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Where can I find the common names for the zoology taxonomy?
Forgive me if my question does not belong here or if I'm using incorrect terms, but I'm not educated in biology at all. I'm investigating the workings of the biological classification system.
I was wondering if there is a list somewhere of all kingdoms, orders, classes, etc., both in Latin and common names?

That list is called Wikipedia. ;-) … Seriously, (almost?) all Wikipedia articles on animals carry both the common and the scientific name.

True, and in fact Wikipedia is my source, but I'm looking for a more convenient format, a list on a single page.

The Tree of Life project has a browse-able tree of all major taxa, but not necessarily all species. You can start at the root of the tree here. Tree of life uses modern phylogenetic nomenclature rather than more traditional Kingdom-Phylum-Class-etc.
Part of the problem that you will run into is that common names differ across regions/countries/languages. This is the point of species binomials. They are language-invariant.

Thanks, thats a very useful site. The information there is largely what I need, I only require english common names. The format isn't ideal for my purposes but I'll find a way to parse it.

Wikispecies might help with common names: http://species.wikimedia.org/wiki/Main_Page

EOL has large collections of common names, and a pretty comprehensive API which should be able to access them somehow (I haven't tried specifically downloading commons name before, though, so I can't promise that it'd work). If you need a list locally, ITIS has downloadable pipe-delimited files containing scientific names and common names (although you'd need to do the mapping yourself). Hope that helps!

EOL gets some of their common names from uBio, which exists explicitly to serve names. I don't know how their API is compared to EOL, but it would be worth checking out.

Kingdoms
The UK accepted system has five kingdoms, for some it's hard to describe a single word common name so I hope you don't mind that I have written brief summaries too:

Animalia are multi-cellular organisms that have adaptations to allow them to move within their environment.  They have membrane bound organelle but not cell walls or chloroplasts. They must absorb nutrients by ingestion.  Common name is animals ;-)
Plantae are multi-cellular organisms that use photosynthesis to harness energy from sunlight.  Their cells contain cell walls & chloroplasts (where cells are exposed to the sun).  Common name is plants
Fungi are multi-cellular organisms with no adaptations to move independently.  They range in size from microscopic to the size of mushrooms (literally, of course).  They absorb their nutrients from their surroundings.  Common name could be mushrooms & molds
Protista are marine organisms that are eukaryotoic (have membrane bound organelles) and some can photosynthesise.  Common name could be algae
Prokaryota (a.k.a. Moneara) are single celled, with a cell wall but with no membrane bound organelles (i.e. they have no smaller 'bits' within the cell separated by a membrane).  They absorb nutrients directly across their membranes or can photosynthesise to make their own nutrients.  Common name could be said to be Bacteria.

Sources: 1, 2, 3 (for Protista)
Phyla and Below
You may wish to try the following website:
ITIS Database - enter a scientific or common name of an organism to get it's full taxonomic tree.  For example the tree for the Panthera leo (Lion).  This site also gives common names of Phylum, Class, Order & Genus - for example the lion is a member of genus Panthera ("roaring cats"). It may be slightly cumbersome but it is a way to get the info you want and is actually quite interesting once you get going, particularly if its just for your curiosity!
Additions after comments by OP
Have been hard at work, however it seems that a centralised repository is certainly elusive!  I've found some sites which go a little of the way to amalgamating scientific and common names on a single page but I'm doubtful that you will be able to get much further than Phylum without having to write a script to harvest data from sites such as ITIS

List of all Phyla for the Animalia Kingdom with common names.
As above for Kingdom Plantae
As above for Kingdom Fungi
As above for Kingdom Protista

Thanks. What you did is to describe the kingdoms in a language common people understand. That's what I'm looking for, but I'd like that kind of information for lower taxonomy levels as well, ideally in a single list. I know I can find the common names of every level using various resources (ITIS,EOL,Wikipedia), but I'm looking to automate parts of this.

@Ferdy Well I've gone back and got you as far as phylum for four of five kingdoms (apparently there is some contention over prokaryota).  I'm beginning to get the impression that the data simply doesn't exist as one long list - sorry, I tried =)


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Why is there such a long interval between ages of sexual maturity and of reproduction in female chimpanzees?
There seems to be some disagreement on the ages at which female chimpanzees typically reach sexual maturity and when they typically first give birth, but regardless, different sources seem to agree that a number of years elapse between these two milestones.
For example, this 2018 paper from Jane Goodall and colleagues found

… an average age of 11.5 years (range 8.5–13.9) at sexual maturity and 14.9 years (range 11.1–22.1) at first birth. These values exceed previously published averages for wild chimpanzees by one or more years. Even in this larger sample, age at first birth is likely underestimated due to the disproportionate number of non-dispersing females, which, on average, give birth two years earlier than dispersing females.

In humans, there is also a substantial lag between these two events, but we understand this as a very common cultural dividing point, which places the first firmly in childhood, and the second (generally/ideally) in adulthood. The maintenance of this interval is controlled by a variety of social and societal practices and institutions, across cultures.
Do we know what maintains the lag between the biological capability for reproduction and the actual first birth in chimpanzees? Presumably there is also some sort of set of social practices among chimpanzee society that maintains this. Do we know to what extent it is controlled by mature matriarchs or patriarchs, or by actions taken by the young females themselves, or some other set of behaviours?

source: Stack Exchange

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

sort: votes


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Isolating a specific gene (specifically TRAV* series of genes) for sequencing
I'm trying to figure out (for pedagogical purposes) the right way to isolate and PCR the regions coding the T-Cell receptor.
My understanding is that I would need to use restriction enzymes that target regions near the start and end of the gene. I was looking at a bunch of different restriction enzymes on this site: https://www.addgene.org/mol-bio-reference/restriction-enzymes/
What I'm not sure about is: how do you pick the combination that will specifically cut out that gene and not any of the other ones? It seems like the restriction enzymes only consist of a few base pairs, and I would guess they can slice at many many sites.
Furthermore once it is cut, how do I isolate just the DNA for the gene I want to sequence as opposed to the rest of the junk DNA?

Restriction enzymes are usually only used when you do molecular cloning using plasmids or other forms of shorter DNA moleclues, since - like you said - using them on genomic DNA would cut it into much more than thousands of pieces.
Instead what you can do is perform your PCR directly on the genomic DNA (or potentially cDNA, if you want to get rid of introns).
Doing PCR on genomic DNA is often a bit tricky (i.e. you'll likely have to try different conditions to get a product), but generally possible. If you want to analyse the whole coding region it might be better to extract mRNA instead of DNA and reverse transcribe it, so that can amplify the coding region as one block, that doesn't contain Introns - PCR on cDNA is also easier than on genomic DNA.
Another thing you need to look out for is that T-Cell-Receptors (similar to antibodies) are different in every T-Cell. This means that you can't use Sanger sequencing, which will only give you a proper result if you input has the exact same sequence. To get the sequences of a mix of T-cells you would need to use next-gen sequencing.

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


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How are fragments isolated during shotgun Sanger sequencing?
For a large genome (say millions of base pairs) -- we split the genome into fragments < 1000bp that are sequenced and can then be put back together computationally.
My understanding is you use some sort of shearing technique to get the DNA into fragments as in: https://en.wikipedia.org/wiki/DNA_fragmentation
Now you have a vat full of random fragments -- how do you sanger sequence these?
From what I can tell if you took the solution with the sheared DNA and ran sanger sequencing you'd get a bunch mixed of fragments mixed together resulting in a lot of noise ... you'd basically get all the runs averaged together. Don't you need to isolate each fragment before running Sanger sequencing?
How is this done?

In the original method, one would clone all of the resulting fragments into a suitable vector, and transform the collection into a bacterial host, to create a so-called library.  By plating the library clones under appropriate conditions you would have a collection of so-called clones, and each clone would be randomly selected and sequenced using the Sanger technique.

So if I understand correctly: Step 1: inject the fragmented plasmids into vectors. Step 2: Pick out an individual vector (e.g a single e-coli) and put it on a petri dish (this represents a single fragment) Step 3: Allow the individual vector to replicate (and thus replicate your fragment) Step 4: Take the culture of vectors, lyse the cells and extract the DNA. Step 5: Run Sanger sequencing

Step 0: Prepare double-stranded DNA cloning vector (usually a circular DNA Plasmid) by digesting, or cutting, it with a site-specific type II restriction enzyme, or endonuclease, and then possibly purify this uniform DNA fragment. Step 0.5: Mix the purified, linearized, cloning vector fragment with the suitably prepared sheared DNA fragments (that you want to sequence), and add ATP, buffer, and an enzyme named DNA ligase.  Specifically, DNA ligase encoded by the genome of bacteriophage T4. Step 0.9: Treat log phase E. coli cells with divalent cations, on ice (making them competent).

Step 1: Mix a small amount of the ligated DNA with the competent cells, give them a heat pulse, add some broth and grow them at 37 briefly, and plate aliquots on LB Plates containing a drug that will select for the rare bacterial cells that have taken up one of the foreign recombinant plasmids (from the DNA ligase reaction). 99.99 % of the bacterial cells will be killed by the drug in the plates, but cells that have taken up a viable copy of the cloning vector will express its selectable marker (a drug resistance gene) and be able to grow, yielding a bacterial colony on the plate).

Step 2: Pick individual colonies, grow them in broth.  Now continue with your Step 3 and Step 4


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How many samples to run an association study on B-Cell receptors
We are trying to find biomarkers on the B-Cell receptor VDJ regions. To do this we plan to run Single cell RNA-Seq (using the solution from 10x genomics https://www.10xgenomics.com/solutions/vdj/)  to get the transcripts, then assembling these using VDJ Puzzle: https://www.biorxiv.org/content/early/2017/08/26/181156
The output will be a list of about 100k base pairs per patient per cell sequenced. I will then have clinical information ... how can I compute the number of patients needed to establish a statistically significant association between SNPs and clinical outcomes / disease state?
Furthermore how many cells would we need to sequence per patient?

