection is still... selected, click inside it, but not on the number (where the cursor becomes hand), and drag it where you want the next lane. And press 2. And so on. Draw all your lanes.
Now, if you misplaced a lane, click the rectangle selection tool, then click on the lane number while the cursor is a hand. It will be selected. If you're having troubles with this, use the shortcuts Ctrl+1 and Ctrl+2 or the menu Analyze - Gels - Select Previous/Next Lane to select between lanes. The cursor turns to normal. Click anywhere inside the lane and drag it on the right place.
If the first lane was bad and you want to remove all lanes, just go to Analyze, Gels and click on Reset.

Hi Cornelius the menu contains only select first and next lane. There is no way to move between lanes. And for me it is also not possible to select lanes with the mouse. But pressing [ctrl/command] [1] removes all lanes but the first and lets me recreate the lanes. That helps a lot.


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What are these root-like structures growing in the upper part of a tree?
In the UK, I saw these root-like structures growing from the upper parts of a tree. I thought they might be parasitic but they're part of the tree itself, and join to the trunk as branches.
What are they?

Do you know what type of tree it is and do you have any better lit photos, it might help to get a full answer.

Likely a duplicate of: https://biology.stackexchange.com/a/77434/16866

In the absence of better photos and a species ID on the tree there are a few options:

Adventitious roots. These are roots produced from parts of the plant apart from the main root system. They are very common in some plants, and some species of trees are well known for doing this. I think Willows, particularly White Willows (Salix alba) will do this naturally when a branch touches the ground, but other species can too. Adventitious roots can also form inside hollows inside the plant where rotting material/soil accumulates.

Witches' broom. This is where a woody plant an abnormal growth, often caused by an infection. I guess you could liken it to a cancer in animals - it's essentially a diseased part of the plant. These typically present as a bundle of quite twisted and dense branches growing from an unusual place on a branch - I think it this is the most likely option here.

A sport. These are also abnormal growths on a plant, but they aren't caused by infection, they are genetic mutations, which result in an abnormal form. If you have a variegated plant (one with multi-coloured leaves, usually streaks of white/cream on green) at home and it produces totally green stems - that's a sport (though often a reversion of a sport in this case as variegation is often produced by sports in the first place and then propagated for the difference), or you might have even seen a normally green plant produce variegation itself. Some sports result in differences in growth habit such as branching patterns.

These aren't roots at all, merely a branch that has fallen and gotten caught. Roots tend to have different textured bark to branches and be less straight, so it is often easy to identify, but I can't tell from this photo.

Very hard to tell from the photo due to the lighting.  Some trees, like the Banyan (https://en.wikipedia.org/wiki/Banyan) grow roots from their branches that run down to the ground and allow the tree to spread out horizontally.


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Nernst equation and equilibrium potential
Solutions A and B are separated by a membrane that is permeable to Ca2+ and impermeable to Cl−.
Solution A contains 10 mM CaCl2 , and solution B
contains 1 mM CaCl2.
Assuming that 2.3 RT/F = 60 mV, Ca2+ will be at electrochemical equilibrium when:
(A) solution A is +60 mV
(B) solution A is +30 mV
(C) solution A is −60 mV
(D) solution A is −30 mV
(E) solution A is +120 mV
(F) solution A is −120 mV
(G) the Ca2+ concentrations of the two solutions are equal
I eliminated A,B and E because of the +ve sign immediately, and G because it doesn't take into account the electrical potential factor.
I also understand the general idea (that Ca2+ ions will cross the membrane but Cl- won't so it will stop when solution A is negative enough for the electrical gradient to be > concentration gradient) but I don't know what to do next.
$ EMF (millivolts) = \pm 61 * log \frac{C_{1}}{C_{2}}$
Using Nernst equation (reproduced from the version in my book), I got that the equilibrium potential is about -60 mV (I did -61log(10/1))
But the book's answer is D which makes me think I might have a huge misunderstanding in the principle itself.

Can you try to format your question to be more readable? As-is it is a complete mess. Show your thinking step-by-step: which numbers actually matter to the answer, what is the equation you are using, etc. And remove the bits about your professor and your university being shut down - yes, that sort of thing is affecting all of us, but it doesn't change the on/offtopicness of questions here.

Thanks for the edits, this is much better looking! One last thing: can you write out the entire Nernst equation, and show where you have substituted numbers for variables? You're very close.

