text:
Island model vs. stepping stone model
Wright's Island model and Kimura's stepping stone model are classic explanations for migration/gene flow o individuals between subpopulations within the field of population genetics.
My question concerns the quantity Nm, the (effective) number of migrants per generation.
In the Island model, where all demes are exchanging migrants at a given time, individuals migrate with a frequency of m, as seen in Wright's approximation for $F_{ST}$
$F_{ST} = \frac{1}{4Nm + 1}$
In Kimura's stepping stone model, individuals can only migrate to an immediately neighbouring subpopulation with a frequency of $\frac{m}{2}$.
My question is:
In the stepping stone model, are there still only $Nm$ individuals migrating, or is it now $\frac{Nm}{2}$?
My thinking is that an individual can either move left or right, each with a frequency of $\frac{m}{2}$, for a total of $\frac{m}{2}$ + $\frac{m}{2}$ = $m$, so that there are still $Nm$ total migrants. Am I correct in my thinking or should it really be  $\frac{Nm}{2}$?

It all depends upon how $m$ is defined and that might vary from a paper to another.

I thought that may be the case. Was SimBit designed assuming $Nm$ or $\frac{Nm}{2}$?

It all depends upon how $m$ is defined and that might vary from a paper to another. The rest, I find, is very much just a question of logic.
In the infinite island model (the model from which Wright's approximation was computed), the total number of migrants is of course, infinite (if $m≠0$). With $d$ demes (or islands), the total number of migrants is $dNm$ if $m$ is defined as the migration rate between any two patches.
Under a linear stepping stone model with only 1 step (because there exist more complex stepping stones models), with $d$ demes (or stones), the total number of migrants is $dNm$ (minus small approximation for the extremities of the world) if $m$ is defined as the migration rate from one deme to an adjacent deme. Half of $dNm$ are migrating toward the left and half of them are migrating toward the right.

I thought that may be the case. Was SimBit designed assuming NmNm or Nm2Nm2?

In SimBit, you can use multiple modes to enter migration information. You can specify the migration rate from any patch to any other patch (mode A).
You can use island where you specify the probability of not migrating (which might arguably be a little unintuitive). If the probability of not migrating is $x$, and there are $d$ demes, then the number of migrants from one deme which patch size is $N$ to a single other deme of interest is $\frac{N(1-x)}{d}$. The number of migrants from this deme to any other deme is $N(1-x)$ and the total number of migrants in the whole (meta)population is $dN(1-x)$.
The mode LSS (Linear Stepping Stone), is a little complex as it is very flexible. You can specify the migration rate from a focal patch to any other patch considering they are place in a linear order. SimBit LSS indeed allows for stepping several stones apart if you want. If for example you input LSS 3 0.1 0.8 0.1 2 it means that the probably to migrate from any patch to a given adjacent patch is 0.1. The probability of migrating is 0.2 and the probability of not migrating is 0.8. With such model, the number of individuals exiting a given patch is $0.2N$ ($0.1N$ on each side) for a patch of size $N$. Assuming all patches have the same size, the total number of migrants for a (meta)population of $d$ patches is $0.2dN$.
Of course, if you allow for patch size to vary with carrying capacity or for migration rate to be affected by population mean fitness, then this expected number of migrants will vary among generations.


text:
Should I use RNAseZAP on my bench and pipettes before RNA extraction?
Should I spray RNAseZAP on my bench and pipettes before working with RNA? I am regularly using RNase at my bench and would like to work with RNA as well. Could traces of RNase on my equipment degrade my RNA?

The common practice in my lab is to work in a laminar flow cabinet and clean it with alcohol, then spray it with the RNAseZAP. I've always heard from my professors that, while DNAses are more uncommon, "RNAses are everywhere". So, zap it early, zap it all.

Do you know if it is safe to use RNAseZAP outside the hood? Can it harm us if we inhale the vapours?

@charlesdarwin I don't know the composition of RNAseZAP, but I don't think it can create harmful vapours. I suggested the hood because it prevents recontamination during the experiment, not for RNAseZAP safety problems (see "RNAses are everywhere")

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text:
Does anyone know what insect is this?

Living in Brasília, central Brazil; currently experiencing rainy warm/hot days.

This looks like it's a female Pelecinid parasitic wasp (see this page for an overview of the family in the western hemisphere); from your location the species is either Pelecinus polyturator or Pelecinus dichrous (all of BugGuide's images are of the former, that being the one also found in the United States).

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What is the practical difference between SC, SD and CSM?
Is there some logic to how SC, SD and CSM yeast dropout media differ from each other? I have encountered these three formulations in Sunrise Science Products' catalog, and it appears that the composition differs quite a bit, but I couldn't find any information on what the purpose of these media is.
Obviously, any nutrients that are "dropped out" (e.g. -Ura) will select yeast cells on the basis of that marker. However, what about SD-Ura, SC-Ura and CSM-Ura?

sunrisescience.com/yeast-media-faq. I assume these simply may have arisen from different labs coming up with different chemically defined medias before these were commercially available (perhaps see refs on sunrise link)


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How can paleontologists identify morphologically different fossils as members of the same species?
I recently saw a documentary about Tyrannosaurus rex, which detailed the growth stages of the dinosaur. Apparently, it underwent a huge growth spurt at around 14 years of age, growing into the massive predator so well known in the popular imagination. From what else I've read, this much seems uncontroversial.
However, it made another claim which is that pre-teen Tyrannosaurs had a radically different morphology from adults. The skull was smaller, the legs much longer and the two-fingered forearms far larger in proportion to the rest of the body.
Given that there is some limited evidence for the animal living and hunting in social groups, the program speculated animals of different ages may have filled different hunting roles. The faster, more agile teens driving prey toward the massive, slower adults which then tackled the actual killing. Lions in Africa hunt in packs in this way, but whether Tyrannosaurs did remains speculative.
Anyway, on seeing the body plan of the young Tyrannosaur, I immediately wondered at how any palaeontologist could identify it as the same species as the adult. And lo, the documentary went on to say that, for some years, it was presumed to be a different species.
So the question is: given the radically different body shapes of these two forms and the limited evidence one can glean from the fossil record, how were scientists able to conclusively identify that young and adult tyrannosaurs were, in fact, members of the same species?

Just to be pedantic about the scientific method, scientists seldom "conclude" anything. They propose a hypothesis, and then collect data to see if their hypothesis can be falsified. Paleontological species hypotheses are frequently overturned as more or better fossils are discovered.

Radically different body shapes and sizes represent overall phenotype. Overall phenotype was used briefly in the 1960s and 1970s for species identification under a statistical distance method called "phenetics". However, phenetics has been rejected as a valid method of species identification. Similarly, although ecologists widely use the Biological Species Concept (Mayr) based on reproduction, taxonomists generally prefer some form of the Phylogenetic Species Concept. In addition, paleontologists find species concepts that require assumptions about reproduction in fossils to be difficult. The phylogenetic species concept uses the presence of fixed morphological characters to identify individuals as members of a species. Fixed characters need not be major, obvious differences. They need only be present in all members of a hypothesized species, and absent outside the species. That they are fixed in all members of a species implies a lack of gene flow, but the definition does not require that. So in the example you gave, juvenile T-rex must have some unique characteristic morphological feature that define them as members of the species (a synapomorphy). In addition, when there are a series of intermediate juvenile fossils, it becomes possible to link them together.


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Can someone help me identify this spider?
Can someone help me identify this spider? Saw it in Malawi; aprox. 5 to 6 cm. Seems like a Solifugae but I cannot go any further... I thank you in advance!

That is a sun spider. It is in the order Solifugae, family Solpugidae. I don't know the species. Looks like genus Zeria.

Just to make it clear - although Solifugids are arachnids, they are not spiders.  Those big heavy 'pincers' in front of the face are the useful ID factor.  They are not venomous (as far as I know), but the pincers can give you quite a nip, like a crab or lobster.

According to museum.wa.gov.au, there are four solifugid species in Malawi. Ceroma johnstonii, Ceroma zomba, Zeria niassa and Zeria paludicola.
Ceroma johnstonii has a grayish-brown tint, not the dark brown, almost black coloration (and red) of your solifugid. Ceroma zomba is only 8 mm in length, much too small even if your estimate of 50-60 mm was referring to the legspan.
Zeria niassa is only 24-28 mm in body length, significantly smaller than what you saw unless you meant legspan. Zeria paludicola is also smaller than your 50-60 mm estimate, so it must have been the legspan, not the length. The only photo I could find of any Zeria species is from eol.org and is of an unspecified species. In the photo, it has a dark brown coloration and a very faint tinge of red on the side of the abdomen.

So your image is either of Zeria niassa or Zeria paludicola.

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Smallest, specific RNA-binding protein - w/ sequence?
I'm looking to synthetically fuse an RNA-binding protein onto another protein, inside a viral vector which has a size-limit. I've considered some options, but I'm wondering what StackExchange will say. What is the smallest protein known that binds to a specific sequence of RNA, and what is that sequence?

This is Stack Exchange Biology. StackOverflow is the computing site.

@David - while in itself obviously true, I don't understand your comment in this context?

He has now corrected an initial mistake / typo.


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Should I use glycogen in isopropanol to precipitate RNA or does glycogen have harmful consequences on downstream protocols such as RNA seq?
I have heard that one can use glycogen in isopropanol to better visualise the RNA pellet after centrifugation. What are the advantages and disadvantages of adding glycogen in isopropanol for RNA quality and quantity?


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Why food is still tasty?
I'm not a biologist, but it seems that plants with disgusting taste have evolutionary advantage to tasty plants. Same about animals.
There are some species that can not be eaten by man (sharks have poisonous meat). Being eaten by a human — is one of major threats for a shrimp. Does it mean that shrimps are going to become less and less tasty (for a human taste)?

Why do you think sharks are poison ?

mercury accumulates in top level predators

@blacksmith37 "Unprocessed shark meat may have a strong odor of ammonia, due to the high urea content that develops as the fish decomposes". You can eat it, but it's unhealthy. In most countries only shark fins are used as food — other parts are concidered waste.

