text:
How to select residues in a selection for protein mutagenesis in PyMOL?
Currently I am creating a selection that has residues 5 angstroms away from a ligand for alanine point mutations at each highlighted residue. Currently, the code is creating the specific selections I want, but it has the error below once selecting the model to use mutagenesis on. I specifically ran this code through PyMOL using File -> Run Script
“Atom” has no attribute “get_id” File "C:\Users\will\AppData\Local\Schrodinger\PyMOL2\lib\site-packages\pmg_qt\pymol_qt_gui.py", line 1192, in file_run self.cmd.run(fname) File "C:\Users\will\AppData\Local\Schrodinger\PyMOL2\lib\site-packages\pymol\parsing.py", line 470, in run run_(path, ns_pymol, ns_pymol) File "C:\Users\will\AppData\Local\Schrodinger\PyMOL2\lib\site-packages\pymol\parsing.py", line 519, in run_file execfile(file,global_ns,local_ns) File "C:\Users\will\AppData\Local\Schrodinger\PyMOL2\lib\site-packages\pymol\parsing.py", line 514, in execfile exec(co, global_ns, local_ns) File "C:/Users/will/PycharmProjects/Binding Residues/bindingresidue.py", line 10, in <module> res_id = residue.get_id()[1]

Here is the code I used:
from pymol import cmd

cmd.load(r"C:\Users\will\.pymol\Acb1test.pdb", "Acb1")
cmd.remove("not chain A and not residue ECI")
cmd.select("eci_residue", "chain A and resn ECI")
cmd.select("binding_residues", "(byres (eci_residue around 5))")
protein = "Acb1"

for residue in cmd.get_model("binding_residues").atom:
   res_id = residue.get_id()[1]
   res_name = residue.get_parent().get_resname()

   if res_name == "ALA":
       cmd.wizard("mutagenesis")
       cmd.wizard().set_mode("ser")
       cmd.get_wizard().do_select(f"chain A and residue{res_id}")
       cmd.get_wizard().apply()
   else:
       cmd.wizard("mutagenesis")
       cmd.get_wizard().set_mode("ala")
       cmd.get_wizard().do_select(f"chain A and residue{res_id}")
       cmd.get_wizard().apply()

   cmd.save(r"C:\Users\will\Acb1test\{protein}_{res_id}.pdb")
   cmd.reinitialize()
   cmd.load(r"C:\Users\will\.pymol\Acb1test.pdb", "Acb1")
   cmd.remove("not chain A and not residue ECI")
   cmd.select("binding_residues", "br. (byres (residue ECI around 5))")

cmd.delete("binding_residues")

I ran this through PyCharm. I expected that after a selection was created with residues 5 angstroms away from the ligand, I could mutate each highlighted residue one by one, and save them to my file. I wished for this process to happen for all residues selected separately, which is why I created a simple loop for the mutagenesis function.

Welcome to the Biology Stack Exchange. Please take the [tour] and visit the [help] for more information on this site and how it works. You might be better requesting migration to our sister site Bioinformatics

Your question is about a software program, not about biology. Have you posted to Pymol users lists — the obvious first port of call? If you find nothing there , SE Bioinformatics would be more suitable.

cross posted https://stackoverflow.com/questions/79048193/how-to-select-residues-in-a-selection-for-protein-mutagenesis-in-pymol

my attempt , input is protein Acb1 from 7t27.pdb ;
code :
from pymol import cmd, stored
import pymol
import time

pymol.finish_launching()
time.sleep(3)

print('\n\n------------------------------------------------')
print('\n  PyMOL Version : ',  cmd.get_version()[0])
print('\n\n------------------------------------------------')

# protein = "Acb1"
cmd.load('7t27.pdb' , 'Acb1')
cmd.remove("not chain A and not residue ECI")
cmd.remove('solvent')
cmd.select("eci_residues", "chain A and resn ECI")
eci_residues ="eci_residues"
cmd.select("binding_residues", "byres {} around {}".format(eci_residues, "3")) ### changed from # cmd.select("binding_residues", "byres (eci_residue around 5))")

def muta(resi, res_name):
    print('\n resi : ', resi, '  resn : ', res_name)
    if res_name == "ALA":
        cmd.wizard("mutagenesis")
        cmd.do("refresh_wizard")
        cmd.get_wizard().set_mode("TRP")
        # cmd.get_wizard().do_select('A/'+resi+"/")
        cmd.get_wizard().do_select(resi+"/")
        # cmd.frame(1) ### rotamer selection ?? check if rotamer exist
        print('before apply !!!!!!!!!!!!!')
        cmd.get_wizard().apply()
        cmd.wizard() # ends wizard
        print('mutated !!!!!!!!!!!!!')
    else:
        pass

stored.residues = dict()

cmd.iterate('binding_residues', 'stored.residues[resi] = resn')

print('\n\n residues : \n', stored.residues , 'lenght : ', len(stored.residues))

for resi ,resn in stored.residues.items():

    # print('resi : ', resi ,'  resn : ', resn)
    muta(resi,resn)

stored.residues = dict()

cmd.iterate('binding_residues', 'stored.residues[resi] = resn')

print('\n\n residues : \n', stored.residues , 'lenght : ', len(stored.residues))

cmd.delete("binding_residues")

output result:
------------------------------------------------

  PyMOL Version :  2.3.0

------------------------------------------------

 residues :
 {'4': 'TYR', '36': 'HIS', '38': 'THR', '41': 'TYR', '66': 'PHE', '68': 'THR', '69': 'GLN', '74': 'ALA', '100': 'TYR', '104': 'ARG', '106': 'HIS', '108': 'THR', '111': 'TYR', '134': 'GLU', '135': 'GLU', '136': 'LEU', '137': 'ASP', '140': 'TRP', '202': 'SO4'} lenght :  19

 resi :  4   resn :  TYR

 resi :  36   resn :  HIS

 resi :  38   resn :  THR

 resi :  41   resn :  TYR

 resi :  66   resn :  PHE

 resi :  68   resn :  THR

 resi :  69   resn :  GLN

 resi :  74   resn :  ALA
PyMOL>refresh_wizard
Selected!
 ExecutiveRMS: RMSD =    0.022 (4 to 4 atoms)
 Mutagenesis: 7 rotamers loaded.
before apply !!!!!!!!!!!!!
mutated !!!!!!!!!!!!!

 resi :  100   resn :  TYR

 resi :  104   resn :  ARG

 resi :  106   resn :  HIS

 resi :  108   resn :  THR

 resi :  111   resn :  TYR

 resi :  134   resn :  GLU

 resi :  135   resn :  GLU

 resi :  136   resn :  LEU

 resi :  137   resn :  ASP

 resi :  140   resn :  TRP

 resi :  202   resn :  SO4

 residues :
 {'4': 'TYR', '36': 'HIS', '38': 'THR', '41': 'TYR', '66': 'PHE', '68': 'THR', '69': 'GLN', '74': 'TRP', '100': 'TYR', '104': 'ARG', '106': 'HIS', '108': 'THR', '111': 'TYR', '134': 'GLU', '135': 'GLU', '136': 'LEU', '137': 'ASP', '140': 'TRP', '202': 'SO4'} lenght :  19

it does 74 ALA ---> 74 TRP :

######################################################
Second Script using the cmd.get_model(string "selection", integer "state" ) :
from pymol import cmd
import pymol
import time

pymol.finish_launching()
time.sleep(3)

print('\n\n------------------------------------------------')
print('\n  PyMOL Version : ',  cmd.get_version()[0])
print('\n\n------------------------------------------------')

cmd.load('7t27.pdb' , 'Acb1')
cmd.remove('solvent')
cmd.remove("not chain A and not residue ECI")
cmd.select("eci_residue", "chain A and resn ECI")
cmd.select("binding_residues", "byres eci_residue around 5")
protein = "Acb1"

print('***' , cmd.get_names('objects' , selection='binding_residues'))

for residue in cmd.get_model("binding_residues").atom:
    cmd.copy("Acb1_copy", "Acb1")
    print('residue , type(residue', residue , type(residue), residue.id , residue.index , residue.resn , residue.resi)
    # res_id = residue.get_id()[1]    ##### AttributeError: 'Atom' object has no attribute 'get_id'
    res_id = residue.resi
    res_name = residue.resn
    protein = "Acb1"

    if res_name == "ALA":

        print('++++++++++++++++++++++++++++++++++++++++++')
        cmd.wizard("mutagenesis")
        cmd.do("refresh_wizard")
        cmd.get_wizard().set_mode("SER")
        cmd.get_wizard().do_select(f"Acb1_copy//A/{res_id}/")
        cmd.get_wizard().apply()
        cmd.wizard()

        cmd.save(f"{protein}_{res_id}.pdb", 'Acb1_copy')

        cmd.delete('Acb1_copy')

    else:

        pass

It does iterate over atoms so the same output file, is overwritten more than once.
The output file Acb1_74.pdb contains the original protein where
the Alanine 74 , the only closer than 5A to ECI ligand is mutated to Serine (yellow original , blue mutated):