The Nernst equation should be:
$\frac{RT}{zF}\ln\left(\frac{\mathrm{Out}}{\mathrm{In}}\right) = 2.3 \frac{RT}{zF}\log_{10}\left(\frac{\mathrm{Out}}{\mathrm{In}}\right)$
You substituted for 2.3 RT/F (approximately 60 or 61 mV: use 60 because your instructor asked you to), but forgot about z. Calcium is divalent (and positive) so for calcium z=2. Substitute this and you can see how you get your answer.
(Also note the "out/in" which is how you get negative numbers when z is positive and out < in )


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Is there variation of AT/CG ratio along species?
Chargaff's rules say that the number of Adenine of the number of Thymine in a genome are equal (nA=nT) and similarly nC=nG. This makes obvious sense knowing that C binds to G and A to T.
But what about the ratio $\frac{nA+nT}{nC+nG}$?
Is there variation along species of this ratio that is higher than expected by random processes? If yes, what causes this variation?

That ratio is essentially, as WYSIWYG pointed out, called GC-content.  In actuality, GC-content is reported as $(G+C)/(A+C+G+T)$, converted to percent; i.e., what percent of the genome is G or C.
There is vast variation in GC-content, both amongst species and within a given species' own genome.  For example, in humans the first intron and exon are generally more GC-rich than following introns/exons.1  Genes themselves are often found in higher GC areas,2,11 in particular CpG islands are found near a large number of (mammalian) promoters.3
Across species, there can be a big difference.  Yeast and Arabidopsis are both around 35%4,5 whereas Plasmodium falciparum is around 24%;6 Carsonella are even lower, at around 16.5%.14  On the other hand, the plankton Emiliania huxleyi is around 65%7.  We can use these differences to study genomic history.  Bacteria often have genes from all over the place thanks to horizontal gene transfer, and GC-content can be used to differentiate between their own genes and those from horizontal gene transfer;8 a good example is the CRISPR-Cas system,9 even in a virus!10
Here's a list of a few things genomic GC-content is correlated with:15

genome size
whether the bacterium is free-living or not
the environment
aerobiosis
nitrogen utilization

In the lab, high GC-content often means a harder region to work with, as the presence of three instead of two bonds (between A and T) requires more energy to break;12 anything involving primers can be made more annoying, including (especially, to some) sequencing.  There is a theory that high GC-content would be an adaptation to high temperatures, to avoid DNA damage, but that is controversial.13,16,17,18

Yes that ratio varies and is generally referred to as GC-content which is expressed as percentage. Earlier, people used GC-content as one of the identifiers for a group of organisms.
Though there have been quite a few studies on the evolution and variation of GC-content, there is still no clear explanation for why certain organisms have a certain level of GC-content- it exerts no great bias on the protein composition though it is argued that it controls protein expression. Chemical mutability is higher for C->U and A->G because of deamination but this might not be the sole criterion. You may refer to this nice review for details.

Well. i read that review fully, just now. Though it is nice, it doesnt summarize everything. But you may find a lot of analysis on this topic. Plus A doesn't get deaminated to G. It becomes Inosine which can base pair with C and thus can be read as G.

GC-content varies greatly among prokaryots, and it is used as a taxonomic characteristic. It is specially elevated in extremophyles, such as halophiles and thermophyles, and it's thought to be an adaptation to high temperature and other chemical and physical stresses. GC bonds are stronger than AT, so it's supossed to acts as a protection agains denaturalizing agents.


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Receptors for red and far-red light in plants: Shade avoidance
Franklin (2009) describes how plants use the ratio of the red wavelength (660-670nm) over the far-red wavelength (725-735nm) (R:FR) in order to avoid shading.
My question is: which receptor is stimulated by the red and which receptor is stimulated by the far-red?
In his paragraph on Phytochromes (3rd page, right column), K. Franklin seems to say that PhyB is responsible for measuring this ratio but I am not sure.

As far as I know there are 5 receptors for far-red and red light which are the phytochroms(phyA-phyE) Its all about the ratio between red and far-red light.
Each phytochrom has an inactive(PR) and an active(PFr) conformation. phyA is the only phytochrom which is activated by far-red light, so its active state is PR. (Only if the ratio between red and far-red light is low.) The other phytochroms, are activated by red light (high ratio between red and far-red).
An active phytochrom blocks the COP1/SPA complex. This complex is a E3 ubiquitin ligase which ubiquinates transcription factors for the light answer like HY5 or HFR1.
Example:
Under normal light conditions, phyB-phyE is active. They block the COP1/SPA complex so the transcription factors for the light answer are not getting ubiquinated. The plant can get a light phenotyp.
In the case that a plant grows under another plant, it gets less red light because the higher growing plant uses it for its photosynthesis. phyB-phyE become inactive. COP1/SPA can ubiquinate the transcriptions factors. The plant gets an low light phenotyp by trying to grow out of the shadow.
The function of phyA is to produce a light phenotyp if there is a lot of far-red light but almost no red light. Than it is getting activated and blocks the COP1/SPA complex. Under red light phyA is not only inactivated it also gets degraded.
I just found a paper for further reading: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2828699/

So the mechanism seems much simpler than what I expected. The ratio is directly "computed" by the phytochrome and the ratio is not "calculated" from the interaction between the molecular pathways activated by the phytochromes. Thanks a lot. I will clearly have a look to the paper your attached.