Things are not fundamentally tasty or disgusting. A dung fly loves that taste of dungs while I personally prefer the taste of an apple and my dog prefers the taste of duck fat. A classic example is the gene family TAS2R and the evolution of bitter taste in rodents and primates.
Predator (incl. herbivores) evolves as to like the taste of what he should be eating (Carlsson et al., 2009). Preys (incl. plants) can eventually play out with their taste though, trying to either taste bad to avoid specific predators or taste good to attract specific predators that may disseminate their seeds. I have failed to find evidence that plants can deceive animals at being more tasty than nourishing but you might still want to have a look at Dethier (1980), Sorensen (1983) and Goff and Klee (2006).
One could therefore expect an evolutionary race (red queen) between preys and predators upon how they taste. It would likely be a rather complex race as most species have several predators and several species they prey upon. However, such race on taste would work only if plants can deceive animals which I failed to find evidence for. Arms race for toxic compounds relating to evolution of taste in animals are very much known though (Edger et al., 2015).

So is it a Red queen taste version?

Yes. But see edit where I made sure to be a bit more safe in not claiming more than it is known. I also added a few references.

Well, my dog likes long-dead deer bones, and eats horse droppings and hoof parings, among other things I don't think I'd find at all tasty.  OTOH, my horse likes to snack on bitterbrush (https://en.wikipedia.org/wiki/Purshia_tridentata ), and eats a lot more hay than I'd care too.  Tastes differ :-)

Right now mankind is a major predator for a lot of species (shrimps for example) — does it mean that in future generations shrimps will evolve to be less attractive for people?

@StanislavGoldenshluger More than half of the world production in shrimps are farmed (according to WWF), so it is not really a good example.


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How long does it take for cancer to be detectable if it grows from a single cell?
Assuming cancer has its origins at a single malfunctioning cell, how long would it take for that cell to grow from the point at which it is malfunctioning enough so that it can be detected by the immune system, to the point at which it be detected with:

Routine modern medical tests
Cancer specific blood test
Noticed by the host (symptoms)

Is the assumption that "cancer has its origin at a single malfunctioning cell" correct?

This will probably be hard to tell - and depends strongly on the type of cell. Some cancers grow very slow, while other are rather fast.

I know some cancers grow fast, but I doubt there is any cancer type where the single cell becomes a symptomatic cancer overnight. Or within a month. I mean the single cell has some barriers to overcome, like the ability to grow blood vessels. I am not familiar with all the barriers however. If one is aware of them, it should be possible to get an average, and min, max estimates for the time.

The barriers you mention are outlined well in the classic Hallmarks of Cancer paper: http://www.cell.com/abstract/S0092-8674(11)00127-9
The main problem with finding a general answer to this question is the large diversity in cancers, and the resulting problem in defining what hallmarks are sufficient to call an individual cell cancerous. There are cancers that can't be detected by the immune system or blood tests and will hide for a very long time symptom-wise, and non-cancerous tumours that can be detected in various ways very early on.
Let's say for your timing reference you simply take the point of neoplasm diagnosis (for neoplasms that turn out to be cancers after testing). At this point, figuring out how much time this cancer has spent being cancerous is very difficult, and to my knowledge has never been done. It could be possible to determine:

The number of genetic or epigenetic malfunctions that made the difference between benign tumour and cancer for this particular neoplasm (once again, hard to define)
An approximate rate of acquiring those malfunctions. Conceptually, one could ex vivo culture the cancer and monitor the rate of aquisition of further mutations in cancer-related loci or epigenetic markers.

Depending on how that rate looks, it may be possible to reverse extrapolate the rate of acquisition before diagnosis, and thereby estimate an approximate timepoint of acquisition of the first proper cancerous malfunction.
Besides that, "it probably took more than a few days" is the only statement I can confidently make, although as far as biological theory goes, it's perfectly possible (though highly unlikely) for a cell to acquire a set of mutations sufficient to become cancerous in a single round of replication.


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Recommendations for textbooks on statistical and quantitative genetics, and genetic epidemiology
I'm looking for a textbook on statistical genetics, quantitative genetics, association mapping, and genetic epidemiology. My interests include, but are not limited to, complex trait analysis, and the mathematical and statistical aspects of these subjects.
I've found a lot of books, below are some that I'm considering:

"Genetics and Analysis of Quantitative Traits" by M. Lynch et al. (amazon link)
"Introduction to Quantitative Genetics" by D. Falconer et al. (amazon link)
"Statistical Genetics: Gene Mapping Through Linkage and Association" by B. Neale et al. (amazon link)
"Statistical Genetics of Quantitative Traits: Linkage, Maps and QTL" by R. Wu et al. (amazon link)

I haven't found anyone else posting this question. There are discussions about population genetics textbooks, but these books have limited information about quantitative genetics, etc.
If anyone has a favorite book, comments about the books above, or anything, I would greatly appreciate it.
Thanks in advance.
EDIT:
Another promising book:

"The Statistics of Gene Mapping" by D. O Siegmund (amazon link)

Related: Books on population or evolutionary genetics?

For statistical genetics, take a look at:
Likelihood, Bayesian, and MCMC Methods in Quantitative Genetics. Daniel
Sorenson and Daniel Gianola. (2002. Springer).

Warning: heavy on math (calculus). If that doesn't scare you, it's excellent guide to non-frequentist statistical methods applied to problems in genetics.

It kind of looks like all but the last chapter are about Bayesian statistics, so you might as well read a different book on that, and then another book on quantitative genetics.

Actually, chapters 5, 6, 7, and 8 (25% of the chapters) cover Bayesian statistics. Chapters 13-16 (another 25%) cover applied quantitative methods. Not sure what book you were looking at.

I see, part IV of the book, chapters 13-16 are about quantitative genetics. Still, chapters 1-12 are about Bayesian statistics and inference, so a really small portion of the book is about quantitative genetics. Looks interesting nonetheless, especially for someone who is unfamiliar with Bayesian statistics and would like to get into it.


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Can pymol show cartoon (secondary structure) for a pdb of multiple frames?
I am using pymol to visualise the secondary structure of protein using its cartoon representation. The pdb file comes from a simulation, which contains multiple frames. After loading the pdb, its secondary structure (e.g. sheet, helix) could not been recognised. Surprisingly, if only one frame is kept, its secondary structure could be seen. So how to enable secondary structure recognition for a pdb file with multiple frames?
An example of the pdb file with multiple frames is shown below.
REMARK    GENERATED BY TRJCONV
TITLE     Protein in water t=   0.00000
REMARK    THIS IS A SIMULATION BOX
CRYST1  116.453  116.453  116.453  90.00  90.00  90.00 P 1           1
MODEL        1
ATOM      1  N   ASP     1      85.582  59.777  48.367  1.000.0000           N
ATOM      2  H1  ASP     1      84.882  59.067  48.507  1.000.0000           H
ATOM      3  H2  ASP     1      85.162  60.617  48.747  1.000.0000           H
... ...
ATOM   6615  OT  ALA   442      28.032  36.877  69.157  1.000.0000           O
ATOM   6616  O   ALA   442      30.092  36.087  68.677  1.000.0000           O
ATOM   6617  HO  ALA   442      30.072  35.867  69.597  1.000.0000           H
TER
ENDMDL
REMARK    GENERATED BY TRJCONV
TITLE     Protein in water t= 1000.00000
REMARK    THIS IS A SIMULATION BOX
CRYST1  116.384  116.384  116.384  90.00  90.00  90.00 P 1           1
MODEL        2
ATOM      1  N   ASP     1      75.052  41.097  56.132  1.000.0000           N
ATOM      2  H1  ASP     1      75.622  41.407  55.352  1.000.0000           H
ATOM      3  H2  ASP     1      75.602  41.357  56.932  1.000.0000           H
ATOM      4  H3  ASP     1      74.682  40.167  56.272  1.000.0000           H
ATOM      5  CA  ASP     1      74.032  42.157  56.202  1.000.0000           C
... ...
ATOM   6615  OT  ALA   442      45.292  49.247  90.922  1.000.0000           O
ATOM   6616  O   ALA   442      47.102  49.617  89.632  1.000.0000           O
ATOM   6617  HO  ALA   442      47.662  49.327  90.342  1.000.0000           H
TER
ENDMDL

I suspect that the PDB is malformed. Is it available online somewhere so I can take a look at it? Alternatively, could you post and excerpt of the HELIX and/or SHEET records from the file?

I notice that the ATOM records don't contain a chain identifier. I'm not sure if that would prevent PyMol from recognizing the secondary structure elements.

@canadianer the chain ID is not the problem, as it works for a single frame

Okay... Does an NMR model with multiple conformers display correctly (5VKV, for example)?

So it must be this particular PDB. If there's anything wrong with the portion of the file you've posted, I don't know what it is. Does the file with multiple models have HELIX/SHEET records?

Ah okay, I can reproduce this. If you compare the original model with the model with the HELIX records removed, you may notice that the secondary structure assignments are not identical. It seems that if no HELIX record is present, PyMol attempts to assign secondary structure itself. For whatever reason, it does not do this if multiple models are present. You should be able to use the dss command to force PyMol to calculate secondary structure in the PDB with multiple models.

yes, exactly! can you please answer it? (so I can accept your answer)

Sure thing; glad it worked for you.

It seems that if no HELIX record is present in the PDB, PyMol attempts to assign secondary structure itself. For whatever reason, it does not do this if multiple MODELs are present. You should be able to use the dss command to force PyMol to calculate secondary structure in a PDB with multiple MODELs.

Thanks for this, it was so easy to get this "fixed"! Works like charm.

@MarcinMagnus You’re welcome!


text:
How does the specificity to bind to antibody differs between 'hot' and 'cold' antigen in radioimmunoassay?
This question is in relation to radioimmunoassay. In this assay, the 'cold' antigen replaces the 'hot' antigen. Why is it so, if both the antigens are same and hence their specificity? Does the radioactive molecule change its specificity?

The specificity is the same, but protein-ligand binding is an equilibrium process. In other words, the antigen is constantly associating with and dissociating from the antibody. As a hot antigen dissociates, it is possible that a cold antigen can take its place, and vice-versa. As the ratio of cold to hot antigen increases, there is a greater probability that cold antigens will take the place of hot antigens.
You can read more on Wikipedia.

@Indresh You’re welcome. If this answered your question, you can mark it as accepted by clicking the check mark.


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How are non identical cattle twins capable of transplanting each others organs?
Non identical cattle twins have different genes and by this their immunesystem works differently so initially it was suspected that eg tissue transplantation from one to the other would be rejected by the immunesystem.
Now it appears that it is possible to succeed in a organtransplantion because there body's lived in the same placenta. But how does their immunesystems get compatible with the cells of the other just through the placenta?