I think that @David's comment is worth noting, but the error tells you where the issue is:
“Atom” has no attribute “get_id”
[snip]
line 10, in <module> res_id = residue.get_id()[1]

Looking at the pymol docs, it looks like what you are iterating over is atoms rather than residues. Atom objects don't have a get_id() method, so that's why it breaks.
You should either figure out how to iterate over residues instead, or access the residue through the atom (possibly atom.resn , better atom.resi).
Here are some examples that might come in handy.


text:
how do I find the number of bp in chromosome 3 by knowing number of bp in chromosome 1?
If i have a number of bp in chromosome 1 for example(298,295,559 bp) can I use this number to find the number of bp in chromosome 3.

Chromosome of what?

human chromosomes

Since chromosomes are numbered according to size, the only thing you can say is that #3 is less than 298,295,559 bp.

http://www.ncbi.nlm.nih.gov/projects/genome/guide/human/

You cannot.  BP numbers vary between the chromosomes.  Chromosomes are numbered by size, so you can always say that 2 is smaller than 1; however, there is no function to determine the exact size of one chromosome based on the exact size of another.

Except for the point raised by MattDMo. At least we can tell that chromosome 3 is shorter than chromosome 1 as they are numbered based on their length (to the exception of sexual chromosomes)

That is certainly true but knowing that two has fewer bp than one and twenty three has fewer than that doesn't really help us determine the number in either based on the number in one.  Perhaps it points at a smaller stack of hay, but doesn't predict where the needle will be.

I agree that It offers little information but it is sufficient to make one of your sentences wrong. You say There's no relation function for the chromosomal number to the number of base pairs it has., while there actually is such a relationship.

Chromosomes vary in length and there is no reason to expect a nice relationship in the relative length of chromosomes.
However, by definition chromosomes are numbered from the longest to the shortest (except for the concern of sexual chromosomes). The chromosome 1 is the longest, the chromosome 2 the second longest and the chromosome 8 is the 8th longest. Following @ping comment Also note that human chromosomes 21 and 22 are numbered the "wrong" way round in that 21 is actually smaller than 22; so even for autosomes using the numbering to determine size rankings doesn't necessarily work.
In consequence, if you know that the chromosome 1 is x bp (base pairs) long, then the only thing you can tell about chromosome 3 is that is has less than x base pairs. Note that x ≈ 250,000,000 base pairs in human.

Also note that human chromosomes 21 and 22 are numbered the "wrong" way round in that 21 is actually smaller than 22; so even for autosomes using the numbering to determine size rankings doesn't necessarily work.

I didn't know that. Thank you, I added your comment in the answer

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sort: votes


text:
How can I search for and find specific biology topics in scientific journals?
I looked on google to find "scientific paper on biological explanation of homosexuality" but nothing comes up that appears reliable or from a journal. Then I looked up "scientific journals" and I found a directory for them, and searched through that directory, but of all the journals, I cant seem to find an efficient way to search for topics in these journals over the web.
Is there a way to efficiently search for specific scientific journal papers, specifically for biology?

https://www.ncbi.nlm.nih.gov/pubmed/ is probably the most common way to search for papers in this area of science.

And scholar.google.com is an alternative to pubmed.

Note that the directory you found, OMICS International, is a predatory publisher according to Beall's list; I would be highly suspicious of any journals you find there.

note pubmed restricts itself to reputable journals, google scholar does not. so use google scholar to find terms then switch to pubmed to look for more detailed papers.

There are two possibilities for searching for scientific articles:
The first one is to use PubMed, a database which has been set up by the National Institute of Health in the US. It contains about 25 Million journal articles. All articles in this database are coming from peer-reviewed journals.

The other one is to use Google Scholar, which is better when you are unsure about search terms. It will give you more results, but you have to be careful here, since not all hits are from peer-reviewed journals, sometimes you get some quite questionable sources.

As a general purpose tool for searching the scientific literature (or even biology in general) I would argue that PubMed is poor. Outside medicine the coverage is hit and miss. The main pro is that it's open for all to search.

While the core focus of PubMed is on the medical literature, the nature of medical research means that coverage of the biosciences is extensive, where the discipline can be related to human health. As a consequence much of genetics, molecular biology and biochemistry is also covered. For additional coverage adding more of the agriculture, environmental and ecological domains try EuropePMC (http://europepmc.org/) which adds literature from the ARGICOLA (http://agricola.nal.usda.gov/) database to the PubMed/MEDLINE/PMC data.

@HamishMcWilliam Well, "much of" isn't really good enought for a general purpose search tool for biology. The fact is that "much of" ecology and evolution (areas where I'm most familiar) isn't covered by either PMC or EuropePMC, and the same goes for e.g. taxonomy. For this particular question, the journals Journal of Homosexuality, Evolution and human behavior or Journal of Human Evolution could be relevant, but neither is covered by PMC.

@fileunderwater Interesting to note that the three journals you mention are categorized as focusing on the humanities by JournalSeek. Checking the list of journals included in PubMed (ftp://ftp.ncbi.nih.gov/pubmed/J_Medline.txt), articles from Journal of Homosexuality (e.g. https://www.ncbi.nlm.nih.gov/pubmed/26914706), Evolution and human behavior (e.g. https://www.ncbi.nlm.nih.gov/pubmed/26880866) and Journal of Human Evolution (e.g. https://www.ncbi.nlm.nih.gov/pubmed/26852814) do appear in PubMed, although they appear to be recent additions so only a limited set of articles are present.

Well, that doesn't really say much. And you don't have to look very far for journals not covered by PMC; Evolutionary applications, Animal conservation, Biodiversity & conservation, Method in Ecology & Evolution, Journal of Biogeography... The list goes on and on and on.

Basically, if you think that searching within PMC gives you an overview of what is published in biology, you get a very incomplete and distorted view, as well as a lot of geographic bias. And as you've noted, single papers can sometimes show up, but that is because authors are sometimes required by funders to deposit them there (e.g. many publicly funded american authors, which will increase the geographical bias on top of the underlying journal bias).

@HamishMcWilliam Don't get me wrong, PMC is good for what it is: an open directory where everybody can search. But you have to be aware of its limitations vs e.g. Web of Knowledge or Scopus. PMC is not a broad general-purpose database of Science (or biology). We should probably move this to chat though.

Worth noting that Web of Science, Scopus, SienceDirect, etc. also do not cover all the scientific literature. In my experience they can be missing stuff which is present in PubMed. So if you looking for broad coverage you have to search all the databases you can access, and even then you will likely be missing stuff. Where stuff is publicly available Google Scholar and web searches may help fill gaps.

@fileunderwater From my experience in various topics of biology, Pubmed is not to bad. The rest can be done with Google scholar, that`s why I recommended both.

Web of knowledge (from Thomson-Reuters) and Scopus (from Elsevier) have the broadest coverage of peer-reviewed journals, if you have access to them through your library. Google scholar is a free option that also covers a lot, but with poorer search options and less quality control. Pubmed is an alternative, but coverage in many areas of biology outside of medicine (or other scientific fields) can be poor.

If you have access to library resources with your university, Scopus is brilliant. It allows you to search specific topics and articles published by a particular author.
http://www.scopus.com/

Short answer: use a free literature search service such as PubMed or EuropePMC. As an example of how to use it for the example you give, searching EuropePMC "evolution of homosexuality" (as a phrase) gets you to this paper, the full text of which is then available straight from the search result.