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Distribution of fitness in wild populations
If I get out in the wild observe wild populations and measure the distribution of fitness $f(w)$ in a given population. What will I find out? Will I observe a Gaussian distribution, a Poisson distribution, an exponential distribution, ….?
It probably depends on the species under consideration, typically it may depend on whether there is an sexual selection in this species. I welcome any insights!

Long for a comment but consider this to be an extended comment and not an exact answer:
At least for Poisson I can say that the random variable should fit the three Poisson postulates. Poisson RV generally describe discrete events in continuous intervals. A fitness function doesn't seem to be such a type of RV; it is a property of a population rather than an event.
I would also not expect it to be exponentially distributed which would mean that probability is highest for the most fit (or most unfit) individual i.e the more fit are more frequent. I assume that it cannot be decided who is the most fit until selection happens. This may still be the case just after a selection event but not otherwise.
It seems that this function should be Gaussian: assuming that there is little variability between individuals and what exists is because of independent events of mutation, these should converge to Gaussian as per the central limit theorem.
But generally the term that best describes this RV is a performance function. Fitness would always be a conditional RV.
For e.g. I would very roughly define fitness like this:
$f(X) = P(m(X)\ |\ p(X),S)$
where $f(x)$ is the fitness of $X$, $m(X)$ is the survival probability of $X$, $p(X)$ is performance in different tasks and $S$ is selection event.


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What model of epistasis best fit the reality?
In theoretical population genetics, it is very common to have to assume a model of epistatic interaction. The two most common models are the additive model and the multiplicative model.
Additive model
Under the additive model the fitness $w$ of an individual carrying all $n$ mutations of effects $[s_1,s_2,...,s_n]$ is
$$w=1-\sum_{i=1}^n s_i$$
, which becomes $w=1-sn$, for the special case when $s=s_i \forall i \in [1,n] $
Multiplicative model
Under the multiplicative model the fitness $w$ of an individual carrying all $n$ mutations of effects $[s_1,s_2,...,s_n]$ is
$$w=\prod_{i=1}^n (1-s_i)$$
, which becomes $w=(1-s)^n$, for the special case when $s=s_i \forall i \in [1,n]  $
Old observation
In Population genetics: a concise guide, Gillespie reused data from Mukai (1968) to plot the following graph

, where the additive $\left(w=1-sn\right)$ and multiplicative  $\left(w=(1-s)^n \right)$ models correspond to the two lines that poorly fit the data. The line that best fit the data is a quadratic model of synergistic epistasis
$$w=1-sn-an^2$$
In all cases, $s$ and $a$ where estimated from these data. We probably have better data and better studies today.
Question
What model of epistatic interaction would you recommend?

Here are some clarifications if needed
Consider $n$ mutations. The fitness of an individual carrying only the first mutation is $1-s_1$. The fitness of an individual carrying only the second mutation is $1-s_2$, etc... the fitness of an individual carrying the $n^{th}$ mutation is $1-s_n$. What is the fitness of the individual carrying all $n$ mutations? Of course, there is no single answer to this question and it will depend on the epistatic interactions between these loci. However, there is probably a general trend that a theoretician would like to consider in its assumptions.

All models are wrong but some are useful :P

I think that if the genes are actually interacting then they are not independent. If they are not independent, their effects cannot be additive. I have not really studied or worked with the models that you mention above but this is a general sort of rule that additive effects are usually because of independence.

If you're fitting real data, try both; if you're doing a purely theoretical model, use whichever is more mathematically convenient. Note that you haven't defined what you mean by "fitness" here; additive effects on growth rate are multiplicative effects on offspring number.

I don't understand what is unclear about my definition of fitness. Fitness is the expected number of offspring of an individual. The statistic I use here $w$ is the fitness of an individual relative to a hypothetical individual that bear absolutely no deleterious mutations (and I ignore the existence of beneficial mutations). I do not talk about the growth rate of a population and would be happy to assume that the carrying capacity is not influenced by the population mean fitness. Thanks


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Why some viruses can spread with aerosol droplets, but others some cannot
Why can some viruses spread with droplet like influenza virus, but some can not like HIV?
Is it due to their physical shape or the protein of their wrapper? Is there any formalized logic decide this before test the virus in lab?
Thanks in advance!