Can you give a source for this? Most commonly, nonidentical twins each have their own placentas, not shared placentas.

It is about cattle see: http://onlinelibrary.wiley.com/doi/10.1111/exd.12227/full

If your question is about cattle, please specify. Humans don't share placentas.


text:
Effects of Free Electrons In a Cell?
I am very new to biology,  currently just a student. Recently I learned of the electron transport chain used in cellular respiration. This  got me thinking. At the end of the chain, the electrons are joined with hydrogen and oxygen forming water.
It  seems that  all cellular activity (that  I've learned about) is very careful to bind any electrons to some byproduct molecule after using them. Thus I get the impression that free electrons in a cell are dangerous. I asked my  teacher about it, but he wasn't sure. So now I am dying to know, what would be the consequences of allowing  a free electron to float about a cell?

It doesn't make much sense to think about 'free' electrons in biological systems, but you might want to read about oxidative stress

To understand biochemistry you need to understand some chemistry, and if you don’t you should learn some before posting such naive questions to this list. As any book will tell you, the electron transport chain is a series of oxidation/reduction reactions that are intermediate in an overall oxidation reaction, e.g. of NADH by oxygen. Chemically, oxidation of a compound is the removal of electrons from the compound which is oxidised, by and to the oxidising agent, which is reduced. The purpose of the electron transport chain is to utilize the energy released. Now delete your question please.

@xusr — This is a schoolboy or undergraduate who is clearly unaware that oxidation involves transfer of electrons. Bryan Krause wants him to read about oxidative stress. You want him to read about paramagnetism. Shouldn‘t you help him to walk first? Even this section from Berg et al. would probably be too much for him.

@xusr — If I have ever abbreviated ‘electron transport chain’ as ETC (and I didn‘t here) it is only because of the word limit of comments. However, this is what the poster asked about. One of the problems with this list is that some of us would like to answer questions at a sophisticated level, but posters are often asking basic questions because they lack chemistry or haven‘t read the chapter in their text properly. If you would like to answer a question on four electron reductions, I'll post one (if I‘m not required to do too much research first ;-) )

@David My comment was directed towards someone who expressed an interest in biology and at least some classroom familiarity with concepts like the electron transport chain. Different people learn differently. This might be someone who was completely turned off by chemistry and won't find the motivation to study it until they find an avenue of interest. This asker has shown quite some insight and free thinking, and they are coming here for some support. I understand you are attempting to do some quality control here, but please mind the impacts of your words. Now delete your comments please.


text:
Test of antibiotic A for sensitivity as surrogate of antibiotic B
I am reading the WHO Global Antimicrobial Resistance Surveillance System (GLASS) - Manual for Early Implementation. it mentioned some of the drug-bug combination that will be put under surveillance in page 8 of the following link, I have screen-captured the page below that I have some questions.
http://apps.who.int/iris/bitstream/10665/188783/1/9789241549400_eng.pdf

For S. aureus, Cefoxitin is selected for surveillance, but the remarks mentioned that Cefoxitin is a surrogate for testing susceptibility to oxacillin (methicillin, nafcillin). I know S. aureus showing resistance to methicillin is MRSA, but why test for Cefoxitin but not test methicillin directly?
The same question goes for S. pneumoniae for Oxacillin as a surrogate for testing reduced susceptibility or resistance to penicillin. Why not directly test for penicillin?
Sorry that I am not a microbiologist, just a data analyst recently working on microbiological data, hope that I won't be asking something too stupid.
Thanks!

I will be interested in seeing if this gets answered. +1

This is not a proper answer as such and it's based on a bit of an 'educated guess' but it was too long for a comment.
I did however, find this article. Unsurprisingly, one of the big drivers of using surrogate antibiotics is down to availability and cost. Some antibiotics, while known about, may not be produced commercially at scale, or be widespread enough for testing facilties around the world to use. Consequently, the WHO can maintain a list of antibiotics with complementary 'cross-talking' modes of action, so that a resistance mechanism can be probed without needing the specific antibiotic.
Another reason for using a surrogate might be to avoid some of this cross-talk. I.e., if you wish to know the effectiveness of (say) imipenem, and you know imipenem and meropenem have the same mode of action, but perhaps the bacteria has a second resistance pathway that  is specific for imipenem - you could use meropenem as a surrogate, knowing that it won't be degraded/removed by pathway 2, and you can still probe the mode of action.*
*(This is a contrived example, I have no idea if you'd ever use those 2 antibiotics in this manner.)
It seems like, from reading online, the real drivers to use surrogate testing however, are purely as an interim measure due to the enormous lag phase between discovery of new drugs, testing, scale up, administrative approval, and then general market availability.

Though I'll add to this I have absolutely no idea why that would be an issue for penicillin which is definitely widely available!


text:
Why outgroups are supposed to be ancestral?
I was reading about phylogenies and found many literatures said that outgroups contain the ancestrial trait, but why is that? Aren't they also experiencing the same amount of evolutionary time and (presumably) changing their characters as well?

http://www.blackwellpublishing.com/ridley/tutorials/The_reconstruction_of_phylogeny13.asp

Yes, sister taxa are, by definition, of equal age. So they evolve independently after the two groups diverge. You are asking about character polarity, and you are exactly right. That is why multiple outgroups are better for inferring which state is ancestral. If an outgroup is state A, and a second more distant outgroup (an out-outgroup) is also state A, and the ingroup has state B, then you can be fairly confident that state A is ancestral. If you look at dozens of characters this way, you will find that any of the three taxa in any combination may have the ancestral state. Imagine the distant outgroup (the out-outgroup) is state A, and both the close outgroup and the ingroup are state B. Then again, you could not know which state is ancestral, and would need a further outgroup. These are inferences, not measurements.


text:
Why does enteral carbohydrate yield higher energy than parenteral?
The following is written in a well-known textbook of surgery:

Each gram of enteric carbohydrate provides 4.0 kilocalories (kcal) of
  energy. Parenterally administered carbohydrates (eg, intravenous
  dextrose) yield 3.4 kcal/g

What is the explanation for this?

Is the textbook refering to the same type of carbohydrate in both case ?

The 3.4 refers to dextrose. What other carbohydrate is given iv?

@Frédéric unfortunately, this is not elaborated upon.

@GrahamChiu theoretically one can also administer fructose or inverted sugar syrup etc., but I don't think they are widely used.

Parenteral carbohydrate is usually dextrose which is actually D-Glucose monohydrate. Monohydrate implies coupling with a water molecule, such that 1 gram contains a lower relative component of glucose, resulting in a lower kcal yield.

The value of 4.0 kcal per gram of dietary carbohydrates is simply a convention used by the Atwater System, which took a single averaged value for each of the available macronutrients found in food. I believe it was meant to represent an average composition of dietary carbohydrates at the time.
However, not all carbohydrates have the exact same heat of combustion. In other words, the amount (weight) of carbohydrate needed to yield a specific amount of energy differs depending on the molecular form of the carbohydrate (1). More specifically, monosaccharides (glucose and fructose) have ~3.75 kcal per gram, disaccharides (sucrose and maltose) ~3.95 kcal per gram, and longer polysaccharides (starches) have 4.15 to 4.20 kcal per gram (2).
The reason for this is again caused by water, specifically the dehydration (loss of water) that occurs as a result of the condensation reaction which forms the glyosidic linkage between monosaccharide monomers (1). For each additional monosaccharide subunit added to a carbohydrate chain, a water molecule is lost (see the example below).

Image credit: https://ib.bioninja.com.au/
So...going back to the original example. The heat of combustion of anhydrous glucose is 3.75 kcal per gram. Glucose (180 g/mol) makes up ~ 90.9% of the weight of dextrose monohydrate (198 g/mol). So, take the heat of combustion of glucose (3.75 kcal/g) multiplied by it's relative proportion in composition of dextrose monohydrate (0.909) and you get 3.75 * 0.909 = 3.4 kcal per gram. The 4.0 kcal per grams of dietary carbohydrate is simply a convention derived from an average value based on work that's over a century old.
References:
1: FAO FOOD AND NUTRITION PAPER 77. Food energy - methods of analysis and conversion factors; Report of a Technical Workshop, Rome, 3-6 December 2002. FOOD AND AGRICULTURE ORGANIZATION OF THE UNITED NATIONS.
2: Agricultural Handbook No. 74. Energy value of food; basis and derivation. Merrill, A., Watt, B. USDA Agricultural Research Branch.


text:
Does "eating less" stimulate cell starvation?
2016 Nobel Prize in physiology or medicine was given for the study of autophagy.
Judging from the description, a healthy cell responds to starvation (and other types of stress) with autophagy.
Does starving of the organism for short amount of time (around a day) cause cell starvation? And, can we say that starving for short amount of time stimulates autophagy?

What is "short amount of time"?

@MartinKlvana around a day


text:
Complete human rDNA sequence
I've been trying to retrieve the complete human rDNA sequence (non-spacers and spacers), which should be about 43-kb in length using Biomart, NCBI, and rnacentral, but I have only been able to find the 13-kb non-spacer sequence. Are the spacer regions not yet sequenced due to difficulty in sequencing a repetitive region? Thanks for your help.

Managed to find the complete sequence of the repeating unit:
https://www.ncbi.nlm.nih.gov/nuccore/U13369

In 1.1 version of (since that version) "Complete genome" assembly of homo sapiens (never achieved before) compared to 1.0 (previous version) 5 last gaps (all somehow in the rDNA) were fixed and now it all is there!
https://genome.ucsc.edu/cgi-bin/hgTracks?genome=t2t-chm13-v1.1&hubUrl=http://t2t.gi.ucsc.edu/chm13/hub/hub.txt
https://www.ncbi.nlm.nih.gov/assembly/GCA_009914755.3
Delta from 1.0 version is there https://s3-us-west-2.amazonaws.com/human-pangenomics/T2T/CHM13/assemblies/changes/v1.0_to_v1.1/v1.0_to_v1.1.chain and delta from patch 13 of GRCh38 is here: https://t2t.gi.ucsc.edu/chm13/hub/t2t-chm13-v1.0/hg38Lastz/t2t-chm13-v1.0.hg38.over.chain.gz

To the best of my knowledge, of the estimated  500 copies of rDNA repeats in the human genome only 1 and half repeats has been sequenced and published. Mammalian rDNA repeats are hard to clone and appear unstable in yeast and e coli.