The best way to find scientific papers on a specific topic is to use a literature search engine. There are five main ones I'm familar with so will discuss specifically: PubMed, Google Scholar, Scopus, Web of Science and EuropePMC.
Each has advantages and disadvantages. There are some published comparisons of different search providers (e.g. Falagas et al. 2008, Anders & Evans 2010, Schultz 2007) but the main difference in practice unless you are at a major university is that PubMed, Google Scholar and EuropePMC are all free, while Scopus and WoS are subscription-only.
Other major differences include:

PubMed is designed for biomedical use, although in my experience
coverage of other areas of the life sciences is acceptable. There are
tutorials on using PubMed here.
Google Scholar includes a lot of 'grey literature' which is not
peer-reviewed, which could be an advantage or a disadvantage. I tend
to steer clear of it unless I am specifically interested in the grey
literature.
Scopus and Web of Science (previously Web of Knowledge) are
subscription service operated by Elsevier and Thomson Reuters
respectively. Both integrate additional article metric functionality
for example H-index and impact factor, although it
doesn't sound like you would need these. I find Scopus slightly
easier to use and a few comparative studies suggest its coverage is
slightly more complete but there's not much to choose between them.
Finally, the 'new kid on the block' is EuropePMC which seems to be
very similar to PubMed but apparently indexes substantially more articles
than PubMed. It also has some nifty functionality such as searching
by grants, linking to ORCIDs etc. It allows search automation via
software packages which is very useful for systematic reviews etc
(others may also do this but if so I haven't found it yet). I think it's becoming my favourite.

As a final cautionary note, different search services cover different journals and have different biases. If you're doing a systematic review paper or meta-analysis the official PRISMA guidelines recommend using at least two different services to minimise this problem.
(Many thanks to the many other users who added useful comments and shorter answers to this question; I'm just trying to collect them all together)

Pubmed: you can find articles about medical fields.
Biological sciences (proquest): a very specific database for biological articles.
Web of science: suitable for interdisciplinary articles.

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text:
Why is your taste affected due to sinuses?
I heard someone say "My sinuses are acting up, I can't taste the food." I don't think the person is lying, they probably believe this but I'm having trouble seeing how the sinuses would affect the taste buds. I realize smell helps identify foods, but it seems like not smelling a food wouldn't affect taste so severely as people make it sound.
I don't have sinus troubles much and haven't experienced this, so I'm not claiming it's fake, I'm just curious to understand how that works.

Scent and taste are intimately connected. Try tasting something flavorful, rinsing your mouth out with water, then holding your nose and tasting it again - it will be much "duller". Taste buds and scent receptors signal to the same part of the brain.

The first thing which is important to note is the difference between taste and flavor.
Taste refers to the chemical sense performed by taste buds present on the tongue, and to date there have been identified 5 tastes: sweet, bitter, sour, salty and umami. Thus I understand obstructed nose and sinuses should have no significant effect on taste.
Flavor, on the other hand, is the final sensation that conveys the information about the food we're eating, and involves not only taste, but also smell, mechanical sensation (like that smooth flavor from cream) and pain and temperature pathways (hot and spicy food, like peppers). Part of the signals from all these receptors located on the mouth (and nasal) cavity ultimately converge to the same location in the brain, where they are processed to create the final flavor (I know taste and smell do converge to the same region, cannot tell the others with full certainty).
So, having obstructed sinuses and nasal cavity can interfere with the smell detection (by not allowing molecules to bind to receptors on the olfactory epithelium), and thus interfere with flavor.
You can check this site which I think explains very well what I am trying to pass on, it is very clear and covers all the physiology that I talked about, allowing you to go deeper into details if you are interested: http://www.cardiff.ac.uk/biosi/staffinfo/jacob/teaching/sensory/taste.html and also http://www.cardiff.ac.uk/biosi/staffinfo/jacob/teaching/sensory/olfact1.html (you have to scroll down to the main text)

any sources to add?

@AliceD I wrote based on what I have been studying over time, from neuroanatomy and anatomy to physiology, and also some autonomous research, but if you search it on google you will probably get the same information, maybe even in Wikipedia!

@Filipe I suggest you search through those sites (and preferably more reputable sites as well) and add some sources to your answer. Otherwise, it will be closed/deleted. See here for a guide to writing good answers on Bio.SE.Thanks

@theforestecologist i feel as if we are giving way to much importance to reputation. I am simply sharing part of the knowledge I have been accumulating over time, from what I have studied in Medical school to what I have read in my personal researches and life experience. That is how it should be taken, as me trying to share what I know with another person, and not the whole and absolute truth - and that's science, in my opinion. I don't think reputation should be so impactful, but rather the facts that are behind what I'm saying.

@FilipeRocha - everyone can claim to be an expert and start babbling away. Although I don't doubt your expertise in this area I'm downvoting your answer as you're blandly ignoring the advice of hi-rep users. Please understand - reputation on this site is a reflection of nothing more than user effort; even laymen can gain a lot of rep here simply by quoting wikipedia. The reason we ask for sources is that it allows users to background read on the topic and get in-depth understanding of your answer.

@Filipe and all that experience makes finding proper sources easier because you already know some sources, you know the proper keywords to find new ones and you can better recognize their validity. Anecdotal information is interesting for sure, but on this site we require that you back up your answers with sources b/c other users don't have the experience to know what is valid or not. If you want to share anecdotal info/answeres on Bio.SE, it is best shared (and welcomed) in the comments.

@theforestecologist thank you for the explanation, it does make sense and if it was me I would also like others to show me where can I find something that I can use to verify or further learn about the topic.  So I went looking for such and found this site which I think explains very well what I was trying to pass on, it is very clear and covers all that I talked about: http://www.cardiff.ac.uk/biosi/staffinfo/jacob/teaching/sensory/taste.html
I hope you find it useful (you have to scroll down to the main text), and once again thank you

@AliceD the answer above is also for you :)

@Filipe Great! Just one last thing: we ask that answers be complete (i.e., not needing comments to "fill-in" further information). Please incorporate your link into your answer. Further, providing context for the link is super useful because some links break over time; as a result, it's useful to provide a bit more than just the link (.e.g, what does the link contain, what part of your answer is it pertinent to, etc.). Copying (and citing) a photo (which that site has numerous) would be a great addition to your answer as well :). Thanks for putting in the effort to improve!

@theforestecologist done :)


text:
Do neural axons extend around connections like this?
I was wondering if axons sometimes connect like this:

Note that I'm not referring to situations where the path of that network is curved and the 3rd / 4th neuron is just as close to the 1st neuron as the 2nd is, I'm talking about situations where the 3rd / 4th neuron is physically 2-3x as far from the first than the second neuron, or more. This is relevant to neural simulation.

Yes, all the time, but there isn't much meaning to the conceptualization of "1st, 2nd, 3rd" neuron. Real, biological neurons in the CNS aren't connected in simple feedforward loops, recurrent connections are common, and individual cells can have both local and distant projections.

@BryanKrause You answered my question but I'd point out that I wasn't suggesting that the system is as simple as a 1-2-3-4 feed forward connection, I'm just referring to the physical location of 4 specific neurons in a much more complex network.

Got it - you might be surprised that many people who come at neuroscience from a background in artificial neural networks take all sorts of biologically goofy assumptions away from it. I will say that in the neocortex, where most of my expertise is, the pure number of contacts between cells is definitely a function of distance, falling off over 200-400um, but there are also projections that go for many mm, even in a small brain like a rodent.

@BryanKrause interesting. This may be too complex for a comment question, but I'll try: Could localization (axon "length" limit) to some extent be beneficial to a neural system, or would a system likely benefit from infinite axon length potential?

I would search for some literature on "small world networks" if I were you - I think this will interest you a lot. Doesn't directly answer the questions you are answering but it will tell you a bit about the types of optimization that are possible.


text:
Has aloe vera been proven to help heal burned skin areas?
I don't like buying into "natural remedy" type things without seeing scientific proof behind them. There's an almost universal belief that aloe vera helps to heal burned skin, and whether that includes assisting in cell regrowth, preventing inflamation, or something else, I haven't bedn able to find any real scientific evidence.
Can anyone cite legitimate scientific evidence that aloe vera has any helpful effect for burned skin? If so, how does it work?