I don't know about the number of cells per patient, but there is a vast literature on power calculation for association studies. Power depends on several parameters. This tool developed by Goncalo Abecasis' group might be of help in exploring power while changing several parameters: http://csg.sph.umich.edu/abecasis/gas_power_calculator/index.html


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Taxonomy problems on algae: Is Cryptophyta a Phylum or a Class rank?
I  am currently interested in algae taxonomy (I am not an expert in the field).
I retrieved the taxonomy of my sequences with their NCBI access number via the taxonkit software (https://bioinf.shenwei.me/taxonkit/usage/).
I noticed that I get Cryptophyta at the Class rank level.
For me -phyta actually corresponds more to the phylum rank.
I checked on NCBI site and is actually tidy in Class rank ( https://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&id=3027&lvl=3&lin=f&keep=1&srchmode=1&unlock) but for example on the algaebase database (http://www.algaebase.org/browse/taxonomy/detail/?taxonid=Xafa8c1d30aa53593), Cryptophyta is classified as Phylum.
Can you tell me why Cryptophyta is rank at the Class level on NCBI and not to the Phylum level ?
Conversely, I retrieve taxonomy with, for example, Phaeophyceae ranked at Phylum level (https://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&id=2870&lvl=3&lin=f&keep=1&srchmode= 1 & unlock) while it is normally a Class on algaebase (http://www.algaebase.org/browse/taxonomy/detail/?taxonid=L8055ac0a94735f3e).
Do you have ideas being considered? I am very interested !
Thank you very much in advance for your answers.
Best regards


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Offspring of parents with different number of chromosomes
Many papers report that dog-whelks (Nucella lapillus) show a distinct chromosomal polymorphism between populations of 2n = 24 up to 2n = 36. Could somebody please tell me how many chromosomes the F1 generation of parents with (male) 2n = 24 and (female) 2n = 27 would have? What would happen to the three unmatched chromosomes?


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Is that true that plant stem cells can be used in humans?
I was reading an article (which seems very fake to me) on sensitive topics, but there was one astonishing statement:

Stem cells are obtained from certain plants that grow all over the world. Once the stem cells have been obtained, the doctor will inject them on the target organ...

I want to ask specialists if this particular statement can be true. If yes, does it imply nucleus replacement in stem cells, or anything like that?
Sorry guys, for the stupid question.

They very likely can't be used. The number of chromosomes won't match and most likely the immune system will mount a response against the plant cells

Absolutely not, plants do not have the same signal pathways and have very different cell biology.

Of course, the stem cells must be obtained from the plant stems ;-)

I’m voting to close this question because it is very poor quality and under researched.

@tyersome, poor quality? It's readable - yes. Under researched? You wish to answer only clever and obvious school-test grade questions? If everyone had the knowledge, no questions would be needed. Don't like this question - don't spend your time here.

https://stemcells.nih.gov/info/basics/6.htm
...
Viruses are currently used to introduce the reprogramming factors into adult cells, and this process must be carefully controlled and tested before the technique can lead to useful treatment for humans. In animal studies, the virus used to introduce the stem cell factors sometimes causes cancers. Researchers are currently investigating non-viral delivery strategies. In any case, this breakthrough discovery has created a powerful new way to "de-differentiate" cells whose developmental fates had been previously assumed to be determined. In addition, tissues derived from iPSCs will be a nearly identical match to the cell donor and thus probably avoid rejection by the immune system. The iPSC strategy creates pluripotent stem cells that, together with studies of other types of pluripotent stem cells, will help researchers learn how to reprogram cells to repair damaged tissues in the human body.
So as that all points out, no, the genetics of it will cause a plant stem cell to be genetically not a match, where it might do something for a little while, but upon that cells first interactions, it will stimulate the immune system to get rid of it, rather than incorporate it.
Anymore, I want to know about how Bone Morphinogenic Proteins (BMP-4 or above) can be injected into an organ, and if that will help stem cells for reviving an organ at all.


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Young family members to learn genetics - Amino Labs?
I'm an engineer but want to learn about biology with a niece and nephew who are early teens. I saw Amino Labs (https://amino.bio/) and thought because I work a lot with my hands, doing hands on exercises would be a good way to learn. I don't like text books and don't think my niece and nephew will appreciate a text book. Has anyone used Amino Labs? Any suggestions?


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Why there are no RBCs in lymphatic vessels?
I know the following.

Leukocytes (white blood cells) are made in the bone marrow, and naive leukocytes go to the blood vessels. So, leukocytes mainly exist in blood vessels.
Endothelial cells wrapping the capillaries have some gaps, but too narrow for RBCs or leukocytes to leak out (or for bacteria to invade. So, bacteria go to lymphatic vessels).
When leukocytes are needed (like when some foreign molecules invade), leukocytes such as macrophages get out of blood vessels to the tissue of interest by the mechanism of  extravasation.

My question is, why there are no RBCs in lymphatic vessels? Is it because they cannot do extravasation, while leukocytes can?

That's exactly right


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How related do life forms need to be to produce hybrids?
Specifically, I'm asking about infertile hybrids like ligers, mules, camas, etc. How closely related do animals need to be?

Related just enough? There probably isn't a single answer across taxa.

"The number of quantitative trait loci fixed for different alleles in different species should increase with time since speciation" (Genetic distance between species predicts novel trait expression in their hybrids). I suppose that the genetic distance of hybrid parents may be larger in plants than in animals.


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Genotype-Phenotype evolution distinction
I understand the difference between the genotype of an organism and the phenotype of an organism, (genotype being the genetic code, phenotype being the physical expression), however I am unsure about what this figure mean when it says "Selection that takes place in the environment is based on the specific phenotype of an organism-its traits, not the underlying genotype".
(misconceptions about evolution)

I thought the genotype controlled the phenotype, so what does the figure mean exactly when its saying that natural selection isn't based on the genotype?
Thank you!

See my comment on Remi.B’s answer below.  To say that the genotype controls the phenotype is true to a first approximation.  It would be more accurate to say the genotype at one locus influences the organism’s phenotype, because the cumulative affect of the genetic background also influences that phenotype.  Hence, there are people walking around carrying one or perhaps even two alleles of mutations linked to specific diseases, yet these people have no disease symptoms (and may never develop them).  Of course there are other mutant alleles with 100 % penetrance and expressivity.

The difficulty is in the semantic. In the sentence

Selection acts on the genotype because that is what is inherited

it is unclear what is meant by "acts on". The point that the author(s) of this misconception were probably trying to make is that what define the reproductive success of an individual is the phenotype of an individual. In other words, it is the expression of those genes that affect the probability of the genes to be passed on but it is not the actual genetic sequence itself (or at least less directly so).
Let's assume a haploid case where at a given gene, allele A means 'tall' and allele B means 'short' and let's assume that size matters in defining fitness. It is ultimately not whether an individual carry the allele A or B that matters but whether the individual is tall or short. If by some fantastically random event there is an individual with allele B that is tall then this individual will rather have the same fitness as the tall individuals and not the same fitness as the B carrier individuals.

Alleles can have variable penetrance, and variable expressivity.  In a diploid species consider the heterozygous individuals all carrying the same dominant allele, or m/+.  If all of those hets display the mutant phenotype, then it is 100 per cent penetrant.  However, if only some of the hets display the mutant phenotype then the allele has variable penetrance (that you can likely measure).  Similarly, among all of the hets displaying the mutant phenotype, there may be different degrees of severity, so the allele could have variable expressivity.  Same can be said for recessive homozygotes.

Of course. Never did I meant that there is a one-to-one function between genotype and phenotype. I would agree that my answer is a bit poorly phrased. I've had a hard time to write a pleasant to read answer here for some reason!

I almost started my comment with “You probably know this . . . “


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Where does NADP+ come from?
Trying to understand Photosynthesis better. I understand the NADP+ is reduced to NADPH in light dependent reactions and NADPH is then recycled back into NADP+ in the Calvin cycle. What I don't understand is where does the NADP+ come from initially?
Specifically I am asking with regards to its presence in the stroma within the chloroplasts of a plant cell. Where do plants get NADP+ from in order to assist in the production of sugar?

The simple answer is that plants synthesize it in the same way as they do most other cellular molecules. You can find the details in standard texts. However, I assume that is not what you are after. If so, you need to explain — at present your question is unclear, at least to me.

Niacin (better known as vitamin B3) and nicotinamide are both precursors of the coenzymes NAD and NADP in vivo. As you can see below, the biosynthesis of NADP+ proceeds as follows, when nicotinamide combines with a basic ingredient, a sugar phosphate:

The sugar phosphate precursor can also form AMP and GMP, also important molecules in the cell, when it reacts with the nucleobases adenine and guanine (A and G from the 'ladder' that bridges the DNA helix).
Just as an additional funfact, some bacteria such as Plasmodium falciparum and Toxoplasma gondii cannot synthesize nicotinamide themselves, because they lack the genes for it. Instead, they salvage the enzymes from eukaryotic hosts. This is an example of an incomplete biochemical toolkit giving rise to parasitism.


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Identification of bird observed in Western Australia near the city of Perth in February
This bird was observed during a holiday in Western Australia near the city of Perth in February 2019. Maybe somebody can help me figure out the species.

I think the bird's name is Willie Wagtail and It's scientific name is Rhipidura leucophrys..

That looks right! Brilliant! Thanks!

Welcome to Biology.SE. You are likely to get a more positive response to your answer if you explain why your identification is correct. Specifically, please [edit] your answer to add discussion of key features that led you to this conclusion and supporting references or at least validated images. Without this your answer is indistinguishable from opinion. ——— You may also wish to take the [tour] and then consult the [help] pages for additional advice on [Answer] effectively on this site.

The white eyebrow  (“leucophrys”) confirms the ID.


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Identification of tree seed pods observed in Western Australia near the city of Perth in February
These where observed during a holiday in Western Australia near the city of Perth in February 2019. I assume they are tree seed pods. But from which tree?