Welcome to Biology.SE! Some of which virus? There are 'a lot' of virsuses...

This is a very general question. I popup this idea during read the book <>

I would recommend first looking at some of the wikipedia pages for some viruses and doing some preliminary research to make your question more precise. This is a very broad question and it is hard to answer unless you can narrow it.

Thank you very much for the help. @MaximilianPress I will check the wikipedia later too. Actually I'm a programmer, love to read books. It's hard for me to start without basic virus knowledges. I will try to ask the question more precisely in the next time. :)

The question you are asking, if I have it right, is about what is called the "mode of transmission" of a virus.
I won't get into too much detail but there are many many factors that play a role. The main one here (in the example of HIV vs influenza) is which cells the virus infects. Influenza infects cells of in the mouth, throat and lungs. So when it grows and ruptures these cells the virus will be let out in your throat, mouth and lungs. So the way it spreads to other people is coming out of these areas on saliva and mucus when coughed or sneezed in droplets.
HIV on the other hand infects cells of the immune system, which are mainly found in the bloodstream as well as mucus cells (that line reproductive tracks). Again without going into too much detail (because mucoid layers are also found in the stomach etc) HIV can spread only from the location where the cells are located that it infects. Because it does not generally infect cells in the mouth and throat it will not be able to access these areas. So it spreads from blood or sexual intercourse, as that is where the cells of the immune system that it infects are located.

Welcome to Biology.SE! This looks like a good answer, but answers are much more likely to receive a favorable response if you include supporting references (primary literature is best). Without that support, your answer is indistinguishable from opinion. This is a good example of how to format references. ——— You may also want to take the [tour] and then consult the help pages for additional advice on [Answer] effectively on this site. Thank you!

Does this means not all the cells of human composed with same chemical surface? If so that is amazing. How could that be? As I superficial knowledge, all the cells of human are mitosis from stem cells. I though all the surface should be the same...

The surfaces of cells have many markers that are different. The DNA will be the same (with exceptions). But the surfaces will be different. For example: Cancer cells that show a different surface will be destroyed by immune cells.

Got it. Thank you!


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What is the best way to learn about gene regulation?
For those of you who already have a decent knowledge of how gene regulation works, how should someone new to the topic acquire a detailed overview?
Is there a particularly good and up-to-date resource?
Is it better to learn from the primary literature? If so, what are the main sub-topics within gene regulation to cover?

I would not learn from the primary literature, the terminology will likely be confusing and there will be a tendency to conflate whatever the current methods are with the concepts.
I'd suggest going for a basic introductory course in the topic, or a textbook. Here is a resource from NHGRI which may be helpful as an introduction.
Here is an online textbook section that might handle the topic at a very basic level. Here is an online version of a traditional standard text at the undergraduate level.
Probably the best somewhat more technical introduction to the basic concepts, without a lot of the fuss, is Mark Ptashne's classic 1986 book on phage lambda.
I saw Ptashne give a talk in the mid 2010s in which he declared (somewhat pompously) that we still didn't understand anything in gene regulation other than phage lambda. No one contradicted him, and I don't think that anyone would contradict him if he said the same thing today.


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Genes are linearly arranged on the chromosome
Could someone please explain the meaning of the statement given by TH Morgan:
"genes are linearly arranged on chromosomes"
Since according to my knowledge there are noncoding parts in between.

Can you give more information about why the existence of noncoding segments precludes a linear arrangement? A linear arrangement of genes could imply the linear arrangement of all the stuff in between, no?

And have you any idea of when TH Morgan said that? And what the state of knowledge about the chemical structure of the chromosome was at the time?

This combines two important findings to which Morgan's lab contributed.

Genes on the chromosome: They could show that mutated phenotypes were linked to the physical entity of chromosomes.
Arranged linearly: They could show that there are distances between different phenotypes correlated to a specific linear arrangement. These distances correspond to the physical distance on these chromosomes (and thus how frequently they are co-inherited). More specifically they showed that distances suggest that the space is linear,  e.g.: in ---A--B-------C-D-   , A would be commonly inherited with B, but less so with C, and even less with D ... ; Theoretically one could have also thought that the chromosomes are circular (as they indeed are in some bacteria) or adopt an even more complex shape, e.g.: some net-like meshwork on which mutated phenotypes / genes sit. In these other cases one would anticipate more complex patterns of co-inheritance among all pairs of genes relative to a linear arrangement.

This is a very good answer and I'd like to upvote it, but it doesn't have references. Please help by adding them. :)

@David I wasn't the one who posted this question!

@Adhish Whoops. Sorry.