Great, that's useful to know. I assume that there must be mutations in at least some of the noncoding regions that would enable positional information for certain sequences.

Yes, there must be sequence variability in the non-coding region. However as rDNA arrays are rather unstable and recombine within a yeast or ecoli host. Hence isolating rDNA repeat array and making a rough map of rDNA repeat arrays is next to impossible.

Reference in support of this assertion please. I thought methodological developments in sequencing meant that this situation could be dealt with.

Welcome to the "gaps" in human genome. Parts of the genome of eukaryote that are very difficult to explore must less experiment with. Here is a reference but it does quite cover recombinational instability of repeat arrays that prevent other methods to study them.  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5098217/

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


text:
Questions about RNA Polymerase
I'm confused about the terminology and directions described in processing DNA to proteins in this paragraph.

RNA polymerase reads a DNA template in the 3’ to 5’ direction to
  synthesize RNA in the 5’ to 3’ direction. Transcription can occur in
  either direction, but not in either direction from a single promoter.
  RNA polymerase can only transcribe in one direction (5’ to 3’) with
  respect to reading one strand of the template DNA in the opposite
  direction (3’ to 5’). In general, each promoter recruits RNA
  polymerase to a particular site and indicates in which the direction
  RNA polymerase will move along the DNA. As RNA polymerase is moving,
  there will be only a single strand that can be used as a template to
  allow 5' to 3' synthesis of a transcript.

Sentence 1:
What's the difference between reading and synthesizing RNA?
Sentence 2:
What's the difference between synthesizing and transcribing?
Sentence 3:
Didn't this just contradict sentence 2?
Sentence 4:
If RNA polymerase is recruited at a site to and directed to "move along" the DNA, what is it doing when it "moves along" (reading? synthesizing? transcribing? wtf?).
Sentence 5:
My understanding is this is the "transcribed strand", not the "coding strand" of DNA, correct?
Question:
I don't understand this paragraph and the more I read it, the more confused I get. Could someone please clarify (preferable with visuals)?

I think if you search youtube for "rna transcription animation" you will find plenty of visual demonstrations.

What's the difference between reading and synthesizing RNA?

What's the difference between reading and writing a book? Synthesizing RNA means producing an RNA based on a sequence in DNA. Reading it means processing RNA that is already produced. Reading also implies that protein will be produced based on the sequence in RNA.

What's the difference between synthesizing and transcribing?

"Synthesize" means to produce any chemical molecule. "Transcribe" is specifically the synthesis of RNA form DNA via a polymerase (as opposed to for instance inorganic synthesis of RNA de novo, as might be done in a chemistry lab).

Didn't this just contradict sentence 2?

It's just saying that genes can be oriented forward or in reverse. Reverse genes are on the opposite strand, so they are still 5' to 3' (the 5' ends of the two strands are on opposite ends of the DNA). But every gene must still have a promoter on its 5' side.
And actually, that bit is not quite true: There are bidirectional promoters that will cause transcription in both directions.

If RNA polymerase is recruited at a site to and directed to "move along" the DNA, what is it doing when it "moves along" (reading? synthesizing? transcribing? wtf?).

Usually, it will transcribe (so it will also synthesize, or "read"). But technically, RNA pols belong to a family of proteins which are "molecular motors", meaning that their fundamental activity is to move along DNA step by step like a little monkey climbing a ladder. With RNA pols, RNA synthesis is coupled to this movement, so each step on DNA also causes a letter to be added to the RNA they are making.
Also, technically the RNA pol is not only moving and making DNA, but also unwinding the two strands of DNA and separating them. But this may be outside the scope of your material.

My understanding is this is the "transcribed strand", not the "coding strand" of DNA, correct?

RNA comes out matching the sequence of the gene (except for T->U), and it is assembled through basepairing to DNA. If it paired with the strand the gene is on, the RNA would come out as the reverse complement of the gene. Instead it is assembled on the opposite strand, which is already the RC of the gene. RC of RC of a sequence is the same sequence. Thus we say RNA is transcribed from the "non-coding" strand, but keep in mind that these coding/non-coding assignments are arbitrary and only used by us humans, the cell does not have a special marking for it (beyond the 5'/3').

I don't understand this paragraph and the more I read it, the more confused I get. Could someone please clarify (preferable with visuals)?

It's very simple: DNA is a directed (because of 5'/3') string of ACTG. It is coupled to another, complementary string that runs opposite to it. The sequence on either strand may be meaningless, or parts of it may encode genes. Genes consist of a promoter, some sequence, and terminator. RNA pols can slide along either strand, but only in 5' to 3' direction, so they will slide in opposite directions on opposite strands, like cars on a two way street. When RNA pol encounters a promoter, it starts synthesizing an RNA: It separates the two strands, and lets single RNTPs basepair with the opposite-direction strand, when they do so it glues their phosphate backbones together. It keeps sliding and making RNA like this until it reaches another sequence, the terminator, at which point it stops assembling RNA and releases it. The RNA snaps off DNA and goes off on its merry way, the two strands of the DNA that were separated by RNA pol come together again.
Thus for every promoter-terminator pair, whatever sequence is in between them will be transcribed into an RNA. These are basically genes. These genes may be on either strand of DNA, and they must always be oriented along the 5' to 3' of the strand they are on. Thus genes on opposite strands will appear "reversed" with respect to each other.

"Sentence 1:
What's the difference between reading and synthesizing RNA?"
Sentence 1  relates to what is the most trivial if most important to not mis-understand: RNA polymerase is said to "work" ( Wikipedia, RNA polymerase) in 5' to 3' direction.
In order to paraphrase your question accordingly: What would "to work" mean in that sentence? It would mean "synthesizing" RNA, it would not mean "reading" DNA (the reading I circumscribe as "unraveling/traveling" from '3 to '5, while, at the same time,  "elongating" in '5 to '3 direction). As it now occurs: The text says "... RNA polymerase reads a DNA template..."! Thus,   changing  your question to "...difference between reading DNA (do not omit "DNA") and synthesizing RNA apparently answers the question. However, that is not the whole story. I think it doesn't come easy to see that, see above, the "work" is like  old fashioned homework (in German: "Stricken"): What you have just seen is what you got to add - to the end (to paraphrase some common acronym).
If polymerase had some bench or large table it'd go "a-head" and work from 5 to 3, not the other way round. Polymerase must put the letter that it had just read as  been ordered to the end of the list that "goes out",  that polymerase thus "table-waited"  from 5 to 3,  which makes "sense". So - "reading" might very well be "synthesizing" in terms of direction - however, defined by mechanism, it is not (it is first in, DNA, first out, RNA, "nothing in store"). Again, in some surprising way - to be specific: in terms of direction -   reading could be, but is not synthesizing.
"Sentence 2:
What's the difference between synthesizing and transcribing?"
Sentence 2 does not use the word transcribing. In the context of sentence 2 synthesing and transcribing are synonymous.
"Sentence 3:
Didn't this just contradict sentence 2?"
Sentence 3 does not preliminarily explain what sentence 4, the following, explains:  "...each promoter  ... indicates in which the direction RNA polymerase will move along the DNA." Thus sentence 3 does not seem to "clear up"  the ambiguity of sentence 2 which lies in the issue of "direction". The word "direction" in sentence two does not make clear how "direction" relates to the concept of direction as the author makes use of in  sentence 1.  One specific gene defines "any" direction (which you wrote about in some answer of yours).*
"Sentence 4:
If RNA polymerase is recruited at a site to and directed to "move along" the DNA, what is it doing when it "moves along" (reading? synthesizing? transcribing? wtf?)."
It transcribes (most general term) by reading (the  template/anti-sense)  DNA and synthesizing RNA (cp. answer on sentence 1 above) accordingly, first in first out, elongating first becomes last (there is no memory).
"Sentence 5:
My understanding is this is the "transcribed strand", not the "coding strand" of DNA, correct?"
Correct.


text:
Where do kombucha SCOBYs get nitrogen?
Kombucha can be brewed even with tiny amounts of inocculate, such as the little bit of sediment at the bottom of store-bought kombuchas. Over 1-2 weeks, this can grow into an inch thick film covering the entire surface of the brew; a very striking accumulation of biomass. Where is the material for this biomass coming from?
It seems like most recipes for kombucha brew consist of:

5.7% sugar
0.7% black tea
10-30% of a previous, "finished" kombucha
SCOBY (optional, the kombucha in the previous step is sufficient)

I can see how the sugar provides carbon, oxygen, hydrogen and energy. Of course, merely providing the elements is not necessarily sufficient, since often enough cells require specific compounds as well. But I'll assume the SCOBY community, in aggregate, is able to transform the sugar into every CHO compound it needs. However, what about nitrogen? The amount of tea seems minute, and tea seems like not a very rich source of protein/amino acids. Sugar doesn't contain nitrogen, and while dead SCOBY constituents from the initial kombucha can conceivably be cannibalized, the cannibalism cannot account for dramatic increase of SCOBY biomass because of conservation of mass.

Short answer:
Nitrogen fixation (i.e, atmospheric nitrogen)
Longer answer:
Nitrogen fixation is the process by which atmospheric nitrogen is converted to forms usable by further biochemical reactions. Some bacteria are capable of nitrogen fixation (and some plants have symbiotic relationships with nitrogen-fixing bacteria); all the others rely on those species directly or indirectly to provide nitrogen.
The microorganisms involve in brewing kombucha tea are actually a collection of different species of bacteria and yeast. The bacteria that are found in kombucha tea include Acetobacter nitrogenifigens and Gluconacetobacter kombuchae, both of which are capable of nitrogen-fixation (and there may be others).
Molasses is also often used as the sugar source for kombucha, and molasses includes some nitrogen-containing compounds.
See the following review for more information:
Jayabalan, R., Malbaša, R. V., Lončar, E. S., Vitas, J. S., & Sathishkumar, M. (2014). A review on kombucha tea—microbiology, composition, fermentation, beneficial effects, toxicity, and tea fungus. Comprehensive Reviews in Food Science and Food Safety, 13(4), 538-550.

I hadn't considered nitrogen from the air, wow!


text:
Can lysozyme also lyse gram-negative bacteria and if yes, how fast?
Lysozyme attacks peptidoglycan, which are found in Gram-positive bacteria. I know someone who uses lysozyme to lyse Escherichia coli, which is Gram-negative. How is that possible? Can lysozyme lyse all bacteria, independently of their Gram status? Does anybody have information on how long I should leave lysozyme in a bacterial solution for it to be effective?