No, there is no reliable proof of its effectiveness (if I remember correctly, one decent study found delayed healing.) And I actually like "natural remedies", which is why I look for supporting studies. But you might cite a source and ask on Skeptics.SE.

A quick Google Scholar search gave me this paper which is a list of abstract of research that suggests it helps with would healing, inflammation and burn wounds


text:
What was the first known organism to exhibit muscle growth based on activity?
Being able to grow bigger muscles to match an organism's personal habits seems like a pretty nifty feature since most organs grow to one specific size, aside from some stretching.
Was this a feature as long as muscle tissue has been around? If not which species had the ability first?

It would depend how you define a muscle no? This article has an informative take on the evolution of muscles. http://www.en.uni-muenchen.de/news/newsarchiv/2012/2012_woerheide.html


text:
Is the brain functionally symmetrical?
I understand that each half of the human brain handles different parts of our thinking. Left brain, right brain, that whole topic.
But in pictures, the brain is always depicted as having symmetrical structure. I'm curious about that. I realize that it might be silly to expect such a complex tool to be truly symmetrical, so my question is:
Is the brain functionally symmetrical or not? By functionally, I'm referring to whether the specialized groups within the brain all exists on both sides or rather each side contains different components.

No. For instance, Broca's area exists only in the frontal lobe of one hemisphere, usually the left. (it's responsible for speech, btw)


text:
Correlated evolution of discrete traits: do traits need to have phylogenetic signal?
I'm doing a phylogenetic analysis using the Discrete program in BayesTraits. Of the  traits I am testing, one of them does not show any phylogenetic signal (using the Fritz and Purvis d-statistic).
Does this mean that a test of correlated evolution using this trait is actually not appropriate? I was surprised that there is actually some support for correlated evolution between this trait with no signal and three other traits (Bayes Factors of 4-12).
Some of my colleagues, who know more about this than I do, think that Discrete analysis can be used if only one trait shows phylogenetic clustering.
I would be very grateful if someone could let me know whether or not this is the case, or point me towards any references for this! Thanks in advance

I have a gut sense that you might be able to learn something even in the absence of phylogenetic signal in one of two characters. I don't have a reference, but I expect that simulations could sort it out.
I'd recommend using data of similar shape simulated on your tree to experiment with how frequently you would expect BFs of that magnitude even with independent evolution.
For example, you could shuffle the state of the non-signal character at the tips of the trees, and see how frequently you get a similar BF from Discrete. This is a heuristic Monte Carlo approach without a strong formal basis, but you could at least evaluate whether something about your phylogeny's structure is pathological and confuses Discrete. This Monte Carlo approach is implemented in Mesquite, providing some methodological precedent.
I'd also recommend running Discrete with MCMC rather than ML, if you have only used ML. For your actual trait data, I'd examine the rate parameters late in the MCMC chain using Tracer. If there are a lot of modes of the rate distribution, then it's possible that the internal reconstructions are too noisy to draw much of a conclusion.
I'd also consider whether you are encountering a multiple testing problem. How many total phylogenetic correlations are you examining? If the answer is "a large number of bivariate correlations", then you do expect to find what appears to be a strong association at some rate even when there is no association.
It would also help to know more about the size of your phylogeny and how the different characters look when mapped onto the tips, or on a sample reconstruction.

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How to theoretically calculate amount of product in first-order reaction?
I was wondering if it was possible to calculate the amount of product theoretically produced from in vivo (human) values to determine if that's the only enzyme causing the increase in amount of product. The rate of the reaction is dependent on enzyme concentration, and assumes that enzyme $K_m << [product]$ (in rats at least).
From the papers I have read, others have calculated the theoretical concentration (in rats) by:
$[product] = (k_{cat}/K_m) * [substrate] * [enzyme]$
However, as far as I remember $K_m$ is dependent on multiple environmental factors and $K_{cat}$ can change as well.
Thus, I'm wondering how I could theoretically calculate it.
Post-edit:
My questions are more this:

Can I use the $K_m$ and $K_{cat}$ I found in papers for the reaction (also found in humans), given that they differ greatly between papers.
Is the equation given above correct for a first-order reaction?
Any papers or books I can read to learn more about this?
Any ideas to calculate this?

I suggest googling the issue a bit, this paper that I found quickly looks like it addresses some of your concerns directly (notably accuracy of K parameter estimates). Also it would help to link some of the resources you seem to have found.

You need to set out your problem — or an example — with actual values, and what you want to calculate. Without this I doubt whether anyone can help you.

The answer to question 2, I think, is an emphatic yes, provided that the substrate conc is way below Km (the Michaelis-Menten equation then describes a first-order reaction).  Two great sources are Fersht Structure and Mechanism in Protein Science and  Frost and Pearson Kinetics and Mechanism

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Nitrate fertilizer problem

Take the above problem. I understand how to do the calculation. However I can't seem to understand the units of the answer in the calculation.

The answers illustrate the units as t/ha^-2 which is equivalent to t(ha)^2. But where do these units arise from? Crop yield is represented by tones per ha in the table above. So wouldn't total crop yield just be tones? I can't seem to find any intuition whatsoever as to why the units are t/ha^-2? Could someone please give me a hint or a solution?

Please do not post text as images. Accurately type the text into your question. Images are not searchable, and cannot be interpreted by screen readers for those with visual impairments. Use the [edit] link to modify your question.

I think this is a mistake in the provided solutions – it should say either $\mathrm{t/ha}$ or $\mathrm{t \, ha}^{-1}$. Furthermore, the answer should be multiplied with the area of fields.
There are two different quantities in this task: yield which is the mass of harvested crops (and has units $\mathrm{t}$), and field yield which is yield per unit of field area (which has units $\mathrm{t/ha}$). In the provided table, you are given field yield, but in the question, the farmer wants to have the highest yield.
The yield if fertilizer is put on one field will be:
$$m=7\;{\rm \frac{t}{ha}}\times 1\;{\rm ha}+3\;{\rm \frac{t}{ha}}\times 1\;{\rm ha}=10\;{\rm t}.$$
The yield if the fertilizer is spread equally on both fields will be:
$$m=4.8\;{\rm \frac{t}{ha}}\times 1\;{\rm ha}+4.8\;{\rm \frac{t}{ha}}\times 1\;{\rm ha}=9.6\;{\rm t}.$$
Therefore, the farmer will produce more crops if he puts all fertilizer on one field.


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What characteristics identify modified 'plant parts' as the respective 'plant parts'?
I was learning about different modifications in plant parts such as modified leaves, stems and roots from my Biology textbook.
Modified parts differ as they are modified for different functions.
For example, the pitfall traps in a pitcher plant are called modified leaves. These have completely different function than normal leaves but are still referred to be leaves.

What characteristics identify such parts to be those parts?

Not an answer but helpful background/vocabulary: https://en.wikipedia.org/wiki/Homology_(biology)


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Is the technology "identitas v1 forensics chip" related to microarray technology?
Available resource but difficult for me to make scence
Relation about crime scene and identitas v1 forensics chip
Is the technology "identitas v1 forensics chip" related to microarray technology?
if true ,as I know, different combination of genes are expressed in different parts of our body which means a certain tissue only makes particular types of mRNA.
Then my question raised: How can a CSI crew reconstruct a person's virtual appearance (for example skin color, face structure) by a piece of microarray with limited tissue (for example cells from saliva) and mRNA?
I mean saliva cells don't make pigment of our body, so how can the eye color or skin color be presumed, for example?
Otherwise, what is the technique "identitas v1 forensics chip "which allow us  to detect several phenotype  simultaneously?
According to the information I Know,"identitas v1 forensics chip" it contains hundreds of thousands of short sequences of DNA that binds to SNPs,where the DNA from the crime scene binds to this chip can allow software to reconstruct the appearance of the person of interest.
the chip is the first to provide data on all these traits simultaneously. Other devices can determine at most two at a time – usually eye and hair colour.

It'recommended to include information in your question rather than just providing the links - could you add some information about this chip to the body of your question?

Sure! I will try to describe it as best as I could.