I don't know the exact species, but this is likely to be a Hakea species. These are a widespread genus of plants in Australia, with a hard persistent woody seed that splits open after heating (usually fire) or plant death (as in your case) to release two seeds.
You can see some photos of seed pods at Project Noah, showing the classic bifurcate seed pod.

That looks plausible to me. Thank you very much!


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Do organisms use detergents to fight off viruses?
Common advice against contracting bacteria or viruses is to wash your hands because soap dissolves the viruses' shell. Does any organism exploit this effect to protect against infection, e.g. by having detergents in their mucous membrane? If not, why not?

I think that only works on enveloped viruses.

To answer your question, consider why soap is effective against bacteria and viruses.  The chemistry of detergents allows them to interrupt the lipid layer that surrounds cells and some viruses.  Viral envelopes, in particular, tend to be composed of host-derived phospholipids and proteins.  So, if an organism were to synthesize a detergent to fight off a pathogen, that detergent would pose a threat to the producing organism, as well.

Edit - most air-breathing animals produce a pulmonary surfactant in their alveolar cells, though the purpose of these molecules is lung function and cell size regulation, not immunity.

@user1136, Yes, insomuch that antimicrobial peptides are membrane-disrupting molecules.  Some bacteria even produce charged peptides for this purpose.  But the OP's question specifically referred to soap / detergent, which I take to mean amphipathic molecules with lipid-like and ionic components

Possibly?
I note that the body of your question refers to bacteria as well as viruses.
The following review discusses the antimicrobial effects of amphipathic bile salts, including a detergent-like mechanism:
Urdaneta V, Casadesus J. 2017. Interactions between bacteria and bile salts in the gastrointestinal and hepatobiliary tracts. Front Med 4:163.

Bile acids are surface active, amphipathic molecules, and their detergent activity damages cell membranes. Not surprisingly, many bile-sensitive mutants of both Gram-negative and Gram-positive bacteria carry mutations that impair membrane integrity. Likewise, electron microscopy studies have described a shrunken phenotype in Propionibacterium freudenreichii cells exposed to bile. Enzymatic assays in E. coli, Clostridium perfringens, and Lactobacillus acidophilus have shown that bile causes leakage of intracellular material. Factors that influence the severity of membrane disruption are as follows:
(i) Concentration of bile, high concentrations will dissolve membrane lipids, causing leakage and cell death. Low concentrations of bile may have more subtle effects on membrane fluidity and permeability by altering membrane-bound proteins or increasing trans-membrane divalent cation flux. Low levels of bile can also alter the hydrophobicity of the cell surface.
...

I haven't looked into this deeply, so I'm not sure how pronounced these effects are in vivo. There are other mechanism by which bile salts exhibit antimicrobial effects (also discussed in the review). Another review suggests that bile salts may have a similar, detergent-like effect on enveloped viruses:
Bertok L. 1977. Physico-chemcial defense of vertebrate organism: the role of bile acids in defence against bacterial endotoxins. Perspect Biol Med 21:70-76.

Attention should be called to the possibility that the detergent effect of bile acids as a physico-chemical defense mechanism may not be confined to protection against bacterial endotoxins. Theiler has noted that yellow fever virus and other arthropod-borne viruses are inactivated by mixing them with bile or sodium deoxycholate. However, the viruses of poliomyelitis, murine encephalomyocarditis, and Coxsackie virus are resistant to bile acid treatment. These observations have become a significant means of virus classification; viruses have been divided into two large groups, one being sensitive and the other resistant to sodium deoxycholate. The potential pathogenic and prophylactic significance of these observations has not been suggested heretofore. It is concluded that only those viruses with lipoprotein coating (peplon) are sensitive to this detergent action under in vitro conditions. Those with no such covering are resistant. The examination of the effect of bile acid on Aujeszky virus of the herpes group has demonstrated in vivo that bile acids do have the capacity to protect the organism from such viruses.

There is also a model for the mechanism of amphipathic antimicrobial peptides that involves a detergent-like action:
Bechinger B, Lohner L. 2006. Detergent-like actions of linear amphipathic cationic antimicrobial peptides. Biochim Biophys Acta 1758:1529-1539.

Whereas detergents at very low detergent-to-lipid ratios can have a neutral effect on model membranes, or can even result in their stabilization, openings might form temporarily at intermediate concentrations, and membrane disintegration becomes apparent at higher peptide-to-lipid ratios. Disintegration of the bilayer takes into account the loss of the membrane barrier, dissipation of the transmembrane electrochemical gradient, loss of cytoplasmic constituents and concomitantly interference with the energy metabolism of living cells, all being observed also with antimicrobial peptides.


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Breakdown of functional human genome by organ/What fraction of the functional human genome is devoted specifically to brain functioning?
Of course, there won't be a precise known answer to the question, as it is not even known precisely what percentage of the genome is functional in the first place - but I am still looking for research.
The book "Principles of Neural Design" claims that "20% of our genome is devoted to coding neural signaling molecules". This seems not only vague, but also suspect to me, as that is more than the fraction of DNA that is known to have a function in the first place - maybe they meant only protein-coding genes?
One hears a lot about the human brain as "the most complicated object in the universe" etc., but I would like to put a number of that and compare the genetic complexity needed to express it to that needed for other body parts.

The complexity of the brain is not necessarily related to the amount of genome involved. Humans have much more complex brains than rodents and yet mostly share the same proteins with only relatively minor modifications.

I think that depends on the definition of "complexity". In terms of "amount of data needed to describe an instance of the system", I agree - but then, counting the degrees of freedom, a rock could have a higher complexity than a human brain. What I was getting at is "amount of data needed to recreate the system" (further restricting to "biological data", not the experiences the brain bases its learning on or randomness), and if the human brain doesn't need much more "code" than a mouse brain, these would indeed be similar according to the definition I am interested in.

I agree with your assessment of that statement as vague. At best, it's a gross oversimplification. For one thing, neurotransmitters are not directly encoded by genes. However, this online fact-sheet published by the NIH state, "at least a third of the genes in the human genome are primarily expressed in the brain." Still a bit vague, but slightly less so. Obviously not a proper answer, hence the comment format.
https://www.ninds.nih.gov/Disorders/Patient-Caregiver-Education/Genes-Work-Brain


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Diastole/systole pressure in transcapillary circulation
The Starling equation factors in hydrostatic pressure and oncotic pressure. Given that the hydrostatic pressure in capillaries is pulsed, alternating between systole and diastole, does reabsorption tend to be favoured in diastole (low hydrostatic pressure, low volume from filtration in systole and therefore high concentration of colloids i.e. high osmotic pressure)?


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Why does Porous-tube Nutrient Delivery System cultivation improve nutritional quality of Okinawa spinach (Gyruna bicolor)?
I wrote a review paper and it involves in growth system of a plant “Okinawa Spinach (Gynura bicolor)”. A research of (Wang, Fu, & Liu, 2015) reported that Porous-tube Nutrient Delivery System (PTNDS) cultivation enhanced calories from 139.5 to 182.3 kJ/100 g dry matter, and carbohydrate from 4.8 to 7.3 g/100 g dry matter and reduced the amount of protein from 7.3 to 4.8 g/100 g dry matter and ash from 1.4 to 1.0 g/ 100 g dry matter, compared with hydroponic culture. PTNDS cultivation also accumulated the nutrition elements of Ca, Cu, Fe and Zn, and reduced Na concentration.
The reviewer asked me that “why the plant grown in PTNDS reduced the total ash but why improved accumulation of Ca, Cu, Fe and Zn.? “My major is food engineering and I’m not expert in this field.
If this area is your expertise or someone knows the answers? Please help me out with it. Thanks very much.
Wang, M., Fu, Y., & Liu, H. (2015). Nutritional status and ion uptake response of Gynura bicolor DC. between Porous-tube and traditional hydroponic growth systems. Acta Astronautica, 113, 13-21.


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Calculating bacterial mutation rate
I'm reading Molecular Biology of the Cell by Alberts et. al and at one point, the authors mention:

One finds that a single gene that encodes an average-sized protein (~$10^3$ coding nulceotide pairs) accumulates a mutation (not necessarily one that would inactivate the protein) approximately once in about $10^6$ bacterial cell generations. Stated differently, bacteria display a mutation rate of about three nucleotide changes per $10^{10}$ nucleotides per cell generation [emphasis mine].

I'm trying to figure out how they came up with the numbers in the text stated in bold. Here's what I have so far:
According to the first sentence, we have $\frac{1}{10^6}$ mutations per $10^3$ nucleotides per cell generation. So per $10^{10}$ nucleotides per generation, we have $\frac{10^{10}}{10^3}\times\frac{1}{10^6} = 10$ mutations, which is not the 3 that they mention. What am I missing here?

One mutation per 10,000 bases per 1,000,000 generations.
1 mutation / 103 bases / 106 generations
= 1 mutation / 109 bases/generation
= 3 mutations / (3*109) bases/generation
= 3 mutations / 109.5 bases/generation
Since all these are rounded approximations, if you started with more precise numbers and round at the end (always round as your final step!), it would be very easy to get 3 mutations / 1010.

Thanks for the answer. Why can't you just jump from the 1 mutation / $10^9$ bases/generation step to deduce 10 mutations / $10^{10}$ bases/generation i.e do what you did but multiply by 10 instead of 3?

@AnIgnorantWanderer I made it 3 to match their estimate. I assume they say 3/10^10 rather than 10/10^10 because that's closer to their actual estimate if they don't round too early.


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Why are telomeres needed to allow DNA replication at the ends of linear chromosomes?
I’m reading Molecular Biology of the Cell by Alberts et. Al and at one point the authors mention the following:

We saw earlier that synthesis of the lagging strand at a replication
fork must occur discontinuously through a backstitching mechanism that
produces short DNA fragments. This mechanism encounters a special
problem when the replication fork reaches an end of a linear
chromosome. The final RNA primer synthesized on the lagging-strand
template cannot be replaced by DNA because there is no 3ʹ-OH end
available for the repair polymerase. Without a mechanism to deal with
this problem, DNA would be lost from the ends of all chromosomes each
time a cell divides [emphasis mine].