Gram-negative bacteria also have peptidoglycan which can be degraded by lysozyme. However they have an outer membrane lying outside the peptidoglycan layer and this will block lysozyme action.
Because of this if you intend to treat Gram-negative bacteria with lysozyme it is necessary to add something that will disrupt the outer membrane—the usual choice is EDTA since removal of magnesium ions by chelation will destabilise the outer membrane.

Do you know what concentration of EDTA and lisozyme would be ideal for killing the bacteria?

I've heard that lysozyme can, even in vivo, attack gram-negative bacteria through some alternative mechanism possibly unrelated to attacking peptidoglycan.

@charlesdarwin Published protocols tend to focus on using EDTA/lysozyme treatment to prepare spheroplasts rather than killing. See https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4223228/ for an example. Note that the authors add sucrose to prevent the cells from lysing i.e. as an osmoprotectant.  Their report indicates that rather short treatments (5 min) are enough to form spheroplasts: in the absence of sucrose these cells would have lysed.

Do you know what they mean by '125 mM EDTA-NaOH'? Is it 125 mM EDTA and 125 mM NaOH?

Also, do you think that the bacterial proteins will be denatured after the lysis of the bacterial cell membrane?


text:
Why aren't 'exons' named 'introns'?
Why are introns called 'introns' when they are the actual ones who are getting spliced out from the pre-mRNA. Shouldn't exons be named introns as they are the ones that are 'in' and are not 'exiting'? On what criteria were they named like this?

It confuses me too. Shrug.

Introns stay inside the nucleus, exons exit the nucleus.

It’s not actually true that introns always stay inside the nucleus. There is a lot of research discussing the role of extranuclear introns playing a role in translation regulation.

I'm amazed how many votes this has got. Shows that there is a general confusion among those new to the topic. If I were still teaching this, I'd make an extra effort to clarify the origin of the expression. I withdraw my close vote.

@David It was in the "Hot Questions" list, which makes it visible to everyone across Stack Exchange.

The terms intron and exon were coined by Walter Gilbert in a renowned 'News and Views' article, Why Genes in Pieces, published in the journal Nature in 1978.
Introns are the intragenic regions and exons are the regions which are expressed.
This is the relevant passage in full:

The notion of the cistron, the genetic unit of function that one thought corresponded to a polypeptide chain, now must be replaced by that of a transcription unit containing regions which will be lost from the mature messenger - which I suggest we call introns (for intragenic regions) - alternating with regions which will be expressed - exons. The gene is a mosaic: expressed sequences held in a matrix of silent DNA, an intronic matrix.

Yeah I got the link of the article from Nature.com . Thanks

Well, as this question seems to be about helping the X- or M- generations get to grips with baby boomer terminology, let me explain how I remember what introns are.
Before Gilbert coined the term (as @xusr explains) original reports of the research that established the mosaic nature of eukaryotic genes refered to

in-tervening sequences.

For example, there was a paper from Phil Leder’s lab in 1978 entitled

Intervening sequence of DNA identified in the structural portion of amouse β-globin gene

So intron was really related to intervening in its origin, and knowning this it is easy to remember which is which — introns and exons.


text:
What is this insect in Southeast Idaho?
This thing ran out of the wall of my dorm hallway. It had a lot of what look like antennae, and it's very fast.

(click to enlarge)

related post: Is this silverfish? My apartment very dry

That is a silverfish, order Zygentoma (also known as Thysanura). Likely genus Lepisma (family Lepismatidae). Zygentoma are insects, and are the sister taxon to Pterygota (winged insects)

I should have added that these are harmless.

Admittedly, that was one of my main concerns

They're harmless to people, but they feed on stuff like paper. Usually the presence of these creatures (not the insect itself) is considered to be related to hygiene issues.

@wie5Ooma Very loosely related. Not like cockroaches. Many clean homes have silverfish. And they don't generally cause much damage to anything.


text:
What causes Pseudomonas fragi to smell sweet?
I am working with Pseudomonas fragi and I could not help but notice that it smells sweet, which probably explains its species name 'fragi' from 'fragum', strawberry in Latin.
Does anybody know what causes this bacterium to smell sweet? It must be some volatile compound that they release in the air? Why would they do that? Do other bacteria release odorant molecules? If so, why?

The strawberry-like odour that you perceived is mainly attributed to three ethyl esters, namely the ethyl esters of butyric, hexanoic and 3-methylbutanoic acid.
There are other odour-active volatiles produced by Pseudomonas fragi, about 26, which are said to add to the richness and complexity of the odour of the three aforementioned main compounds.
Source:
Analysis of odor-active volatiles from Pseudomonas fragi grown in milk - Cormier et al. 1991
The study by Cormier et al. should be a good starting point for further reading as it references a variety of scientists who have worked on this.


text:
Why is translation so much faster in prokaryotes than eukaryotes?
Prokaryotes perform transcription and translation much faster than eukaryotes. If memory serves, a single 70S prokaryotic ribosome can incorporate around 20 amino acids per second, whereas the 80S eukaryotic counterpart is much slower, at around 2 amino acids per second. Is the reason for this known? The only possibility I can think of is that prokaryotic mRNAs are often polycistronic, whereas eukaryotic mRNAs are not and tend to involve co-translational protein folding. Slower translation may be able to improve folding accuracy. Other than that, I can't think of any reason the 80S ribosome would be physically slower than the 70S ribosome. It's not like DNA replication where accuracy is exceedingly more important in multicellular organisms than in fast-replicating unicellular prokaryotes.

I have made some minor corrections to your post. Ribosomes do not pump out amino acids, they form peptide bonds between them. (If they pump out anythng it is proteins.) Proteins cannot be polycistronic, only mRNAs or transcription units. There are poly-proteins, but mainly in eukaryotic viruses like polio. Your suggestion about folding is difficult to understand. Prokaryotic proteins are folded co-translationally just as eukaryotic ones are.

Transcription speed also varies across species. http://book.bionumbers.org/wp-content/uploads/2014/08/540-t1-ErrorRateInTranscriptionAndTranslation-1.png.

Unless the poster can cite more recent papers to support the assertion regarding a difference in rates of prokaryotic and eukaryotic protein synthesis, I would say that this is incorrect.
Lacroute and Stent (1968) reported a rate of 15 amino acids per sec for β-galactosidase in Escherichia coli, whereas Knopf and Lamfrom (1965) reported a rate of 7 amino acids per sec for globin chains in rabbit reticulocytes. This does not appear much different to me, especially as a recent study by Li et al. (2014) showed that the rate of protein synthesis varies with the complexity of the assembly (if any) into which a protein is incorporated.

My assertion mainly came from memory, and was reinforced by a quick search that showed a Quora question asking the same thing. Perhaps my memory was just mistaken!

I can imagine circumstances (growth on rich medium) where bacterial protein synthesis is faster, and I need to comb through the suplementary material in the Li paper to see if I can find an update on the 60s figures. When I've done that I'll post an addendum, also discussing what might be rate-limiting for translation.


text:
book on human sexuality evolution
i am interested in Lynn Margulis' book Mystery Dance: On the Evolution of Human Sexuality.
i don't find it in libraries and it's too old and i am too poor for paying 20 euros for a 1991 book.
Does anybody know a more modern book about human sexuality evolution?

Perhaps The Evolution of Desire by David M. Buss. I haven't read it myself (yet), but I've had it recommended.

Wild connection by Jennifer Verdolin is good, it shows the source of many of humanities sexual behaviors, but it really depends on what you are looking for is there a specific area you are trying to learn about?
The Third chimpanzee might interest you, it compares human behavior to the other chimpanzee species, sex is only a small part but it is there.
I a can warn you against a book I used to like,sperm wars by Baker, A lot of the research is his own and there have been a lot of issues with people being unable to replicate many of them, so a lot of it untrustworthy, which is a shame because I really liked his writing style.


text:
Is there gas exchange in the fingers?
I saw A documentary many years ago that said that hemoglobin will take in O2 in the fingers and toes. I have Not been able to find any information on this. But it would seem that being so close to the surface some gas exchange would occur, and more so in the fingers and toes than the teunk.

At first I was skeptical about this question but then I did some researching and apparently, a certain amount of oxygen is indeed taken up from the surroundings through the upper layers of our skin. In fact, the paper titled "The cutaneous uptake of atmospheric oxygen contributes significantly to the oxygen supply of human dermis and epidermis. states that

the upper skin layers to a depth of of 0.25-0.40 mm are almost
  exclusively supplied by external oxygen, whereas the oxygen transport
  of the blood has a minor influence.

Here is another paper that you would find interesting. In short, I would say that its not just the fingers but O2 diffusion into cells take place over the whole body.


text:
Different kind of M13 primer
I m looking for universal primers M13. I found different version. For instance :

M13 (-21) Forward TGTAAAACGACGGCCAGT
M13 (-40) GTTTTCCCAGTCACGAC

What's the meaning of (-21) and (-40 )

This dates back to the 1980's when these M13 primers were first cloned.
Heidecker G, Messing J, Gronenborn B. 1980. A versatile primer for DNA sequencing in the M13mp2 cloning system. Gene 10(1):69-73.
In this paper, they discuss the construction of a primer for sequencing of the M13mp2 phage vector. An EcoRI/AluI digest releases a 92 bp fragment from a portion of the lac operon. This fragment contains what are now called the M13 forward -21 and -40 primers. I do not know who first named these primers but, counting from the centre of the EcoRI palindrome, I think it's clear where these names came from:


text:
How does the "giant mosquito", Psorophora ciliata manifest it's "aggresive and vicious" behavior?
On Psorophora ciliata Wikipedia states:

Not only are these mosquitoes vicious and aggressive towards humans
and other animals as adults but, P. ciliata larvae are known for
preying on other mosquito species' larvae and even tadpoles. [2]

Emphasis mine.
Now every mosquito is kinda aggressive by drinking your blood and being generally annoying. So what makes Psorophora ciliata especially aggressive? Does it scream expletives or what does it do?

The key is "toward humans". There are so many species of mosquito, and many of them prefer other animals to feed upon. I also suspect that the Wikipedia article may have been a bit hyperbolic. My guess is that it just has a strong preference for humans. I'd put this in the answer box, but I am really just guessing.