Interesting question. The answer lies encoded in our DNA. If you take eye color for example, the genes important here are well known. The most important are OCA2, HERC2, SLC24A4 and TYR.
These are involved in different parts of the pigmentation process, any mutations in these genes lead to changes in pigmentation. Since also the variants, which lead to a altered pigmentation are known, you only need to analyze some cells containing genomic DNA from your suspect to check for these mutations (or SNP, single nucleotide polymorphisms).
The same is true for hair and skin color. So if you identify one or several mutations in the MC1R gene, you can be pretty sure, that your suspect is red haired, has pretty light skin and a high chance for green eyes.
This technique doesn't need to know the exact expression of a certain gene, but needs information on the cause for a phenotype (like skin, hair or eye color) and the causative gene.
The "Identitas v1 forensics chip" is a microarray chip, unfortunately, the company website is not really a source for information. You can find some in the New Scientist article you linked. This is basically a microarray (or chip) where all the forensically interesting and known SNPs about how a person looks like are analyzed.
It gives basic information (or at least a chance) how a persons looks like, what CSI does in the series is usually widely exagerated.

Thanks a lot! But I feel sorry for my incomplete and unclear description to my question. I still wonder  if  "identitas v1 forensics chip" have any connection with microarray and how they work? if true ,how can the SNPs be detected when they don't express?


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Why we need an egg cell donor and a surrogate mother in an organism cloning process?
Could a whole set of artificial organism-cloning process only be operated on the  somatic nuclear donor ,which means for example ,can we extract the somatic nuclear from animal "A" and put it into the egg cell plasma also from animal "A"  then implant it into the animal"A"'s uterus to clone "A" ?

Could a whole set of artificial organism-cloning process only be
  operated on a somatic nuclear donor?

No, this would not be possible. Single-cell reprogramming would enable you to reset the potency status of that cell up, yielding an embryonic stem cell (ESC). However, ESC do not have the ability to generate extra-embryonic structures (e.g. placenta), which are known to be required for providing oxygen and nutrients to the embryo, amongst other relevant functions.
Theoretically, it could be possible to replicate the embryological environment, and I think this is the second part of your statement. Nevertheless, in practice this is not possible... the amount of signals and parameters that one would need to control simultaneously is far too extensive.
I don't quite see the point of having an enucleated egg and performing somatic cell transfer, when you're not really interested in implantation in utero. Somatic cell reprogramming would be sufficient (see iPSC)

thanks ! Now I gain some new knowledge now , but there is a little bit misunderstood , what I mean is that ,for example ,if we get a somatic cell from animal "A" , can we just transfer that cell to animal A's uterus to clone animal"A",instead of finding another surrogate mother or egg cell donor?

@Snake From your comment and your newly edited question I see what you mean. You are wondering whether it is possible to clone an animal by using its own somatic cells AND eggs.
I do not have extensive experience with transgenic production, but I have a hypothesis on why the same female is not used as a donor and for implantation: oocyte extraction is an invasive method that may be destructive (i.e. the donor female dies). Therefore, it is not possible to use the same female and a foster mother is required.

the trick is ovum come with a whole package of signal pathways built in before fertilization that you need to trigger implantation and embryonic development. In theory you could engineer these (search artificial ovum)  but it is drastically easier and less expensive to just use existing ovum organisms produce for essentially free.
could you use ovum and somatic components from the same organism that is the surrogate mother, sure, but there is not much reason to do so. You still need a donor egg and surrogate mother they just all happen to be the same individual.


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Why was the study of "Concordance of Monozygotic and Dizygotic twins for traits" designed in this way?
I am confused by the twin study 'Concordance of Monozygotic and Dizygotic twins for traits.' My questions arose from 3:17-4:17 of the video
And this is the related data I  have referred
I have the following questions:
1 Is the dizygotic twins also separated in different families? If true, didn't the DZ group lack the Control Variables of 'same environment 'or'identical genes'? Or should we make the '50% identical genes' as control variables?
2 why do we need Dizygotic-Twin groups in the experiment, if we need to find the environmental influences why not just find a pair of unrelated individuals and set them at a same family (environment)? Alternatively, is it necessary to compare the monozygotic groups with dizygotic groups instead of any others that aren't dizygotic twins?

It's unclear what your questions are and you should avoid asking so many questions at once, and questions should be able to stand alone (we should not need to watch the (bad) video).

Thanks for your suggestion,I have isolated my questions .

I established the other question   Hope you can check it out.

My interpretation of the first question is why do traits determined by the environment appear to be equally similar among monozygotic and dizygotic twins in these twin studies. The studies he is talking about look at twins that are separated and adopted in to different families. These different families provide a different environment for either twin, and with enough samples, you can compare similarity between dizygotic and identical twins. So imagine you measure the trait of interest (height) in all individuals, and find that identical twins more closely resemble each other than dizygotic twins do. This would indicate that height is somewhat genetically determined - the more genetically similar pairs were more phenotypically similar.
Why use mono- and dizygotic twins individuals to test environmental effects? Comparing mono- and dizygotic twins is a good experimental design - it removes the effects of being a twin (nutritional environment in the womb may differ if you use monozygotic twins vs single born siblings), effects of year and season of birth, effects of womb environment among the two single born individuals, and in one group you have zero genetic variance, while both groups should have the same amount of environmental variance. Read here about heritability, he gets the explanation wrong in the video, heritability is not a measure of how genetic something is, it is how much of the phenotypic variation ($V_P$) is explained by additive genetic variation ($V_A$).
$$h^2 = V_A/V_P$$

Thanks for your answer ,but I still have some questions about the first part of your answers. If there is a TRAIT determined by environment ,  both the identical twin group and fraternal twin group have 100 samples in each of two families.  After the research , in identical  or fraternal group , it is found that both families have 30 of 100 samples that have TRAIT,so 30% people have same trait in the  group.My question is why the difference of both  environments can cause that 30% same TRAIT, and also equally similar to those in the other group.

If the trait was genetic then the trait would be more common in the group that is more genetically similar (the identical twins), but if the trait is entirely environmental (and assuming both groups experience the same environmental variation - requires large unbiased sampling effort) then there is no reason for either group to differ in the frequency of the trait.

For example; if trait is caused by exposure to chemical-A and 30% of people are exposed to chemical-A then both groups should have a trait frequency of 0.3 (or 30%). However, if trait is determined by genetics, then identical twins are identical for trait, i.e. if one has trait, the other in the pair also has trait, while in the non-identical twins the presence of trait in one twin is not as informative about the other in the pair (the second twin may have trait, but not necessarily)


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Perplexing by the way of estimating the shared or different genes between humans and chimps
We share 98.5% genes with chimps (it means we have 98.5% same DNA sequeces ),so there is about one percent difference .It means we can approximately differ from them by one base pair every hundred base pairs on average.
The following is my question.
A human receive 3 billion base pairs from each of parents ,and has six billions in total .Do the math by using one hundred to divide six billions and then it equals sixty millions.
Due to that, The person have ,on average ,sixty-million-nucleotide differences with a chimp.
However,the professor of the online courses I attended said it's thirty-million-letter differences.
Dose that mean it's counted on haploid?Why?
Also ,I'm not sure that about one percent difference is calculated on one base pair or one nucleotide every thousand base pairs or nucleotides .Because he mentioned the both.
This is the course ,my questions occur at 1:58
In another course , similar questions occur at 3:11

I do not really understand your question. What do you mean by 98.5% gene sharing? Do 98.5% of human genes have a homologous gene in chimpanzees? Or is there 98.5% sequence identity in human and chimpanzee genes (and if so, is the difference due to fixed differences?)? Is the one bp per 100 bp difference only related to gene regions? And I can by no means guess what you mean with your last sentence.

Each of us ,on average ,varies from a chimp by about one nucleotide at particular loci every hundred basis.

I'm the first-learner in this realm ,so I can't clearly explain that so much,but as what I learned,the conception could be a bit similar with SNP(Single Nucleotide Polymorphisms),but SNP only apply on a paticular species.

I tried to explain the concepts in my answer. Note that there in fact are SNP between species, so called shared alleles or trans-species polymorphisms.

You might want to read through the answers here: Do apes and humans share 99% of DNA or 99% of genes? What is the difference?

Even though I am not sure I understand your question completely, I want to try to explain to you the genetic difference between humans and chimpanzees. I will work through your questions:

We share 98.5% genes with chimps ,so there is about one percent difference .It means we can approximately differ from them by one base pair every hundred base pairs on average.