They use this explanation as a motivation for why telomeres are needed. But I don’t quite understand it. Below is a diagram that they show earlier. It seems to me like the process shown can just as easily be done at the ends of chromosomes. In particular, if we imagine that the left-most primer has no DNA following it, it seems to me like polymerase can just do what it normally does to replicate the DNA until the end is reached. Where’s the problem?

How is the 3’ end of the orange strand replicated?

@canadianer I see. But what is meant by "there is no 3ʹ-OH end available for the repair polymerase"?

It means that DNA polymerase only extends existing chains and doesn’t create new chains de novo. In other words, it needs a primer.

@canadianer right but why is there no 3’-OH end available?

This just means that because the final part of the 'reading' is in the 3'-OH to 5'-OH direction (R to L in the orange lagging strand), the last available component for synthesis of an RNA primer by the DNA primase is from that latter 5'-OH towards the 3'-OH end of the strand.  So, the final 3'-OH component of that strand cannot be synthesised: there is no 5'-OH component to its right in the diagram. Telomeres perform other functions; nature is fantastically efficient. The whole thing is an immensely beautiful wave (interference) dynamic in 3-D, wrapped around the tetrahedral form of histones.

@jeremiah but why can another primer not be added right at the 3'-OH end (at the rightmost end of the lagging strand template)?

This video: https://www.youtube.com/watch?v=2NS0jBPurWQ answered my question

The final 3'-OH component cannot be 'read' due to the absence of a further 5'-OH to its right: the requisite directional sense for the initiation of a further primer is absent. I'm glad you found the video -- that's the point.

And yes, the video clarifies it all very nicely.  The key information is the absence of the 3'-OH at the correct end of the Okazaki fragment (right in the video), to prime further DNA synthesis.  So, thank you for that: I'm a wanderer too.


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Why do quaking aspens quake?
I've just finished reading The Hidden Lives of Trees by Peter Wohlleben, which I thoroughly enjoyed.
According to the author, the advantage of shaking the leaves is that both sides of the leaf are exposed to the sun, and therefore both sides can photosynthesize. This would be in contrast to other species, where the underside is reserved for breathing and transpiring. However, to me (a complete amateur), the underside of a quaking aspen seems paler in colour and doesn't "look" like it's any more suited to photosynthesis than the underside of any other leaf.
In addition, I can't find any other sources that back this claim. Most other sources (for example https://www.nature.com/scitable/knowledge/library/case-study-the-glorious-golden-and-gigantic-13261308/) seem to claim the shaking of the leaves reduces the risks that come with too much sunlight, which damages the leaves and actually lowers the rate of photosynthesis.
My question is therefore, what is the most convincing advantage the quaking aspen gains from this characteristic ?

I would have to ask whether there is in fact any particular advantage, and indeed, whether aspens "quake" much more than other broad-leafed trees.  My casual observation is that they really don't, it's just that they're often the only deciduous tree in areas with conifer forests, so the leaf movement stands out.

Quaking aspens do indeed "quake" in the merest of breezes, but aspen leaves are very light compared to maple or oak leaves and ave a flat petiole, another surface to catch the breeze. Maybe there is no benefit, it just is what it is. It's not like they attract other trees this way.

@jamesqf - If they didn't move more in a gentle breeze, they probably would not have been called quaking aspens.

@anongoodnurse: Many other deciduous trees - cottonwoods, willows, maples, ash - have leaves that move in similiarly gentle breezes.  But (at least in the western US) aspens are typically found in isolated groves (near springs, streams, & other places where there's plenty of water, surrounded by conifers, so the movement is noticable.

Hmm "why" do they quake? Impossible to know. The best the scientific process can do is determine if quaking provides any physiological or ecological advantages to the trees. I do not know of any specific research examining this (not too unusual) "phenomenon"  in quaking aspen, but I'll dig around to see if I can find any interesting papers for you...

Conjecturally: P. tremuloides is an early successional (i.e.,"foundational") species, and as a result is typically going to be exposed to more sunlight (due to less other plants shading them out). Their foundational role also means they use more of their energy to develop fast-growing foliage to out-compete other plants for sun (and therefore have less energy for developing UV defenses). I would guess that the added heat of the direct sun and less robust UV protection would decrease fitness, and so the plant would benefit from having less horizontal and still leaves. Natural selection etc..

Robberecht & Caldwell (1978) demonstrate that P. tremuloides experiences substantial UV protection from epidermal compounds. However, this could be interpreted in 2 ways relative to my previous comment. 1) reaffirming the need for and past evolution of traits to protect against high UV (which we know is common in its habitat). Or 2) no need for additional UV protection due to having adequate epidermal protection -- therefore reducing the odds of UV damage being the selective driver for quaking. Heat is still an issue though...

Dillaway & Kruger (2010) might also provide some insight relevant to my hypothesis above, but it's too late -- 2 am -- for me to read, so I'll just place this citation here for reference for the AM.


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electrostatic charge of viruses, especially Coronaviruses
I am searching for (and failing to find) literature about the electric charge (+/-) of viruses, specifically the Coronaviruses.  I am aware that it is a complicated issue, including interaction of pH and electrostatic charges, etc.  However, I note that electrostatic charge of various materials is investigated for barrier protection, suggesting that there are normal average or overall charges for viruses.  Can anyone comment on this?
Especially, I want to know, at neural pH, are Coronaviruses more likely to adhere to a negatively or positively charged surface?
Thanks.

This is a great biological question! It asks a lot about how empirical science is done in the field of modern biology! I'm glad we encourage such questions from curious people who want to learn more.
Via: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4213776/#!po=1.19048

All viruses are coated with proteins and contain genetic material which can either be DNA or RNA. Since both nucleic acids have phosphodiester bonds, the genetic material provides a partial negative charge to the virus. The viral nucleic acid genomes are wrapped in proteins that can be neutral, negative, or positive in charge. Therefore, the net charge of a virus depends upon the cumulative charges of the genetic material and the protein.

So the electric charge of a virus particle depends on the constitutive parts of the virus of interest; particularly if enveloped or non-enveloped; the outward-facing heads of the phospholipid bilayer membrane of an enveloped virus will carry a negative charge.
Two references in the above paper may help with a deeper dive into the subject:

Lodish H. et al. Molecular Cell Biology (ed 4.). (W. H. Freeman, New York, 2000). (Google Scholar)
Michen B. & Graule T. Isoelectric points of viruses B. J Applied Micb. 109, 388–397 (2010). (PubMed) (Google Scholar)

I couldn't find any papers on the electrical properties of novel coronavirus specifically. But looking into SARS-CoV may be suggestive of general properties. Its envelope proteins have a positive charge that help with targeting and infecting ACE2-expressing cells (https://clarivate.com/wp-content/uploads/dlm_uploads/2020/01/CORONAVIRUS-REPORT-1.30.2020.pdf).

Does it really mean that viruses are not electrically neutral (i.e., they are essentially ions) or is it mostly disbalance of charge, i.e., polarization and higher electric moments?

Many viruses appear to have an average isoelectric point (pI) that is below a pH of 7. This means that, at the pH of water, such viruses carry a net negative charge. Other viruses with a pI greater than 7 have a net positive charge. A pH-based separation column can be used for purification. https://sfamjournals.onlinelibrary.wiley.com/doi/pdf/10.1111/j.1365-2672.2010.04663.x https://pubmed.ncbi.nlm.nih.gov/18778829/ https://en.wikipedia.org/wiki/Chromatofocusing

sorry, I didn't realise at first that you are talking about viruses in a solution, rather than isolated viral particles.


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Maximum length for PCR amplification
Is there a recommendation for how long a target sequence for PCR amplification should be?
If there is how do you amplify a target sequence that exceeds the recommended length?

The answer depends a lot on the polymerase you are using. Some are engineered for better processivity, by fusion of a processivity-enhancing domain (Wang et al, Nucleic Acids Res. 2004), but even the best one will struggle after a few tens of kilobases.
You can push the length of the amplicons a little by playing around with conditions but to produce something significantly larger than the average limit of your polymerase, you will usually need to amplify smaller fragments, and then assemble them together. This is the strategy that was used to synthesize the 1079kbp synthetic genome of M. mycoides JCVI-syn1.0, the first "artifical genome" (Hutchison et al, Science 2016); the authors first amplified many fragments of 1.4kbp, and assembled them in vitro. To easily assemble large fragments in vitro, common one-pot enzymatic techniques include the so-called Gibson assembly (Gibson et al, Nature Methods 2009) and Golden gate assembly (Engler et al, PLoS One, 2008) for example.


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Why do vertebrates have an oesophagus?
As far as I know, the oesophagus in vertebrates has no digestive or absorptive function. It is simply a conduit from the mouth to more distal parts of the gastrointestinal tract. Why have it at all, then? What evolutionary advantage does it give? Why not have the stomach start right where the mouth/pharynx ends?
Could it be to make space for the heart?
A Google search did not yield any useful answers.

Some fish do this, but if you want a neck (and if you live on land you do) you need to space things out. narrower fish use it to give space for the gills.

Because of the lungs - they need their own space to expand and contract.

That's a cool question! I think (just a thought, hence not an answer) the stomach needs space since it moves to churn food, and there are already have two vital 'moving' organs in the thoracic cavity. Additionally, it would be easier to have a lower position for the stomach to transfer the chyme down to the intestines, rectum, anus and finally eliminate it from a point far away from the mouth- for hygienic purposes.

@Varsh04802_Lr That's a possibility. But the words 'mouth' and 'hygienic' should not be used in the same sentence. The human oral cavity is home to hundreds of species of bacteria (see https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1287824/). It's so filthy, some even call it the glorified rectum.


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What is the difference between phyletic and phenotypic gradualism?
As I understand it, Phenotypic gradualism describes the development of new traits as a series of incremental steps.  How is Phyletic gradualism different?

By "phenotypic gradualism", did you mean "phyletic gradualism"?