@KarlKjer Yeah, I was also suspicious about the statement on wikipedia. But that's why I asked. Those mosquitoes have attracted some media attention, so I'm hoping some real research was done. If the statement on wikipedia is proven inflated by some scientific research we can edit it.


text:
Why people don't harvest Locusts when infestation happeds?
We've heard about tremendous amount of money losses even leading to famine due to crop destruction from locust infestation over and over again, but all these grasshoppers are a valuable protein, probably way more valuable than the destroyed crops. Although most people from many cultures won't eat such insects, these can be ground to flour and stored to be fed to omnivore livestock like pigs or sold for profit or exchanged for grains.
Is there edible energy in the insect swarms? Can this be made into livestock feed? If not, is the reason this isn't common practice biological or economical?

The problem, Nigel, is that crops can be stored for months, whereas locusts are a mostly perishable food.

I don't think so. Dry proteins for commercial use can be stored for quite some time. Also after some research, it turns out that Meat and bone meal (MBM) has a shelf life of 12 months. Furthermore, there is a ton of consumable insects sold online vacuum-packed and cooked. And to top all this we live in a global economy where it won't matter anyway.

You have made my point for me. What you propose is much costlier than harvesting wheat, which needs very little by way of processing after harvesting. :) A global economy might not be an inconvenience to you, but to the farmers whose crops are consumed by locusts, I imagine they could hardly care less about global economies.

Locusts have been harvested in Thailand and Australia they call them sky-prawns. They deep-fry them and consume them happily.
http://www.bugsfeed.com/locust
http://www.fao.org/docrep/017/i3246e/i3246e.pdf
In Thailand Orthoptera or
grasshoppers include Patanga succincta,
Locusta migratoria, Acrida sp.,
Cyrtacanthacris tatarica and Oxya
japonica japonica (Thunb.)
(Hanboonsong et al. 2001; RaƩ anapan
2000). All of them are pests of
economic crops such as maize and
rice. Grasshopper species, parƟ cularly
Patanga succincta and Locusta
migratoria, used to be one of the
major pests of maize and rice. Today
they have become one of the most
popular edible insects since they were
introduced for human consumpƟ on
by entomologists − a campaign to eat
grasshoppers had been launched
because control efforts had been
unsuccessful. For example, in 1983
this was launched by local offi cials and
villagers in Prachin Buri Province
collected more than 10 tonnes for use
as food (Lewvanich et al. 1999).*


text:
Can cancer cells transmit from one organism to another?
I know cancer cells are very resilient, so would it be possible for them to survive outside of the original organism for long enough to be absorbed by another? Furthermore, would that type of "infection" be possible?

Yes. Devil facial tumour disease is an example:
https://en.wikipedia.org/wiki/Devil_facial_tumour_disease
Look here for other examples of transmissible cancers.
I have not heard of any human transmissible cancer.


text:
Can I kill bacteria with distilled water?
Given that bacteria are hypertonic (contain more salts) compared to distilled water, and that they rely on ion concentration differences across the plasma membrane to survive, can I kill a bacterial solution by adding an excessive amount of distilled water to make them explode? If I add distilled water on a surface, are the bacteria on it going to die?

Counter question: If you think this is so easy, why are surface disinfectants used instead of water?

maybe because disinfectants have a wider spectrum of species that they can kill? maybe distilled water would kill some species but not all? I don't know. I would like an explanation of why then distilled water is not used as a disinfectant.

In addition to @Superbest's answer, distilled water does not remain 'distilled water' from the moment it touches a washcloth, sponge, surface, etc. You would need to literally flood your counters with the stuff to do any disinfecting, and at that rate, probably anything you use (e.g. tap water) might be just as effective.

@Chris: this is the kind of answer/comment which shuts down interest and research. "Because" comes just below in the rank. And then "Don't ask stupid questions".

@WoJ: There are four types of answers, and counter-question is one of them.

@MartinKlvana: sure, but it does not help when someone does not know the subject. If you ask me "Can we have smaller particle accelerators?", to what I say "if this was that easy we would not have built CERN", does this helps you? And - more importantly - does this gives you food for thought? Saying "we could, but because of this and that it is not easy/feasible". This is an answer which is helpful.

Indeed, bacteria are susceptible to osmotic stress from being in pure water. They are also susceptible to starvation in such an environment.
However, wild bacteria tend to have many mechanisms that protect against this and allow them to survive in spite of being exposed to water. Note, also, that freshwater can serve as a habitat for many species of bacteria: Consider ponds, streams, lakes, etc.
Thus bacteria which you encounter in everyday life will likely have been those that survived osmotic stress in the first place. And drying, and mild disinfectants, and sunlight, and temperature variation... So it is unlikely that water alone will kill them.
Here is a recent article on this topic: http://jgp.rupress.org/content/early/2015/04/07/jgp.201411296.short
And here's one about how osmotic stress affects susceptibility to other antibacterial effects: https://www.sciencedirect.com/science/article/pii/S0740002014001890


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Can someone identify this Brazilian bird?
Photographing and documenting the local fauna (Brasília, DF, Brazil - Near Coordinates [-15.696506 -47.860013]), I found this rather unusual-looking bird whose name I couldn't find:

(Image was now uploaded to Wikimedia under my account "AlephGuira")
Possibly useful information:

One was seen preying on
what looked like Taturanas (https://en.wikipedia.org/wiki/Lonomia), but due to their venomous nature, I'm not sure.
The observed flock was composed of 7 birds.
There seems to be sexual dimorphism (The other one, not pictured, seems to be smaller, has shorter head feathers, whiter wings and lacks the orange-pointed beak).
They were first seen on a Pequi Tree (https://en.wikipedia.org/wiki/Caryocar_brasiliense).

These look very similar to the Guira cuckoo (Guira guira) which are found in this part of Brazil.

Source: https://en.wikipedia.org/wiki/Guira_cuckoo


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Peach pits with two seeds: Are the seeds identical twins?
I have Prunus persica peach pits that have two seeds.
My question is simple:
Do the seeds have the same DNA? (are they identical twins?)

For what it's worth, this seems to be happening in about 1-5% of my peach pits.

Polyembryony occurs when a single fertilized egg produces more than 1 embryo. This is the process that produces genetically identical twins.
Although polyembryony is common in some plants, I found limited information about polyembryony in peaches. I decided to broaden my search into drupes more generally. Drupes or "stone fruits" are the fruits with a fleshy outside (exocarp and mesocarp) and a hard inner shell (endocarp) around typically a single seed. Peaches are part of this category, as are almonds (the almond itself is the inner seed), cherries, and coffee.
The best citations I found reach back into history a bit.
From Webber, J. M. (1940). Polyembryony. The Botanical Review, 6(11), 575-598.:

Cases of the first class of false polyembryony
  commonly occur in such drupes as almonds, plums and peaches.
  Although these drupes normally have a single seed within the hard
  seed-like endocarp, sometimes two or even three are found. ' During
  formation, each of the plural seeds develops from a separate
  ovule, provided with a separate funiculus and micropyle. Similar
  cases of such false polyembryony have recently been reported in
  Coffea (63) and Sandoricum (47, 49).

This passage would suggest that most likely what you are observing is false polyembryony. Immediately prior to this passage, the "first class" refers to:

those in which more than one ovule develops in a normally 1-ovulate seed-like structure or locule

as contrasted with the second type:

occasionally two of the developing ovules unite to form what appears to be a single composite ovule.

Another source, Zdruikovskaya-Rikhter, A. I. (1970). The phenomenon of polyembryony in the peach. Tr. Nikitsk. botan. sad, 46, 173-177. is in Russian and only available to me in abstract form in English. The abstract reads:

In a number of varieties, two and sometimes three megaspores were functional, giving rise to several embryo sacs. On fertilization, embryos develop in these, causing the phenomenon of pseudopolyembryony.

Therefore this source seems to agree with the first.
However, a more recent paper Martínez-Gómez, P., & Gradziel, T. M. (2003). Sexual polyembryony in almond. Sexual plant reproduction, 16(3), 135-139., focused on almonds, suggests that certain almond cultivars are prone to true polyembryony, though it seems like the additional seeds are often a bit stunted and have high mortality. They also reference a paper purporting to mention polyembryony in peach, Toyama, T. K. (1974). Haploidy in peach. HortScience, 9, 187-188., though I cannot find this article in anything but Japanese - the title, however, suggests that these may be haploid polyembryos, which also occur with the almonds - these are indeed from division of the same embryo, but because they are haploid they would not actually be genetically identical, since each is taking half of the diploid chromosomes.
With only these limited descriptions to go by, which seem to be mostly observational rather than backed by any systematic study, I would hesitantly conclude that most likely what you are seeing is a fruit in which two separate ovules developed together, and therefore could be as genetically different as any two different peaches from the same tree. True polyembryos seem to be possible in stone fruits, but as a mostly rare occurrence that is only common in particular strains - when it does occur, it may be via haploidy, which means the seeds will still be genetically distinct.

Paging @CowperKettle if you have anything to add from the Russian source in my answer here - I'd be particularly interested if they have anything to say on the incidence of polyembryony and if they distinguish between true polyembryony and pseudopolyembryony.

Great answer! I was looking for an answer to this question, but I didn't know the term "polyembryony" and I couldn't find anything. Now I know, thanks!

An answer provided by Washington State University:

Peach is self-pollinated.  The actual characteristic part of the fruit
  that we eat is from maternal tissue but the seed inside the pit
  results from the sexual recombination that occurs following
  pollination and fertilization.  Technically, I would not think it to
  be a “clone”.  Even in the rare case when a double flower forms and
  when both pistils are viable and fertilized ovules result, the seed
  would have both maternal and paternal DNA and sexual recombination
  could expect to result in different progeny.
An interesting example of a seeded fruit where the seed are effective
  clones can occur with citrus and it is called “nucellar embryony”.
  These seeds are of maternal origin (nonzygotic) only and, if
  germinated, they will be clones of the mother.

Of course they are.
They're both from the same peach, so they both have identical DNA. It's like when a mother has twins or triplets, all of the babies will have the same genetic code, since they all came from the same egg. So if there are two cores in a peach, since the peach and both of it's cores are from the same tree, both cores will have identical DNA. :)

Please look up the meaning of genetic code. Also, did you never meet a twin couple made up of a make and a female?https://www.healthychildren.org/English/family-life/family-dynamics/Pages/The-Difference-Between-Identical-and-Fraternal-Twins.aspx


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Why does decreasing ion channel density result in an action potential not firing?
I'm pretty confused, when i run a simulation of an action potential reducing the sodium and potassium channel densities gradually over time results in an action potential not being fired, and when i only reduce sodium channel density it stops the action potential from firing even faster. My question is why? what role does density have in firing an action potential?