It is correct that humans and chimpanzees differ approximately every 100 nucleotides in their DNA sequence. This is does not mean that 98.5% of the genes are shared. It means that humans have about 98.5% (more precisely about 98.8%, The Chimpanzee Sequencing and Analysis Consortium, 2005) sequence identity with chimpanzees, disregarding indels. The main part of this difference (about 85% of the 30 - 35 Mio. different nucleotides) comes from fixed differences: a fixed difference is a position in the haploid genome in which every human has, say, a G and every chimpanzee has a T. Accordingly, the site is different between the two species for every individual of the respective species. The smaller part (about 15%) comes from sites that are either variable (SNP) in humans or variable in chimpanzees, or in both (there is even a small number of very old variants, i.e. shared alleles between humans and chimpanzees, e.g. see Azevedo et al., 2015). Note that the estimates get better the more individuals of the respective species are sequenced and compared.

A human receive 3 billion base pairs from each of parents ,and has six billions in total .Do the math by using one hundred to divide six billions and then it equals sixty millions.
Due to that, The person have ,on average ,sixty-million-nucleotide differences with a chimp.
However,the professor of the online courses I attended said it's thirty-million-letter differences.
Dose that mean it's counted on haploid?Why?

Yes, it is counted on the haploid genome. I would not make any sense to count it on the diploid genome. When looking at my last paragraph you might see why: Remember, we are looking at (i) fixed differences (both copies of a diploid human genome differ from both copies of a diploid chimpanzee genome) or (ii) at variable sites. Assume you find one site in one haploid genome that fulfills either (i) or (ii). If you then look at the same site in the other copy of the genome you already know that the position is either (i) or (ii). This means that it has already been counted as a difference. If you counted it again, in the worst case, over the complete genome, you would count everything twice. In general, you would strongly overestimate the absolute difference.

Also ,I'm not sure that about one percent difference is calculated on one base pair or one nucleotide every thousand base pairs or nucleotides .Because he mentioned the both.

I do not understand this. I had a brief look at the video and heard him talking of one nucleotide per thousand. He compares the sequence difference between human-chimpanzee (98.8% overlap, approx. 1 per 100, about 1.2% fixed differences and SNPS) and human-human (99.9% overlap, approx. 1 per 1000, 0.1% SNP), pairs. Note that in the last case we cannot look at fixed differences as there are no fixed differences between human populations. The 0.1% difference are the percentage of SNP in the human genome.

I'm sincerely appreciated for your detailed answers,after reading the first and second parts ,the third question has been solved . But I am not sure that I really make sense of the difference between sequence identity and genes,can you explain that for me?

According to your second answer ,I have question about "the same site".Does that mean the certain alleles at homologous chromosomes which control a certain gene have the completely same DNA sequences? –

What you seem to be mixing is having (i) homologous genes and (ii) identical sequence. (i) does not imply (ii). You can easily have the same gene but non-identical sequence, i.e. different variants of that gene. Within species we call that alleles, between species homology. Additionally, only a few percent or so of DNA codes for gene products (e.g. protein, miRNA, tRNA, rRNA, ...). So the vast majority of sequence differences between humans and chimpanzees lies outside of genes.

sorry , I have thought for a while ,my third question still exist ,the sentence might look weird , what I want to ask is that "why do we sometimes say one base pair of every hundred base pairs instead of saying one nucleotide of every hundred nucleotides?

To response the comment of  AlexDeLarge ,if the sequence of"the same" site is not identical ",how can we consider the one side by the other ?

@terdon: The Chimpanzee Sequencing and Analysis Consortium treated indels and nucleotide differences separately and "calculate[d] the genome-wide nucleotide divergence between human and chimpanzee to be 1.23%" which includes intergenic regions and introns.

@Snake: A site is one nucleotide. The vast majority of sites are equal between humans and chimpanzees (as you know, about 98.8%). Accordingly, you can easily identify the same site on the homologous chromosome even though the site itself is not identical.


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At what rate does C-BSE occur spontaneously?
BSE is back in the news here in the UK thanks to a new detection in Scotland. I haven't looked into transmissible spongiform encephalopathies much for a decade or so, but as I understand it the general model for TSEs is that an initial spontaneous misfolding of the protein PrP catalyses the misfolding of other PrP proteins until (over a fairly long incubation period) spongiform structural changes, amyloid plaque formation and other pathological changes cause CNS disease typically manifesting as behavioural changes. Ingesting a dose of misfolded protein can infect new hosts of the same species, and thus farming practices which include feeding animal byproducts to the same species can inadvertently amplify transmission, which resulted in the BSE epidemic in the UK back in the 1990s. Rarely, this transmission process can cross the species barrier.
I can find references to spontaneous scrapie in sheep and spontaneous CJD in humans, but very little on classical BSE in cattle. I do remember that there was a theory that BSE orginated when cattle were fed meat-and-bone-meal (MBM) from scrapie-afflicted sheep. I have found one peer-reviewed article suggesting that at least one type of atypical BSE (H-BSE) can occur spontaneously. I have also found one popular-science article that sounds like it describes spontaneous BSE, but it's unclear whether this is C-BSE or the H-BSE finding above (it's behind a paywall) and it's over ten years old, so I don't know what further developments there have been in this area.
Can classical BSE (C-BSE) arise spontaneously in cattle populations, and if so at what rate?

This paper suggests it was still be an unanswered question in 2006: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3291375/


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How can I create R8 (homopolymer repeat) filter without using illumina pipeline?
illumina instruments have built-in -or online- analysis software for variant analysis (CASAVA). This software can filter out the false positive variants near the homopolymer repeats (AAAAAAAA) and filter them with "R8" tag.
Is it possible to make homopolymer repeat filter without using illumina's own pipeline? (with another software?)
P.S I noticed that, GATK have HomopolymerRun script that makes similar job. But it is no longer supported and recommended.

Yes you can do it with perl or awk or other such languages.

Does it mean that there is no software for such filtration? Should I write my own script? There should be an easier way.

People have made such scripts. Try this one called prinseq. It runs on perl


text:
What is the effective population size of a simple two deme metapopulation?
I am confused as to how to compute the effective population size $N_e$ of a theoretical structured population. Let's consider here a simple case study.
Imagine a 2-deme metapopulation. Each deme is of constant size $N$ with a (forward and backward) migration rate $m$. Mating is random within each deme.
What is the effective population size of such population? In other words, how fast does the population loses heterozygosity through time?

this book looks useful - see page 109 (there is restricted access) https://books.google.se/books?hl=en&lr=&id=pjo5FP5gpFIC&oi=fnd&pg=PA87&dq=effective+population+size+metapopulation&ots=J_z6Ygwl_X&sig=O0Op0mXXYKHdW2OweT8CJKew79Y&redir_esc=y#v=onepage&q=migration&f=false

There is no single effective population size when there is population structure. Suppose structure is strong, $Nm \ll 1$. If you start with very high heterozygosity, it will first decay at a rate close to $1/N$, then more slowly at a rate close to $m$ after the diversity within each deme has been lost.


text:
How do (commensal and mutualist) microorganisms colonize the seminal vesicles?
Human's seminal fluid has it's own microbiome (Javurek et al. 2016). How do species of this microbiome (bacteria and eukaryotes) colonize the seminal vesicles?
It is possible that different species would colonize the seminal fluid through different means. What are the possible ways by which such colonization could happen?


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How to refer to person-derived and place-derived species names
Are there words that categorize latin specific epithets by how they're derived? Specifically, I was wondering if there exist adjectives to refer to:
Person-derived species names as in Nothura darwini (these could be "eponymic" or "eponymous" perhaps, but that seems grammatically wrong )
Place-derived species names as in Amolops hongkongensis (would these be "toponmyous", or maybe "loconymous"?)

I think generally both could be called latinisations, as the practice with species names is to take the name and try to translate/modify it into an appropriate Latin genitive case.  As far as a word the gets specific enough to reffer to eponymic latinisations, no I don't think there is one.  I searched through the OED a few times but I don't think there is one.  Do you have reason to coin the term?  I would be excited if I was proven wrong.