I will assume that by "phenotypic gradualism", you actually meant "phyletic gradualism".
Phyletic simply refers to evolution of a lineage. It is relatively rarely used term. phyletic gradualism comes in opposition to punctuated equilibrium. Punctuated equilibrium is the notion that a lot of evolutionary change in a lineage takes place over short periods of time interspaced by period of time where very little evolutionary change happen. Gradualism is the notion that evolutionary changes happen very uniformly over time. For more information have a look at evo101 > More on punctuated equilibrium

Actually my text, Zoology by Hickman, Robertson et al, differentiates between Phenotypic gradualism and Phyletic gradualism, hence my question.

Can you please give a direct quote that talks about the difference between these two concepts. That might help


text:
Rank-specific rules for taxonomic classification
There appears to be a very specific (although not universally agreed) list of characteristics that describe what a "species" is--and the list applies to ALL species.  Are there similar generic rules or characteristics for the other taxonomic ranks that do not resort to characteristics of existing members of the rank? For example, I've seen "number of lobes on leaves" used to place a particular flower in a particular Family or Order.  Is there anything that applies across ALL Families, or across ALL Orders, etc., of the tree of life?

Somewhat related: How could humans have interbred with Neanderthals if we're a different species?

I agree that the overall answer is "no, there aren't consistent standards for what constitutes a taxonomic level". Perhaps someday we'll be able to say that an animal phylum denotes X years of divergence or Y amount of sequence similarity, but making those same judgements for extinct organisms or microbes is a lot messier. See Wikipedia on bacterial phyla for an example of how taxonomists are still debating whether bacteria should be said to have phyla at all, or whether they're more like kingdoms, or whether we should just use a different word entirely.
However, at the detailed level of one taxon here and one taxon there, evolutionary biologists and taxonomists can work toward greater local consistency. If it's discovered that species X is very different from the other species in its genus, and indeed it's as evolutionarily distant from them as the species in other genera are, then there's a reasonable argument for it to be "promoted" into its own genus. Other taxonomists working on the same group of organisms can choose to use that change as a precedent; and when people revise entire trees at the family or order level, they may be able to apply roughly the same standard throughout. It would be nice to think that through such processes we'll start creeping toward some sort of overall consistency; but I don't think it's likely to happen any time soon across kingdom- or domain-level barriers.

In short, no. Species are unique, in that they are thought to be biologically real categories that would exist whether there were humans trying to classify them or not. There are a variety of definitions for species, involving fixed characters that imply a lack of gene-flow. However, all higher categories, from genera on up are designed by humans to be able to talk about these groups. Each category is defined by phylogenetic relationships, but taxonomists have wide leeway to decide how broadly or narrowly to subdivide groups. (Lumpers vs. Splitters). For example, all ants are in the same family. Yet all it would take to change this would be for some ant taxonomist to submit a paper that divided ants into however many families s/he wanted to. The peer reviewers would then decide if such a division was reasonable, and once published, it would be the new taxonomy. There are no broad rules, other than peer review. Not age: one family could be 1 million years old, and another, 100 million. Not the magnitude of phenotypic or genotypic variation: some groups are radically different from one-another, and still in the same category, while other groups are heavily subdivided and barely distinguishable.

I would disagree that "once published, it would be the new taxonomy". It would be a new taxonomy. Many taxa have organizations or authorities that confer "official" status on a selected tree for a selected set of taxa. It's true that trees or authorities can go in and out of style, and that they're only as authoritative as the experts in the field who follow them. But in most areas, you can't arbitrarily decide to lump or split something and have it "stick", whether it's peer-reviewed or not. If the science is good and it's reviewed by appropriate experts, then maybe; if not, no.


text:
speciation in a single population
Most examples of speciation describe a population splitting (via various mechanisms) into two or more populations that eventually become separate species from one another.  However, what if the population never splits? In other words, at some point in the evolution of a single species, an individual member would become (theoretically) unable to reproduce with its own ancestors--thereby becoming a distinct new species.  How can we say that this has happened, given the impossibility of the example?

Allopatric speciation

Allopatric speciation [..], also referred to as geographic speciation, vicariant speciation, or its earlier name, the dumbbell model, is a mode of speciation that occurs when biological populations of the same species become isolated from each other to an extent that prevents or interferes with gene flow.

Sympatric speciation

Sympatric speciation is the process through which new species evolve from a single ancestral species while inhabiting the same geographic region. In evolutionary biology and biogeography, sympatric and sympatry are terms referring to organisms whose ranges overlap or are even identical, so that they occur together at least in some places.

Yes, sympatric speciation appears to be a thing but estimates of how common that is avery hard to come by.
Now, what you describe is not so much sympatric speciation as you refer to a case of reproductive isolation between extant individuals and their ancestors. I am not sure that was really what you had in mind because otherwise you would have not put it in opposition to allopatric speciation but it is what you seem to phrase. Of course, such type of "temporal reproductive isolation" is obviously a thing.

Thanks for adding the sympatric clarification... yes, this is what I'm referring to.  Obviously there is reproductive isolation...isolated by time, not geography.  So at what point do we say that speciation has occurred; how do we know that a given individual has become the next iteration of speciation?

@charlie-k3 now you are simply asking questions about definitions, not biological facts or theories. You're focusing on one definition of "species", of the many that exist, and you're choosing one that is explicitly not designed to address the question you're asking. Wikipedia introduces the question and there are many other discussions. Remi.b might want to update his answer with other pointers.

@charlieK3 Your follow-up question is an entirely other question and should be asked on a separate post. If the current question has been answered, please check it and consider opening a new post for your new question. That being said, before you open a new post, please have a look at How could humans have interbred with Neanderthals if we're a different species? that might already help you a lot.

actually I'm not asking for the definition of a species, and I know there are many. 2) my first and second questions are variations on the same concept.  3) I'm specifically NOT asking the "Neandertals" question, as stated in my first post, because that is an example two separate species descended from a  common ancestor.  It's OK to answer "I don't know."

I don't understand your follow-up question. To me your follow-up question seems to be How can you tell whether two populations are of the same or of different species in the special case where one population is ancestral to the other one? The answer is it depends upon the definition of species you are willing to considerate, whether or not the two populations of consideration exist in the same time or not. If I misunderstood your follow-up question, can you please clarify it?

Btw, It's OK to answer "I don't know." can be considered a bit rude. It suggests that I am being too pretentious (or dishonest for some other reason) to admit that I don't know what I don't know. Please believe, my goals are to help, to improve my knowledge in biology, to improve my communications skills and not to impress.

Allow me to try this again.  I am specifically NOT describing a situation with or comparison between two (or more) extant species.  I am referring to ONE extant species (say a hermit crab, E.gilli).  At some point in the evolutionary past, E. gilli did not exist--because its ancestor had not yet evolved into E. gilli.   Agreed?  If so, how can we show when speciation has occurred, i.e. when the ancestor evolved into E. gilli ?   For the purposes of this question, let's assume the definition of a species is that in which reproduction is possible and produces fertile offspring.

@charlieK3 Yes, I understood that you are talking about question of species distinction among two populations where one is the ancestor of the other (and hence only one is extant). You have now suggested a definition of species to work with which is good. The definition is not sufficient as explain in the post How could humans have interbred with Neanderthals if we're a different species? but let's work with that anyway....

Reproduction is not possible as they don't exist at the same time but of course, I expect it is not what you want to hear. Maybe you want to hear there is no absolute solution to test whether two individuals would be fertile without actually trying to mate them. Of course, some cases are obvious (such as reproduction between an oak tree and a snow leopard) but there is no general solution for knowing whether two individuals can reproduce without actually trying to make them mate.


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which carbohydrates are produced in the Calvin Cycle?
I understand the structure of simple carbohydrates (di- and monosaccharides, etc.,) but I'm encountering inconsistent/confusing nomenclature while trying to understand the Calvin Cycle.  One source shows that "the carbohydrate products of the Calvin cycle are three-carbon sugar phosphate molecules, or 'triose phosphates', namely, glyceraldehyde-3-phosphate (G3P)."  Are F6P and E4P also carbohydrates?  Are ALL n-carbon sugar phosphate molecules classified as carbohydrates?

yes they do.  you can delete your comment.

Sorry typo. I meant F6P and I meant product. But think about where I’m coming from. The Calvin cycle may have many intermediates, but it is means to convert three molecules of carbon dioxide to a triose phosphate product. The subsequent conversion of triose to hexose may be part of the dark reactions but is not part of the Calvin Cycle. It just feeds into a linear pathway akin to gluconeogenesis.

doesn't address my question at all

If your question is not in the title but about the definition of carbohydrate, you can easily find the answer on the web rather than posting here. Hint: try the Berg chapter on Carbohydrates and the following section 11.1. The phosphate does not contribute to the definition but does not cause an exclusion.


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Basic questions about human genome project
The "human genome" was sequenced by the Human Genome Project around 2000.  But I don't understand what was done and what its significance is.  Questions:

Wasn't a single person's genome sequenced?  I.e. we have the 3.3 billion base pairs for some individual, right?  So how does that pertain to me since I undoubtedly have different alleles than that person.
Isn't most of our DNA so-called "junk DNA?"  Did the human genome project distinguish the portions that code for proteins from this junk area?
What determines a "gene"?  How do we know where one gene begins and ends, especially given that a gene can comprise up to 2 million base pairs?
Suppose I have the 3.3 billion base pairs for some individual.  What can I do with that information?  Don't I need to know much much more in order to make any use of those data?

We welcome new contributors to SE Biology, but expect them to check out what questions are appropriate on this site, even if they have used other SE sites. This section of the help should make it clear that posters are expected to ask specific questions and show evidence of having researched them themselves before posting. Yours is a set of four basic questions, for which you show no evidence of having consulted the obvious source. I have therefore voted to close.