It is very straightforward. More the density of sodium channels, more the influx of sodium ions. More the influx of sodium ions, more the depolarization. If there are sufficient sodium channels, then the large influx of sodium ions will cause membrane depolarization above the threshold value, thus resulting in firing. If the density of channel is reduced, the depolarization value will not cross the threshold. Thus causing a net change in membrane potential, but not firing.
Potassium channel acts in coordination with sodium channel. Only if there is an influx of positive sodium ions into the cell, potassium channel will act and release potassium ions outside the cell in order to maintain the membrane potential. If sodium channel is reduced, no further processes happen, thus no firing.

Actually, the depolarization can still cross the threshold given sufficient synaptic input even with a reduced sodium channel density.
Also, in the case where only sodium channel density is reduced, the rate of sodium influx will be lower than the rate of potassium outflux and hence action potentials will be harder to produce


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Virus immunity from animal to humans
There are number of virus which have animal as reservior and jump to human to cause disease. Why dont we use antibodies of animal to cure humans?
Like rabies in bats.

I think you're asking why don't we take antibodies from previously-infected host animals and treat humans with them. In principle, that could work, but it's impractical as you describe it. You give the example of "rabies in bats". Imagine trying to get enough blood from a 25-gram bat to treat a single person. Farming bats is hardly practical, and if you're bleeding wild bats, you're probably collecting both known and unknown viruses that you're then injecting into your patient. So this is completely impractical with wild animals, which are the donors of most of the diseases in question.
However, there's nothing magical about the antibodies from the original wild animal. (This seems to be widely misunderstood, probably from movies that make medically idiotic and impossible claims.) Any antibody can be potentially valuable for treatment, whether it comes from the original host or not, and whether it comes from the live pathogen or from a vaccine made from the pathogen.
So a more practical approach is to infect a large, easily-handled domestic animal with the pathogen in question; or better yet, with a vaccine made from killed pathogens, so there's no risk of the animal getting sick or or infecting your patient. This used to be done with rabies, in fact, using equine hyper-immune serum to treat rabies patients (Production of hyperimmune antirabies serum in horses).
However, there are major problems even with this approach. It's difficult, it means keeping large numbers of large and potentially uncooperative animals around for long period, etc. Here is a WHO document reviewing some of the problems with this approach.
A third approach is to make monoclonal antibodies. This is the most popular approach now; it lets you make sterile, safe antibodies with completely defined characteristics, with minimal risk of contamination, under controlled conditions.
There are many monoclonal antibodies out there that are used in modern medicine, including some that are used to treat pathogens. However, it's worth pointing out that antibodies are not magical panaceas; they're often much less effective than conventional antibiotic or antivirals and are often more expensive and less practical to use.


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Relation between OD with different microbial growth
Equal volumes of cell suspensions of Escherichia coli, Saccharomyces cerevisiae, Streptococcus lactis and Mycoplasma pneumoniae, all have the same OD600nm = 0.50. Which cell suspension would have the minimum and maximum number of cells, respectively?

Welcome to Bio.SE! What efforts did you make to answer this homework assignment? If you can't provide them, I'm afraid your question will be downvoted and closed. (see https://biology.stackexchange.com/help/homework)

Difficult to say with the information you have given. Here is a paper on the subject if you are interested. The relationship between OD and cell count depends on morphology and size, which in turn depend on culture condition, strain, etc...

Based on size, and if this is a homework question, you might expect yeast to be the largest and Mycoplasma to be the smallest.


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Is it fine to state every learned behavior has an innate component ? ie. Behavior X is largely/ mostly laerned with an innate component
For example human acquisition of language, can we say it is learned, but has an innate component -- because there is a particular structure of the tongue, and perhaps also a specific cognitive ability which is requisite to speaking/ learning a language.
The aforementioned requisites are ones which are reliant on genetics, thus can we say there are innate components to it, even though it is largely, based on experience, as stated in the assertion below.
"The behavior of language acquisition is based on experience, and subject to continual refinement and therefore can be classified as largely learned, however, due to the requisites it also has an innate component to it"

Think of a cake. Is a cake determined by its ingredients or by its preparation (mixing, baking, etc)? It's a meaningless question. The cake is determined by both.
Now think of two cakes. In principal, we can now begin to talk about the causes of their differences. For example, if they had identical ingredients but were prepared differently, then we could say that the differences in the resulting cakes were due to different preparation.
Humans are baked cakes. Quantitative genetics is a field which tries to estimate to which extend differences between organisms are due to genetic factors. Learned behaviors are consistently found to be heritable in quantitative genetics studies. For example, adult vocabulary size is substantially heritable. It is not that the words are literally transmitted to the offspring, but rather genes that influence the cognitive abilities, interests and personality of the individual. That vocabulary size is "heritable" means that a substantial portion of the differences between individuals' vocabulary sizes are due to genetic differences (although by no means only due to genetic differences).
In short, what I'm trying to get at, is that you can only talk about the relative contributions of genes and environment if you're talking about it in the context of differences between individuals. In that case, yes, learned behaviors have an innate component.

Re: vocabulary size being heritable, In the child psychiatry literature, shared environment accounts for the largest component of the variability in vocabulary size, followed by unique environment, then genetic factors. This is seen in English and Chinese.  Where do you see data that "vocabulary size is substantially heritable"?

@DanHall Nope. Shared environment accounts for nearly nothing in vocabulary size. (Once the person is entering adulthood.)

can you share your data?

@DanHall For example, vocabulary tests are well known to load fairly highly on g, and it's well known that g has little shared environmental influence. But there are also studies that directly estimate heritability in vocabulary, see for example (van der Berg, Posthuma, Boomsma: A Longitudinal Genetic Study of Vocabulary Knowledge in Adults).

Are there in fact any (practically reachable) limits on vocabulary size?  Personally, I have a good vocabulary in English (including Shakespearean and a good bit of Middle English), the technical jargon of several disciplines, and a reasonable bit of several other languages, yet previously-learned vocabulary doesn't seem to disappear when I add new.  So where is the heritability?

@jamesqf Can you clarify more precisely what you want answered? Perhaps you have some misunderstanding of what heritability means. More likely, I simply don't understand what exactly you're asking.

@Eff: What I'm asking is how it's possible for vocabulary size to be inherited, when 1) So much of one's vocabulary depends on environment - learning another language or the jargon of a profession demands a large increase in vocabulary; and 2) The practical limit on the size of vocabulary seems to be the amount of time one has to learn.  Within that constrant it seems to be limitless.

@jamesqf As for your (2), you can simply control for age if you wish. Whether vocabulary is limitless, perhaps it will help to think in percentiles. For example, a person may have a vocabulary in the 85th percentile (of a particular population in question). Yes, it is possible for a person to suddenly gain a huge boost in vocabulary for whatever reason. However, when you look at population level, there will almost certainly be fairly high stability in a statistical sense. Rank order people, then test them later again. The rank orders will correlate substantially (not perfectly, obviously).

@jamesqf For your first point that so much of vocabulary being environmental. Well, that has to be tested before you know that. The main goal of the entire field of quantitative genetics is to estimate to which extend differences within a population are due to genetic differences of any sort or environmental differences of any sort. For example, the study I referenced in a previous comment estimated that >50% of variance is explained by genetic differences. This means that genetics matter, but since it is not 100%, the environment clearly matters as well.

@jamesqf How can vocabulary size be (partly) heritable? The reason is, that while external factors may have an influence on vocabulary, so does individual factors. How good is the person's memory? How much does the person read? How interested is the person in learning new things, and how easily does the individual learn? Etc. All of these things are influenced by the individual's psychology and brain. And genes are important for the creation of the brain.

@ Eff: The problem is that all of those are so strongly affected by environment and personal choice that teasing out any heritable effect seems impossible.  A heritable factor would have to affect the POTENTIAL vocabulary size, not actual (since that is so strongly a product of environment), and again, the potential size seems effectively unlimited.

@jamesqf "A heritable factor would have to affect the POTENTIAL vocabulary size, not actual..." No. I strongly advise you to look up what heritability actually means in the field quantitative genetics. What I am saying is completely mainstream science. However, here is a fact that you may find interesting. Identical twins who are separated at birth have more similar verbal abilities in adulthood than non-related adoptives who were reared together in the exact same family and went to the same school and had same teachers. Just because you think it is impossible, that doesn't mean it is.


text:
A doubt in biotech question
Which type of gene does not occur naturally in living organisms?

Bt gene
Endogenous cytoplasmic defense gene

The answer is 2.
I can't find out what this gene is! Does it mean the gene for methylation and restriction enzyme synthesis or some such thing? Does it even exist?
P.s. I am just a student and do not have in-depth knowledge of biotech.

where does this question come from? "Bt gene" seems to have something to do with transgenic corn https://entomology.ca.uky.edu/ef130

Endogenous just means that it is naturally occurring in the organism:
http://www.dictionary.com/browse/endogenous
endogenous cytoplasmic defense gene is a general description of a gene that is cytoplasmic and whose function is defending the organism. There isn't THE Endogenous cytoplasmic defense gene. There are many endogenous cytoplasmic defense genes. Note that it is the protein coded in the gene that is cytoplasmic, not the gene itself. It should say 'gene for endogenous cytoplasmic defense protein'.

Cytoplasmic gene means plasmid and stuff?

Why is the answer that if it does occur in organisms?


text:
Does anybody know what kind of snake is this?
FYI the snake is dead and currently in my freezer, I got it from a guy and forgot to ask what kind it is.

Can you please edit your question and add the location where this snake was found?

I am from Czech Republic, but the snake is definitely exotic, it was a pet.

Is it pictured with the head upside down?

I need a better picture. thaw it, put it in some kind of position so that I can see the back,and give me a length measurement.At least.