This isn't a purpose-driven query – just trying to write a sentence and looking for le bon mot. As an update, I did find a few thousand google hits for "eponymous taxa", but also some criticism of that phrase; and nothing similar for place-derived names.

According to A Source-Book of Biological Names and Terms by Jaeger, the appropriate terms are the simple, obvious ones:
"Geographical" for place-derived names and
"Personal" for person-derived names.


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Which mRNAs enter P-bodies?
Processing bodies (P-bodies) are distinct foci within the cytoplasm of the eukaryotic cell consisting of many enzymes involved in mRNA turnover (ref). They play a fundamental role in RNA silencing/interference, particularly as an antiviral response, since they are the key site for siRNA-bound RISCs (small interfering RNA-bound RNA-induced silencing complexes) to degrade mRNA with an exogenous origin. Some mRNAs entering P-bodies then leave and re-initiate translation, and the switching mechanism for this is currently poorly understood.
However, I'm not clear on whether all mRNAs pass through P-bodies at some point, when not actively involved in translation. Is there is a separate step by which mRNAs of exogenous origin are specifically (or more rapidly) recruited to P-bodies - and, if this happens, how are they specifically targeted for this uptake?
It seems rather odd if RNAi has evolved to give viruses two independent targets for evasion, but if the only requirement for recruitment to a P-body (and potentially degraded via RNAi) is to not be currently involved in translation, wouldn't that select for viral proteins to be more highly translated (and therefore postpone movement to the P-body)? I don't really understand why mRNA processing doesn't simply occur in the cytoplasm.
The paper cited above says "The available evidence indicates that P bodies are sites where mRNAs that are not being translated accumulate, the information carried by associated proteins and regulatory RNAs is integrated, and their fate — either translation, silencing or decay — is decided", but this is from 2007 and I'm aware RNAi is a very fast-moving field.

I don't really understand why mRNA processing doesn't simply occur in the cytoplasm.
To be clear, P-bodies are in the cytoplasm (ie they are not separated by a membrane). There is also dynamic exchange of components between the ribonucleoprotein complex and free cytoplasmic pool (1):

Most P-body components are distributed diffusely throughout the cytoplasm as well as being localized in P bodies. Quantitative information regarding the fractionation of these proteins between the cytoplasm and P bodies is still lacking, but given the volume of P bodies relative to that of the cytoplasm, the diffuse cytoplasmic fraction could be significantly larger, although the concentration of mRNA-decay factors might be much higher in P bodies. Also, P-body components dynamically exchange with the cytoplasmic pool, which indicates that decay enzymes and co-activators are not confined to P bodies. So, it is probable that mRNA decay also occurs, and might even be initiated, in the diffuse cytoplasm, and that P bodies arise by association of mRNA-decay intermediates induced by interactions between decay enzymes and cofactors. The concentration of mRNA-decay intermediates and mRNA-decay enzymes in P bodies would be expected to increase the speed of degradation and, in turn, reduce any potential competition between these RNA fragments and normal mRNAs for limiting cellular proteins involved in mRNA regulation.

I'm not clear on whether all mRNAs pass through P-bodies at some point, when not actively involved in translation.
mRNA can also be degraded by exosomes (1):

In eukaryotic cells, degradation of bulk mRNA occurs by two alternative pathways, both of which are preceded by removal of the poly(A) tail by deadenylases. Following this first rate-limiting step, mRNAs can undergo 3'→5' exonucleolytic decay, which is catalysed by the exosome... Alternatively, after deadenylation, the cap structure is removed by the decapping enzyme DCP2, rendering the mRNA susceptible to 5'→3' digestion by XRN1 [a P-body associated protein].

Also see (2), and this image therein:

If the only requirement for recruitment to a P-body (and potentially degraded via RNAi) is to not be currently involved in translation, wouldn't that select for viral proteins to be more highly translated?
That is, in fact, not the requirement (3)

Recruitment of mRNA to PBs is not an occurrence of non-translation, rather requires active silencing via miRNA or RNAi mechanisms.

They reference another paper (4):

Recent studies with mammalian cells have shown that P-body integrity is not required for ARE-mediated mRNA decay or silencing mediated by fully or partially complementary exogenous, transfected small interfering RNAs (siRNAs). In this study, we investigated the requirement for P-body integrity in NMD, mRNA decay, and silencing mediated by miRNAs and long double-stranded RNAs (dsRNAs). We show that these pathways are unaffected in cells lacking detectable, wild-type P bodies. However, although P bodies are not required for silencing, active silencing pathways are required for P-body formation in Drosophila melanogaster cells, indicating that P bodies are not the cause but a consequence of silencing.

Is there is a separate step by which mRNAs of exogenous origin are specifically (or more rapidly) recruited to P-bodies - and, if this happens, how are they specifically targeted for this uptake?
The RISC complex can be involved in initial recognition and cleavage of viral RNA and the resulting fragments are subsequently degraded by the exosome or P-body associated proteins. RNAi associated components have been observed to be localised with P-bodies (1):

Endonucleolytic cleavage of siRNA or plant miRNA targets is catalysed by the C-terminal PIWI domain of Argonaute proteins... Following this endonucleolytic cleavage, the resulting mRNA fragments are handed over to the general mRNA-decay machinery. In D. melanogaster, 5' and 3' mRNA fragments that are generated by Argonaute-mediated endonucleolytic cleavage are degraded by the exosome... and by XRN1, respectively.

You can also consider the R-gene viral defence mechanism in plants which induces P-body formation and suppression of translation in an RNAi independent manner (5):

Plant NB-LRR proteins [R-genes] confer resistance to multiple pathogens, including viruses. Although the recognition of viruses by NB-LRR proteins is highly specific, previous studies have suggested that NB-LRR activation results in a response that targets all viruses in the infected cell... NB-LRR signaling does not result in the degradation of viral transcripts, but rather prevents them from associating with ribosomes and translating their genetic material. This indicates that defense against viruses involves the repression of viral RNA translation... As a consequence..., NB-LRR responses induce a dramatic increase in the biogenesis of RNA processing bodies (PBs). We demonstrate that other pathways that induce translational repression, such as UV irradiation and RNAi, also induce PBs. However, by investigating the phosphorylation status of eIF2α and by using suppressors of RNAi we show that the mechanisms leading to PB induction by NB-LRR signaling are different from these stimuli, thus defining a distinct type of translational control and anti-viral mechanism in plants.

There are many articles discussing how viruses subvert and/or repurpose P-body mediated decay if you want some further reading (3), (6), (7).

Wow - very comprehensive, thank you very much! I suppose I should leave the bounty unawarded for a couple of days in case someone's preparing something even more impressive, but I can't really see that happening.

@arboviral You're welcome! Yes leave the bounty; let's hope someone adds more information.


text:
Identify caterpillars and, if possible, parasitoid (Sabah, north Borneo)
Someone on Twitter posted some photos yesterday of a lump of mud that, when knocked off a chair by accident, revealed a number of caterpillars:
https://twitter.com/solomilne/status/956135158381334528
I've uploaded one of the photos below. The assumption (which seems reasonable, but I suppose isn't certain) is that they were left there by a parasitoid.
Can anyone identify the caterpillars, confirm whether they are likely to have been left by a parasitoid and if so identify a likely culprit? The sample was from a forested area in Sabah, northern Borneo; I've requested a size from the person who posted the photos.

These are wasp larvae, but likely not parasitoids. They are the larvae of predatory Sphecid or Crabronid wasps, both of which build mud nests, generally provisioned with spiders or other arthropods that have been killed (and by some wasp species, dismembered) or paralyzed by the female (mother) wasp. It looks like one or two of them may be pupae (closer to eclosing--"hatching"--as adults) instead of larvae. If kept carefully they can be raised to adulthood for identification (at least by an expert familiar with the aculeate, or stinging, wasp fauna of that part of the world).


text:
Passing virus/diseases immunity to newborn
From my understanding, our white blood cells 'learn' to fight off viruses and other pathogens that make us sick (or that they encounter because of vaccination) so that the subsequent encounters with same strain will not make us as sick; our immune system is able to fend off much better.
Newborns are protected with mother's antibodies via placenta and breast milk. My question is, can immunity be passed from mother to child via hereditary mechanisms, or does the child have a completely fresh set of 'default' defenses? Is that the reason why we get sick so easily when young?