Okay, a quick answer since I don't have time to go into all the details:
1) As correctly mentioned in the comments already the human genome project had multiple DNA donors, however up 70% of the final genome assembly was from a single person. In order to gt a deeper understanding of the genomic variance in the human population we now have the 1000 genomes project.
2) The fact a such a large portion of the human genome is not gene-coding (the term junk-DNA is not really correct/misleading since quite a bit of it does have unknown or regulatory functions) was not really known before the completion of the human genome project - only after we knew the full genome sequence this became obvious.
3) Genes can either be detected experimentally by doing transcriptome sequencing and comparing the recovered RNA sequences to the genome. This tells us which parts of the genome are in fact transcribed (and includes more than just protein coding genes). It's also possible to find genes just by analysing the genome sequence and looking for open reading frames (in exons), transcription start sites and other known elements. However, this method is only good for finding protein coding genes, other genes (i.e. miRNA or lincRNA) will most likely not be found.
4) Yes, the full genome sequence of an individual alone doesn't tell you anything. In order to get interpretable / useful information out of it you need to compare it with other database sources, such as the SNP-database.

The answer to 1. is wrong: The HGP sequenced a small number of individuals from european descent. Without doing so, they wouldn't have been able to find differences between different allels in the individuals. Celera on the other hand sequenced mostly the DNA of Craig Venter.

@Chris — "The answer to 1…". Quite. The poster has four questions. That is what needs addressing in my opinion. When the answer is a book chapter, people here will provide "quick answers" of limited utility.

@Chris Yep, I didn't check the sources there properly. I edit my answer.


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At what cold temperature at thermoreceptors human feel pain (e.g. in fingers)?
I've tried web search but have not found that specific answer. As far as I know at least some people feel pain (e.g. in fingers) when exposed to cold for prolonged amounts of time. E.g. here sciencedirect - thermoreceptor

The temperatures that individuals report as painful vary, although
temperatures above 45 °C and below 15 °C are generally considered to
be painful.

As I understand 15 °C refers to ambient temperature, probably when full body is exposed to it for prolonged time resulting in gradually drop of internal temperature. But at what temperature at the thermoreceptors (nerve sensory endings) pain signals are produced and after what time threshold? Are they (temperature level and time duration thresholds) same for different parts of the body?
That answer here Why do people feel extreme cold at different temperatures compared to other people of same body structure? implies feeling depend on many things, like differences in clothing,  distributions of body fat which does not look like they would change an answer to my question and some others, like neurotransmitter sensitivity which look to me like they could. However, I think there could be definitive answer to my question in the form of a reasonable range.

You are looking for the temperature threshold for noxious cold. It is believed that TRPA1 is the channel involved in the sensation of noxious cold. As for the physiology, the threshold is usually said to be 15 °C (ref1, ref2). As far as I understand it, this threshold indeed refers to the local ambient temperature (not, as you say, for the whole body exposure).

@Domen, just to confirm: do you mean "ambient" to the thermoreceptor, not ambient to body part / skin where / near where it is located?


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Gene vs Protein homology
I am trying to find homologs for some proteins and I am wondering if it is better to find it by comparing the proteins or the coding genes or either is fine.

Think. What is likely to be more conserved — protein sequence or nucleotide sequence?

In most* scenarios you will probably want to look at a comparison of proteins following some additional matching that considers more than a single gene/protein. Luckily, this is a very common problem and one can often look up homologs through existing reference databases such as https://www.ncbi.nlm.nih.gov/homologene
Further, if genes are not present, their documentation will provide a good overview on ways to find homologs in other organisms.
*in some very special scenarios, gene sequences might be more suitable. For instance if one wanted to study similarity of non-coding regions of a gene. However these exceptions would seem beyond the general character of the question.


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What M9 stands for
Can anyone tell me what M9 stands for in M9 medium?
I have tried googling but I still cannot find it.

I wasn't able to find an original source either but I wouldn't be surprised if it was the 9th version of some minimal medium that was used; M could be minimal or medium or a non-English equivalent. That doesn't mean the history isn't interesting for curiosity's sake but it won't tell you anything else. In any case, the modern M9 has multiple recipes that deviate slightly from one another anyways.

https://www.thermofisher.com/order/catalog/product/A1374401

Original usage seems to be Miller J.H. (1972) Experiments in Molecular Genetics.


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Can fruit be affected by antifreeze in soil?
Due to an accident about 2L of car antifreeze (ethylene glycol & corrosion inhibitors) was spilled around the soil at the base of a fig tree. I am wondering if there is any way the antifreeze can enter the fruit? Will soil bacteria break it down over the course of time? I did a web search that indicated that antifreexe can be harmful to plant roots and can stunt their growth. I could not find any information indicating whether it has any chance of actually entering fruit. I wonder if the ethane glycol (ethane 1, 2 diol) molecule is too large to enter the root system. Your advice would be appreciated.
Kind regards
Chris


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The "truce of the watering hole" -- is it completely discredited?
In short, the idea comes from Kipling that animals observe a sort of truce around watering holes and prey animals do not have to be on guard (as much?) from predators in the vicinity.
I have read that this is false, that predators might even wait around watering holes for prey. However: Cleaning stations in the ocean seem to have rules and a truce (and a fish violating these rules, primarily not to attack other fish waiting to be cleaned is attacked by other fish of various species). So the idea of a truce at waterholes, perhaps only partially observed, is not that far fetched.
I wonder too if lions, for example, at some level understand that in order to survive they need prey to be able to eat/drink and breed. While this also sounds too sophisticated, is it any more sophisticated than the behavior of killing cubs so that females come into heat?

Comments are not for extended discussion; this conversation has been moved to chat.

Cleaning stations offer a pretty strong individual incentive not to attack, those that attack do not get cleaned and thus get riddled with parasites. Watering holes are just the opposite there is no advantage to not attacking and in fact a decent advantage for attacking, (a meal) many predators hang around watering holes just because the draw prey.
To put it another way the genes from lion A say hunt things at the watering hole, the genes from lion B say don't, Lion A is going to have more meals and thus more offspring than lion B therefore the genes to hunt at the waterhole will spread. Lion B gains no benefit from not hunting at watering holes that can offset the very large and immediate advantage lion A gets. This is a good general test to why group selection generally doesn't work, even if all lions were type B as soon as lion A occurs from a mutation it has a huge advantage and drives out lion B's genes.
There is quite a lot of evidence that predators often concentrate around watering holes, heck this is how crocodiles make a living. The idea that lions do not is an out dated and stems from early observations done only during the day (when lions are mostly inactive yet close to watering holes to hunt at night), spread by fiction writers and reinforced by advertising and poorly researched articles.
https://www.nrcresearchpress.com/doi/abs/10.1139/z77-235#.XkxeG2hKhPZ
https://academic.oup.com/beheco/article/23/5/970/232520
The Serengeti Lion: A Study of Predator-Prey Relations
By George B. Schaller
Seasonal Diet and Prey Preference of the African Lion in a Waterhole-Driven Semi-Arid Savanna

If you look at predators as being "farmers" of a sort, the lions, etc. realize that absolutely terrorizing their prey would result in probably their finding another watering hole where predators are more judicious about what they hunt.

@releseabe except watering holes are few and far between and there are many predators each using them, so prey have no choice, also if the prey can move so can the predators.  there is again no benefit.


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Do Glycosides in plant seeds serve some other function than protecting the seeds?
Many plants have toxins like glycosides in the seeds and I think other parts of the plant and the accepted reason for this I believe is to discourage animals that ingest the seeds from digesting theses seeds -- the goal is for the animals to eat the fruit and disperse the seeds where they can subsequently grow. (The seed has not just toxins but also very tough shells often as in stone fruit like cherries and peaches.)
My question is whether these toxins when the plant begins to grow have some other biological function?

There are a lot of different glycosides with many functions. you may need to be more specific.

@John -- i am asking if any toxic compound in the seed has some function beyond protecting the seed from being eaten.


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How are elements like iron recognized and routed to the right places for use in the body?
I asked this in Chemistry and it was suggested to ask it here. I wondered how the genome, which afaik does not contain iron or calcium as "reference" copies, nonetheless produces an organism that uses certain elements. If it create proteins which bind preferentially to iron or calcium, how then are such elements routed to sites where they can be bound? Are there proteins in addition to those which bind to elements that are responsible for routing? I should mention that I am a software developer and imagine mechanisms analogous to computer code.

Hi and welcome to Biology.SE! It's unclear to me whether you're wondering about iron uptake into blood from consumed food or iron uptake by cells from blood. Or are you asking how individual iron ions reach binding sites on iron-binding proteins? Chemically, proteins that bind ions are no different from proteins that bind other organic molecules, and the genome contains codes for proteins that specifically bind almost every class of chemicals out there. You can get some basics re:iron here: https://en.wikipedia.org/wiki/Human_iron_metabolism#Mechanisms_of_iron_regulation

We welcome new users to SE Biology, but unfortunately your question has problems which will be apparent when you take time to read the introductory tour and the help. First, you really have to show evidence of your own research before posting a question. if you had done this you would see the second problem, that your question is much too broad. Different elements are handled in different ways. You seem to think there is a general problem here in relation to the elemental composition of the genome, but I see none. Please explain further.

@com.prehensible please refrain from answering in the comments. Please turn this into an answer. I'll delete your comment shortly. Problem is that answers in disguise demotivates others from writing quality answers.

As another software developer, I should point out that analogies between computer hardware or software and biological systems can be misleading sometimes. What do you mean by "reference copies" in the genome?