This is Orthriophis taeniurus ridleyi, a synonym is Elaphe taeniura. It has a few common names,some are  Ridley's beauty snake,Cave beauty and Cave racer.
https://www.biolib.cz/en/taxon/id310150/
https://www.naturepl.com/search?s=orthriophis+taeniurus+ridleyi2581
https://www.zootierliste.de/en/?klasse=3&ordnung=305&familie=30513&art=21102660
https://www.thainationalparks.com/species/orthriophis-taeniurus
https://en.wikipedia.org/wiki/Beauty_rat_snake
https://www.reptarium.cz/en/taxonomy/Orthriophis-taeniurus/2581


text:
What's the ratio of saturated to unsaturated fatty acids in human cell membrane?
It's well established that the fluidity of a cell is largely dependent upon the ratio of saturated to unsaturated fatty acids that exist within the membrane, but, what exactly are the values for this ratio?
Given that cells maintain a constant degree of fluidity (assuming constant environmental conditions), I would think this ratio could be properly defined.
I've tried looking through several molecular biology books and I Googled for about 30 minutes, but nothing..
Can anyone provide this ratio, or, explain why it's not obtainable?

This paper provides some data for rats.

i never use Google for specific scientific queries. i always use PubMed: https://www.ncbi.nlm.nih.gov/pubmed

@MartinKlvana Google scholar is a very good alternative to PubMed.


text:
Why there is no fluorescent light from my DAPI-stained Hibiscus Rosa Sinensis Pollen?
I currently work with fluorescence microscope to observe generative and vegetative cells within hibiscus rosa sinensis pollen. I used DAPI to stain pollens but there is no light that indicate the existence of both generative and vegetative cells. I simply stained the pollens with 50 ppb DAPI without other procedure. I have referred this steps from Sexual Plant Reproduction textbook from Cresti and Tiezzi, here is the link : le.ac.uk/bl/phh4/openpubs/SPR_HH_pollen_stigma_crestiLR.pdf. From the book, it simply states "For DAPI staining, fresh or fixed pollen is stained on a slide in a drop of 0.005% DAPI (diamidinophenylindole), and the nuclei observed under a fluorescent microscope after 5-30 min (UV excitation, blue DAPI fluorescence).
The result is make me confused because there was no fluorescent light but only reflected light by pollen itself.
I will be very glad if anyone can suggests me what should i do or highlights an error in my steps.

What do you see after the staining? No light at all? How DAPI staining should allow you to distinguish between generative and vegetative cells?

I saw light, certainly. But the light is light that was reflected by an object, not from the fluorescence phenomenon. I am not sure that DAPI can distinguish or make a different look for generative and vegetative cells because DAPI is only a compound that bind the A-T rich region and make the objects that were bounded by it able to emit a light due to fluorescence, not react specifically with generative or vegetative cells and make some different features (or another) between them. cmiiw.

So apparently the problem is that the staining itself didn't work at all. Probably the DAPI didn't penetrate in the cells. Did you solubilized the cell wall somehow? Can you detail all the procedure you followed prior to DAPI staining?

Yes sure, I did it very simple (according to my reference (the textbook that i mentioned before) and suggestion from my lecturer). I just poured the pollens from the Hibiscus r. anther above the aquabidest at specimen glass,  then dropped 50 ppb of DAPI above it and cover it with coverglass. And i think i miss the step of solubilizing the cell wall. Would you mind telling me how the protocol that should I do to solubilizing the cell wall of Hibiscus pollen? Or there is any reference that i can refer to do that?

Actually, this is only a step that my lecturer suggests to check whether or not my DAPI still viable to emit a fluorescence light. The core of my research is to staining a chromosomes with DAPI and observe its image under the microscope using a photonics jet phenomenon.

Could you add the protocol you followed in your question? It gives useful insight on what you did. Also, the textbook reference as it is now is not that useful; can you find a link redirecting to the part you're citing?

I got the ebook for book that i mentioned from here : https://www.le.ac.uk/bl/phh4/openpubs/SPR_HH_pollen_stigma_crestiLR.pdf, it simply says, "For DAPI staining, fresh or fixed pollen is stained on a slide in a
drop of 0.005% DAPI (diamidinophenylindole), and the nuclei observed
under a fluorescent microscope after 5-30 min (UV excitation, blue
DAPI fluorescence)."

Ok, edit your question with all the new information you provided in the comments.

@LinuxBlanket ok i have edited it. Would you mind to telling me the procedure to solubilize pollen wall so the DAPI can penetrate and stain both generative and vegetative cells? Thanks


text:
What is a genome?
By genome do we mean a consensus sequence of DNA or a set of sequences that ideally captures all possible variations?

Like with everything, people mean different things in different contexts when talking about the genome.
You can see this in different levels:

genome of a cell: the entire genetic material contained within a cell
genome of an organism: the entire genetic material contained in an organism. For an multicellular organism, this could refer to the average genome between cells. However, technology does not allow us to access this average of all cells. In more practical situations, this could refer to the reconstructed genome taken from cells in the mouth or blood.
genome of a species: the genome of an individual taken to be representative of a species. In more practical terms, this can be the genome of an individual that was captured and sequenced by humans. In the case of humans, several individuals donated their DNA towards the sequencing of THE human genome
metagenome of an environment: the set of genetic information found in an environment, e.g. the metagenome of a human intestine, the metagenome of a river, etc.

Graph genomes are on the rise for species genomes and they will allow for the inclusion of genetic variability between individuals.


text:
Scanning Electron Microscope images of wheat grains
I took SEM images of wheat grains but I see some granular particles on its surface and I don't understand what they are?

Is it some kind of deformation of the bran layer due to drying? Or is it the gold-palladium alloy coating which is done for SEM analysis of non-metals?


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Simplest known form of aerobic glycolysis
What is the simplest known way that an organism performs aerobic glycolysis? In other words, what is the simplest known way known to convert glucose into $\ce{H2O}$ and $\ce{CO2}$, other than by burning it?
In general, the (relatively conserved) pathway is glycolysis $\ce{->}$ pyruvate decarboxylation $\ce{->}$ citric acid cycle $\ce{->}$ oxidative phosphorylation, but perhaps there exist simpler pathways with possibly a lower energy yield.
I am interested in a way to convert glucose into water and carbon dioxide under (near-)physiological conditions, with a reaction timeframe of 12 hours, give or take. Specifically, I'd like to get rid of sugar as tidily as possible, disregarding energetic benefits. In that sense, I am interested in the (bio-)chemistries of organisms, not in the energy yield.
I am aware, of course, that sugar is used as an energy source by organisms, and they generally want to accumulate it, or at least, decompose it as efficiently as possible. It may well be that the "shortcut" I'm looking for is not known.
Several publications sort of address this topic, but I haven't found a fitting answer so far. In fact, the closest research to what I'm looking for I've found is a publication from 1931 by Degering and Upson; they describe iron pyrophosphate as a catalyst for sugar oxidation. However, they work with far higher reaction times (up to about 3 weeks) and somewhat high temperatures (around 40-90 °C as opposed to 0-35 °C) than I'd like.
I've also tried looking for shortcuts within the pathways using KEGG database. Glucose is COMPOUND C00031 and is referenced in 32 pathways; I've looked at the Glycolysis pathway (map00010) and have found no pathway other than the generally known one.

Do you know why organisms converting glucose to carbon dioxide and water? It is unclear whether you do and what precisely you are asking. Do you think it is an end in itself? Why are you interested in aerobic glycolysis rather than anaerobic? Are you interested in energy yield or the varieties of chemistries in organisms? What do you mean by ‘efficient’? Have you consulted any of the numerous articles on glycolysis? Please clarify your question.

@David Thank you for your valuable remarks; I have edited the post to cover all your questions. Hopefully, it makes more sense now.

@David I see from your profile that you are also competent in the field of Bioinformatics, very nice! I will add some more info on what I've tried, then.

Protists are the thing. Not my field, but I found this review in following up a question (since closed) recently.


text:
How do special NK cells get to the uterus?
When an embryo is creating a placenta in the uterus, some special kinds of Natural killers cell of the mother will move and gather towards this placenta (for exmaple for growth components increasing blood of the placenta). But how do these NK cells know where to go....do they kind of 'smell' the uterus?

They are attracted via chemokines, which are molecules that NK cells sense and move towards the increased chemical gradient.


text:
Carbohydrate diet and dental health
I read that human started carbohydrates rich diet after adopting agriculture before that meat was main energy source which has comparatively less carbohydrate. High carbohydrate started destroying human teeth.
Would a keto diet (high protein fat) diet and low carb diet reduce cavity in teeth?

Where's your reference for the claim?

@GrahamChiu http://www.businessinsider.com/growing-crops-human-cavities-increase-2016-3     there are plenty other sources on google

Please run an English spelling check (and preferably a grammar check too) before posting. They come free on web browsers. You should at least check that the five words of your title are spelled correctly. And pay heed to @GrahamChiu. You need to cite your sources for assertions in your question. It is not enough to say there are plenty on Google (by which I assume you mean the web). If you cite them we can judge their quality. Are they papers in a peer-reviewed journal or just quack health site?


text:
PCR efficiency or DNA yield with single primer
How to calculate number of DNA molecules synthesized after 'n' no. cycles with single primer (either only forward primer or reverse primer)? Is there any formula to calculate the DNA yield after such PCR?
Supposing, I am setting a PCR reaction for 100 template DNA molecules for 30 cycles, with only one primer - forward primer for target gene. How many DNA molecules will be generated at the end of 30 cycles. All other conditions remain the same.
Thanks.

Technically, if you use only 1 primer, it will not be PCR anymore.
But that's what gonna happen if you have 100 template DNA molecules (made of strand A and complimentary strand B) and abundance of primer (say, 10x, or 1000 molecules):

At first cycle primers will bind to template DNA, but only to one strand (for example, A)
DNA polymerase will extend those primers, creating complimentary strands B'. Some strands B' will be shorter than template because DNA pol is not perfect
DNA-primer complex will melt at the beginning of cycle 2
At the beginning of cycle 2 primer molecules will again bind to template, again to strands A, and process continues

Since there is no step where strand A is being copied, this process will be linear, not a "chain reaction". At each cycle you will get the same amount of strands B'.
It is hard to say how much B' molecules you will get at each cycle, but at the end of 30 cycles, it will be at best 30x of the first cycle. Remember, though, that DNA polymerase degrades, and cycle 30 will be less efficient than cycle 1.
Assuming perfect polymerase, and that extension time is long enough, you will get 100 strands B' on cycle 1, 100 strands B' on cycle 2 and so on. At the end of 30 cycles you will have 30x100 strands B', and 100 strands A and 100 strands B.