A wikipedia source gives you general informations and precise details about the locations and methods of absorption and distribution. Reading the page is well recommended, I will add the quote to save others time:
en.wikipedia.org/wiki/Human_iron_metabolism#Dietary_iron_uptake :

Like most mineral nutrients, the majority of the iron absorbed from
  digested food or supplements is absorbed in the duodenum by
  enterocytes of the duodenal lining. These cells have special molecules
  that allow them to move iron into the body. To be absorbed, dietary
  iron can be absorbed as part of a protein such as heme protein or iron
  must be in its ferrous Fe2+ form.
A ferric reductase enzyme on the enterocytes’ brush border, duodenal
  cytochrome B (Dcytb), reduces ferric Fe3+ to Fe2+.[9]
A protein called divalent metal transporter 1 (DMT1), which can
  transport several divalent metals across the plasma membrane, then
  transports iron across the enterocyte’s cell membrane into the cell.
These intestinal lining cells can then either store the iron as
  ferritin, which is accomplished by Fe3+ binding to apoferritin (in
  which case the iron will leave the body when the cell dies and is
  sloughed off into feces), or the cell can release it into the body via
  the only known iron exporter in mammals, ferroportin.
Hephaestin, a ferroxidase that can oxidize Fe2+ to Fe3+ and is found
  mainly in the small intestine, helps ferroportin transfer iron across
  the basolateral end of the intestine cells. In contrast, ferroportin
  is post-translationally repressed by hepcidin, a 25-amino acid peptide
  hormone.
The body regulates iron levels by regulating each of these steps. For
  instance, enterocytes synthesize more Dcytb, DMT1 and ferroportin in
  response to iron deficiency anemia.[10] Iron absorption from diet is
  enhanced in the presence of vitamin C and diminished by excess
  calcium, zinc, or manganese.

The fundamental question is, how can an element be "recognized" without any sample to compare it to? How are proteins able to bind iron from among any number of things that might be encountered?

Enzyms have specificity, a lock and key method, a preferential fit method. The DNA keeps information on millions of external constructs, it is only a code, so it can code anything, not only mineral specific enzymes, it can code about 146 heptillion different enzymes, which change randomly and are selected by evolution or equivalent purpose(for enzymes). If the enzymes are randomly generated to begin with, the coding/cell memory structure doesn't need to have a "reference" copy of the mineral. it's quite a complicated deep theory, you can embark on readings about enzyme specificity/history.

By the way, nobody knows the precise science of enzyme binding and evolution, it's one of the most complex things in biology. you can learn lots of theories, dozens of well written research, about enzyme binding and evolution, for example here: http://www.plantphysiol.org/content/125/1/54 there's another website with all 10,000 or so enzymes known to science, and apparently 75k enzymes are expected in the human body, and a lot more proteins. So, in computing there is no parallel, and computers are good at simple biomimicry, but advanced copying of nature is generally too disorderly for pc's.


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Is there any evidence that genes which are associated with physically adjacent structures are located near each other within the genome?
I am not sure if there are individual genes for, say, fingers and if so, would such genes be near the genes that affect hand growth? If not "near" in the Euclidean sense, could there be a different metric where genes for associated structures could be considered near?

There aren’t genes for fingers, and the answer to the question of whether genes for associated functions are physically associated in the genome depends on the organism. You need to research the genetics of limb development before asking this sort of specific question.

@David: can you suggest links or search terms? I of course did try to search but got only general results. If there is an organism which had this property, can you give me an example? I am not merely interested in limb development but general rules for how the genome is laid out.

I shouldn’t answer in comments, but if you were hoping there were rules — in anything other than bacteria — I’m afraid you will be disappointed. Try searching for operons and gene clusters.

https://en.m.wikipedia.org/wiki/Hox_gene#Colinearity

@canadianer — You really ought to answer rather than comment, as the example you give would appear to be the exception rather than the rule, which the poor computer scientist (for I imagine that is what the poster is) will get the wrong impression.

@David: pretty good guess except I am a comfortable (by no means wealthy) computer scientist.

@releseabe — Apologies for the "poor", but both on this list and in life I have repeatedly encountered numerical scientists interested in finding problems in biology to apply their skills to. Among the problems that arise are 1. Biology (even the molecular variety) doesn't genearlly follow clean rules, 2. The low-hanging fruit has already been picked, 3. Although biology is intellectually stupid (speaking as an ex-chemist) you need to learn some to understand the problems.(Others on the list will hate me for saying this.)


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Lions protecting girl in Ethopia -- how plausible is it that they understood situation?
Several years ago we read of a girl who was apparently threatened by humans being protected by lions who chases off the males and stayed with the girl. Explanations like, "her crying resembled that of a cub" etc. were invoked.
Why is it so hard to believe that adult lions who almost certainly know the difference between a lion cub and a human could not have been acting altruistically as they sometimes apparently do with, for example, prey animals that they sometimes encounter? If a domesticated dog or cat protects a human, we accept that they know what they are doing, do not confuse the human with their own young. Lions are plausibly more intelligent than a dog or cat or at least within the dog/cat range.

It would be great if you link the article which reports this and also the ones that provide the explanations?


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Was there a time in Earth's history when some animal life existed on land but humans could not have breathed?
I understand that higher oxygen content allowed insects and arachnids to grow much larger than today and I wonder if this additional oxygen would have been toxic or unhealthy for modern humans?

Why humans? We are just a moderately large bipedal mammal.

because i am human.

There isn't evidence that the worldwide air has ever been toxic compared to today since animals came to land 530+ million years ago.
At some times in history, there has been lots of mercury vapor and perhaps other poisons in the atmosphere, for example recent research indicates that the late dinosaurs had at least 10 times as much environmental mercury from the Deccan traps eruptions which give most of southern india it's current geology. That said, the air would have been breathable, but some apex predators would have had mercury poisoning from their diets. Imprecise studies have found mercury levels in sediment go up to 1000 ppb for hundreds of years, compared to perhaps 100 ppb as they are today... other studies may find that there were higher mercury spikes, up to 30 times those of today perhaps. https://www.researchgate.net/figure/Temporal-correlation-of-mercury-records-with-other-indicators-of-Large-Igneous-Province_fig15_328051765
For oxygen, ever since the first insects emerged on land 530 million years ago, the oxygen levels have been safe for humans. https://en.wikipedia.org/wiki/Timeline_of_the_evolutionary_history_of_life


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Methanol and brain damage -- special affinity for optic nerve or just really toxic?
Methanol is known for causing blindness. One explanation I have read is that the optic nerve is especially active and so methanol will be preferentially taken up by the cells there which then die.
But I assume methanol is also bad for neurons concerned with, for example, memory and cognition. But is this wrong? Could it be that methanol for some reason tends to cause temporary or permanent blindness but is no more toxic to other neurons than ethanol is?

Methanol toxicity is relatively rare and comparatively little is known about its etiology. I found a correspondence published in the journal Nature in 2004, it seems to a good review of the literature, given that I could not find a recent review on the topic. Please take a look, especially at the sources that the following paragraph cites:

Methanol is particularly toxic to the optic nerve, leading to acute
blindness. Based on a histopathological study, the retrolaminar optic
nerve myelin sheath seems to be selectively vulnerable to methanol
poisoning due to its anatomical structure. In the acute phase, the
hyperaemia and swelling of the optic disc has a papilloedema-like
appearance. The axoplasmic flow stasis at the nerve head and
alteration of the myelin sheath in the retrolaminar nerve segment were
demonstrated in experiments using rhesus monkeys. The pathogenesis is
presumed to be histotoxic anoxia in a vascular watershed area, which
is the result of direct inhibition of cytochrome oxidase by formic
acid. Additionally, the increasing pressure following oedema in the
visual pathway might further aggravate the deterioration due to
ischaemic changes. Therefore, effective methods to treat the oedema
might be important, such as the use of intravenous steroids and
diuretics. The mechanism of subsequent optic atrophy in patients with
methanol poisoning is still unknown, it was suggested to be due to
progressive demyelination. The distinct glaucomatous-like cupping of
the optic disc suggests extensive loss of retina ganglion cells, which
has been thought to result from retrograde degeneration of optic nerve
axons.

It seems that in our best understanding, the optic-specificity of the action of methanol seems to be due to the nature of the myelin sheath that insulates the optic nerve.

Thanks, interesting. But methanol I would guess is still not good for the brain overall, perhaps the same or perhaps worse than grain alcohol for areas concerned with memory, etc.

What makes you think it only affects the eyes? Paraphrasing Wikipedia, upon ingestion, symptoms include decreased levels of consciousness, impaired (or loss of) coordination, vomiting, abdominal pain, smelly breath, kidney failure, and (alas!) blindness or vision loss. That doesn't sound to me like it only affects the retina.

@S Pr: I did not say only eyes but basically I am trying to understand two things: why it seems to be especially bad for the optic nerve and whether it is more toxic in general than ethanol.

@releseabe Methanol is at least an order of magnitude more toxic than ethanol. The treatment for methanol toxicity used to be IV ethanol in an attempt to displace the methanol. I know of no cases of blindness following profound intoxication; death occurs before anyone reports blindness.

@anongoodnurse: Never heard of intravenous ethanol as treatment, very interesting.


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Do animals with very small eyes see microscopic objects?
I understand that many small creatures have very elementary eyes: they are not scaled-down versions of the human eye but as I understand it often just light-sensitive organs for detecting movement.
However, a mouse I would guess has an eye that is like the human eye but probably less than 1% the size. So does that mean that a mouse sees details that humans can't?
There has been recent evidence that ants might recognize their own reflections. Now, I know the structure of insect eyes is very different from mammalian eyes but if indeed they can recognize themselves in a mirror, that implies that their eyes can perceive very small details.
I could also imagine that things like wavelength mean that details of very small objects simply can't be perceived by bouncing visible light off of them -- that is why their are electron microscopes and so I could believe that mice, etc. can see bacteria, etc. any better than we can.


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Is there any evidence that humans isolated from each other genetically are less able to produce viable offspring?
I would guess that before a new species originates, members of subgroups might have difficulty in interbreeding. Is this possible?

Humans as a species are very genetically homogenous, will little genetic diversity compared to our sister species. Basically there is so little human genetic diversity this would be all but impossible to test.

@John: As a practical test, American Indians and Europeans (Africans, too) were genetically isolated for at least 10K years - probably longer considering that the Indians' ancestors came from eastern Asia - yet there are plenty of us who are descended from both groups.  I understand the same practical test has been applied in Australia, too.

@jamesqf 10K years sounds like a lot but it really isn't especially when starting with low diversity. humans lave less genetic diversity than a single subspecies of chimpanzee. which have an order of magnitude more variation. https://www.sciencedaily.com/releases/2012/03/120302101706.htm and https://en.wikipedia.org/wiki/Human_genetic_variation

@John: True, but as a practical answer to the question, we can only look at groups of humans that have been separated for various periods and see if they actually do have trouble interbreeding.  The American and Australian examples are the cases I can think of where groups of humans have been reproductively isolated for the longest periods.  Unless you include Neandertals, and I don't think there's enough data to say whether there were functional problems with interbreeding.

@jamesqf your issue will be American and Australian lines are fairly closely related. Most of human genetic diversity is in Africa. Australian and native American only diverged 70,000 years ago. If you want the longest isolation sub-Saharan African and South America would be your best bet. that will be at minimum 120,000 years of divergence, if not more. but you will run in to a big problem because human fertility rates vary drastically due to standard of living, by as much as 8 fold across all populations.

@John: But the question is not about genetic diversity, it's about reproductive isolation.  If you want to look at South American and SS-African, take the population of Brazil as your example.  I think you won't find any reproductive problems.  Fertility rates vs standard of living (however defined) is an entirely different question, one that gets into technology, culture, and individual choice, not simple biology.

@jamesqf I recognize fertility is a different question but it is a confounding to what we want to study, When you try to study cross fertilization your measurements are going to be swamped by other factors effecting fertility. Your study size would have to be absolutely massive to deal with this. this will confound reproductive isolations as well because so many places experienced colonization and establishing a lack of crossbreeding will be difficult to demonstrate for populations large enough for your needs.

@releseabe You will need to be more specific. Can you point to a specific source, or dataset, or other citation that you would like to know more about? Here is a non-technical description of reproductive isolation: https://www.sparknotes.com/biology/evolution/reproductiveisolation/section2/#:~:text=Hybrid%20Infertility,a%20horse%20with%20a%20donkey. Here is a more technical treatment: https://www.nature.com/scitable/topicpage/hybrid-incompatibility-and-speciation-820/

@MaximilianPress: i know that the Australian aborigines are a group that had been in isolation from other populations. i have never read that Europeans and this group can't have fertile offspring but i am wondering if there is any statistical effect: higher incidence of stillbirth or other issues.

@releseabe I'd suggest updating your question with that information specifically. Something like: "have human people of X group been separated from human people of Y group long enough to form reproductive incompatibilities?" I would suggest looking into this yourself also. I'm adding an answer but this may get more specific data.

@MaximilianPress: i think the question is clear and i dont want to limit it to two specific groups.

@John: Perhaps you're missing the point I have been trying to make, which is that the hypothesis of some human groups having difficulty reproducing with other groups due t genetic isolation (or indeed, anything else) has been disproven by experiment.

@jamesqf and my point is that any such experiment would likely be doomed to failure due to confounding factors. broad fertility is just too confounded by other fertility factors do do anything resembling a conclusive study. You would need hundreds of thousands of breeding pairs for just two groups to study isolated populations.

@John: But those "experiments" have been performed, naturally, when humans from long-isolated groups meet and have offspring.

@thats not the experiment the experiment is compiling that data and trying to calculate statistical significance. and if your confounding variables are powerful, you need a huge N to get useful calculation. An N that would have to be in the tens of thousands between just two isolated groups. (adding more groups would confounding and thus increase N) I don't know of any isolated groups that crossbreed in the hundreds of thousands with another group that is also considered isolated. Almost by definition if they are crossbreeding in those numbers they are not isolated.

Studies looking into this have not found any evidence of reproductive incompatibility in humans, at least not by the mechanisms other animals use.
Some studies looking at co-variation of reproductive genes find nominal positive associations between particular alleles within specific populations. This suggests (unsurprisingly) that there is functional variation of reproductive genes in humans, but again there is no evidence that it leads to the classic reproductive isolation case (e.g. here).
Some such co-occurring genetic variation of reproductive genes is also observed across populations, but again if it's across human populations it is probably not doing a great job of isolating them.
In all of these situations, the statistical evidence seems to be rather weak. If these gene-gene associations are "real", they do not seem to be very strong at all or to have much effect on fertility, echoing comments from @John.


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Self-study genetics
I'm new at the field of genomics. I'm a theoretical physicist by training and now we would like to translate some of the ideas to the DNA, possibly in real genomic instances. The concrete example would be the line contained for example in this book, charge migration in DNA.
Before jumping to this specific line of research, I would like to understand more fully the general theory on DNA and genomics. I have read that Lewis, Genes is kind of standard, but I'm too far from this text at this time. What books would you recommend to self study from scratch?
Extra points will go to someone who can give also references for a basic course in molecular biology; it has been a while since I took chemistry, so I have been rusty at this topic also.

What does "I'm too far from this text at this time" mean?

I used "Essential cell biology" by Albert et al,
and then "Molecular biology of the cell" for  more detail. Also by them.
Experts originally from other fields contribute greatly to biology, so dont be discouraged. For self education (which I did before formal study) I recommend incremental learning based on learning everything about a drug, disease, molecule etc of interest and work out from there.
In "Biochemistry" by Lehninger, browse and look at the side panels and pictures and work through the interesting ones.
Good luck


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Universal clock for humans contained in the telomeric sequences?
I don't know if this would make sense, but imagine that we could only suffer from natural aging (not diseases whatsoever involved). Is there an estimate of what is our natural maximum lifespan that a human can have?
I learned that the telomeric sequences protect sensible information in DNA, and that somatic cells suffer from a cut of these sequences in each replication. So I wonder if this is a natural clock, and if it has been estimated how much time do we have naturally.

If the clock is universal, it obviously doesn't run at the same rate for everyone.

I should have written on average for the human beings.


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Codons at for transcription vs translation
Why are start and stop codons present at translation level but not at transcription level? And how will I obtain a protein at transcription level?
Thanks in advance

After transcription, you don't get a protein but an mRNA. Is this unclear to you or is something else unclear to you?

@Remi.b Ya that's unclear too :(. Why is that the case? And why aren't any start and stop codons present at that time? Thanks

It is hard to know how many things are unclear to you from your question. Hence, the best anyone can do would be to write a whole introduction to the so-called "central dogma of molecular biology", which makes your question too broad, IMO. Plus, many such introductions already exist online. For example, have a look at Khan Academy, wikipedia or many other source of information.

Codons are only meaningful for translation, since that is when the nucleo-based DNA/RNA sequence information is translated into a protein sequence based on the triplet code. Before that step codons don't really have 'meaning'.
During transcription the start & stop codons are already present, but they are ignored by the RNA polymerase, because it works on a single base at a time.
The equivalent 'start' and 'stop' signs for transcription are promoters and poly-adenylation-sites (at least for eukaryotic mRNA). Both are recognised by additional proteins, that help regulate transcription:

transcription factors bind the promoters on the DNA and recruit RNA polymerase to that site so that transcription can start
poly-adenylation-site are specific sequences that lead to the addition of the poly-A tail to the nascent mRNA. This process also leads to termaination of transcription, however the exact mechanism isn't quite clear.

Thanks a lot. It cleared a lot of my concepts. I just have one more specific question. I am given a particular DNA sequence. What will be the mRNA molecule as a result of transcription of that DNA segment?

I hope the question is clear. Please help. I'll be grateful to you!

The mRNA that binds to a template strand will complement the template. For the sequence AATC, the mRNA will be UUAG (remember that in RNA, uracil is used instead of thymine)


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Understanding food composition data from USDA for Vitamin A
When researching the nutritional value of carrots the Vitamin A comes in two  measurements as RAE and UI:

https://ndb.nal.usda.gov/ndb/foods/show/11124?n1=%7BQv%3D1%7D&fgcd=&man=&lfacet=&count=&max=25&sort=default&qlookup=Carrots%2C+raw&offset=&format=Abridged&new=&measureby=&ds=&Qv=1&qt=&qp=&qa=&qn=&q=&ing=
After reading the following article
https://ods.od.nih.gov/factsheets/VitaminA-HealthProfessional/
I understand that IU can be transferred to RAE, but I wonder if in case of USDA does two records represent the same value or they are supposed to be combined? :shy:
If you had previous experience working with this database I will be more then glad to hear you opinion about that :)

The corrected answer: It seems that the both rows from your table show the same thing: the sum amount of all vitamin A-related substances, but in different units; the 1st row in RAE and the 2nd row in IU.
As I said before, according to ods.nih.gov, 1 IU retinol = 0.3 mcg RAE, but this conversation is true only for retinol (the true, "pre-formed" vitamin A), which is found only in animal foods.
The main vitamin A-like substance in plant foods, such as carrots, is beta-carotene and the conversion rate is: 1 IU beta-carotene = 0.05 mcg RAE, so the 20-fold difference between 835 mcg RAE and 16,706 IU now makes sense.
Why to complicate this?
Large amounts of vitamin A (retinol) can be toxic. The upper tolerable level (the amount that should cause no side effects and is not nearly toxic) for retinol for adults is 3,000 mcg RAE. For example, 100 g of chicken liver contains 4,296 RAE of retinol. (You can also see that for the liver, 4296 RAE/14378 IU = 0.3, so this explains again that the two rows are the same thing.)
You can see that the same IU of vitamin A in animal foods is translated into much more RAE than in plant foods. This is also why high IU of vitamin A in animal foods can be (potentially) much more toxic that the same IU of plant foods.

@volna, I had to correct my answer entirely....


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GWAS: marker map based on old genome assembly - can I use the new assembly to look for SNP positions?
I have an old set of pig SNP data and the positions were mapped using v10.2 of the assembly.
I submitted a GWAS paper for review, and the reviewer wants to know if any of the significant SNPs that were located in previously unknown genes are now in known genes, with the release of the latest assembly last year.
I was under the impression that I had to use the assembly the marker map was based on to see where SNPs are located. Is this correct or can I use the new assembly?
Many thanks in advance!

Why haven't you tried using LiftOver to convert the coordinates?
https://genome.ucsc.edu/cgi-bin/hgLiftOver

I didn't even know this was possible! Thank you!

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