So what happens to bottle fed infants?

^ that's something to ponder too

well, you have your answer.

(@GrahamChiu that's a comment - if you want to post it as an answer go ahead, but I suspect it might need more work...)

Welcome to Biology.SE! It sounds like you've tried doing some research already and know something about adaptive immunity and maternal antibody transfer - can you include the sources you found so we can work out how much you already understand? (Showing how much research you've already done usually helps get positive responses, too.)

And innate immunity, as well as possibly microchimeric cells

@arboviral I dont have much sources, it's just a question that is stuck in my mind without any answers.

@GrahamChiu what happens to bottle fed infants? Humans get passive immunity across the placenta, so human bottle-fed newborns are OK. Many other species do require colostrum for passive protection; if they're bottle-fed and never receive first milk, then they're more susceptible to infection until their own immune system is fully mature.

@iayork that wasn't my point which was to say that adaptive immunity exists

@GrahamChiu yeah your detailed question certainly made that clear and justifies your condescending smugness.

@iayork I guess you've never heard of Socrates then.

Newborn mammals get something called "passive immunity", in which the mother's antibodies are passed across to the fetus or newborn. Depending on the species, this can happen by the antibodies crossing the placenta, or more commonly by being transferred in the first milk the mother forms, "colostrum", which is very rich in antibodies. (At the same time, the newborn has special adaptations to absorb antibodies from the colostrum into its body; this only works for a short period after birth.)

Passive immunity
IgG Placental Transfer in Healthy and Pathological Pregnancies
Colostrum

This allows the newborn to have a temporary resistance to whatever pathogens happen to be common in its immediate environment (because presumably the mother would have been exposed to them). It's very much temporary, lasting typically a few weeks or so before the transferred antibodies half-life away. During this time, the newborn has a chance to start developing its own active immunity, which is dynamic and lasts much longer.
Edit to add:
Are there other modes of heritable immunity? Sort of but probably not what you're thinking of. Innate immune responses are often triggered through recognition of molecular patterns that are common to many different pathogens ("Pathogen-associated molecular patterns" or PAMPS). The receptors that recognize these patterns are inherited, and they are essential for starting innate immune responses which are in turn very important for starting acquired immune responses. So yes, every newborn mammal, and reptile, fish, sea urchin, arthropod, nematode, etc. inherits mechanisms for recognizing pathogens.
However, it's important to understand that these don't change during the mother's lifetime. This system doesn't provide any inheritance of recognition of pathogens that are locally important, or that the mother has met during her lifetime. This is the basic toolkit that every individual of the species (often, that every individual in the genus, or kingdom) has, that's needed to answer the general question "Is this a dangerous situation? Should I activate the immune response?"
In other words, as far as the innate system is concerned, "the child has a completely fresh set of 'default' defenses"; the only non-default information that's passed from mother to newborn is via the passive immunity described above.

I'm not sure this answers the question - it sounds like OP already knows something about maternal antibodies (("Newborns are protected with mother's antibodies via placenta and breast milk") but is asking whether other mechanisms for passing on immunity also exist.

http://europepmc.org/articles/PMC3959733

maybe this would be another question itself. U state that the receptors that recognize these patterns are inherited. but why would a mum that is vaccinated against a certain virus, would not pass that knowledge to the child? Since vaccination works by teaching the immune system to recognise the viral signature. Or this inherited immunity is for other kind of illnesses?

why would a mum that is vaccinated against a certain virus, would not pass that knowledge to the child -- She does, via the passive immunity I mentioned at the start. Why not pass down dynamic immunity? Probably because it's better to develop your own immunity to the pathogens you actually see yourself, rather than the ones your mother saw in 1962, or your great-great-grandfather saw in 1880. Passive immunity gives a brief coverage of possibly-relevant agents until you develop your own to the guaranteed-relevant ones.


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I found this insect in Utah, USA. What is it?
I keep seeing this insect around my house. What is it?

Here is another image:

A better pic would help. Keep this one for reference to the size, but could you post another?

sure. I may need to look for one again. let me see if I took a regular one.

ok The image is too high quality for me to load it here so I put a link to it right under the other image which is on this page.

This might not directly related to your question but as you found the animal inside your house you should REALLY make an effort to get rid of it. It can be a real plague and infest all your dry foodstuffs like cereals, pasta, nuts, ... !

It looks very much like the Indian meal moth, Plodia interpunctella, to me. The size, morphology of the antenna and wing tips, and the pale band of scales are all fairly distinctive. (The proboscis isn't very clear in the photo below but it is in most other images you could find via Google; I just couldn't find a better one with a license allowing me to post it here.)

(Image by Kaldari (Own work) [Public domain], via Wikimedia Commons; URL https://upload.wikimedia.org/wikipedia/commons/5/50/Indianmeal_moth_2009.jpg)


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The drawing of genetic crosses
I'm preparing myself for the GRE. The quantitative stuff has all been going well. I'm aiming for a geology grad scheme. In the event of having to take subject specific tests, I'm teaching myself a few "out there" things in science.
I'm going through biology and looking at genetics for the first time since high school(!)
I just had a question here really to do with genetic crosses. I've been looking at Mendel and the experiments he carried out. One specifically looking at short pea plants. I'm looking at an example where all F1 plants are tall (F1 being the generation of plants). In the example the F2 generation are created in selfing the F1 plants.
Now, I've got my head around the science involved, but I just basically wondered if any biologists here could show me how to make a genetic cross of F2 in order that I could show the genotypes and phenotypes of the offspring.
This isn't necessary but I feel as though it would help my understanding.
At the moment I'm drawing a two by two grid. I suppose I need to fill it with the appropriate alleles?
Thanks.

One of my most valuable sources has been this:
http://www.indiana.edu/~p1013447/dictionary/mendel.htm

The diagram that you are looking for is called a punnet square.

What's a GRE? (I have Googled it now, but I wanted to make you aware that's not a widely known term outside the US - you might want to explain it).

(I also added the 'homework' tag. Please don't consider this as a negative - in my opinion this is an example of a 'good' homework tag!)

The cross you're studying is Mendel's monohybrid cross. Which looks something like this.

Now here, the genotype of F1 gen plants is Tt.
To draw this cross, proceed exactly like you decided. Draw the 2/2 grid and cross the alleles Tt x Tt
Your cross should look like this (ignore the plant drawings):

(Source: classes.midlandstech.com)


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Is eating cooked food an evolved behavior or rather an intelligent one, passed down via culture?
I was just eating a rather rare steak when I started wondering whether eating foods cooked was something I would instinctively want to do if the practice hadn't been taught to me.
So, is cooking food an evolved behavior, inspired by nutritional value or health benefits, or is it a practice learned, and passed down through culture alone?

I think cultural. It is too a complex behavior to be simply evolved. In addition, many species will not even come close to fire. Plus, you have to learn cooking. lastly, the nutritional benefits are questionable although it is definitely beneficial for health as it kills germs. So in terms of evolution there could be a pressure on evolving this behavior, but again, I think it is too a complex thing to be hardwired into the brain.

@ChrisStronks I think there are nutritional benefits to cooking food, compare human teeth and digestive tracts to those in gorillas and chimps. We just aren't able to process raw food as well as they do, so cooking replaces part of the digestive process. This implies we've been cooking long enough to have an evolutionary effect, otherwise there wouldn't have been time to lose the large guts. It is speculated that spending less energy on digestive tracts allowed humans to develop larger brains. If true, it's an interesting interaction between a learned behavior (cooking) and evolution.

@user137: it is not the evolutionary consequence of cooking that is under question, it is the evolution of cooking itself that is questioned.

I think it is easy to decide this. Do we have an instinct to cook something after we killed it? I don't think so... At least I never felt it... There are stories about missing children have been living in the forest for many years, etc... If they cannot make fire (I think so), then there is no such an instinct, because without fire you won't cook... (Except if they have an instinct to build a microwave oven or use geothermal energy...)

@inf3rno having an instinct to do something is not the same thing as being able to do it, I am sure you would agree humans have an instinct to reproduce even if some fail. An instinct could be something as simple as preference, and on average humans prefer cooked foods, particularly meats and starches. Then you have things like language that is instinctual but still has to be learned.

@John Sure, but you have everything to reproduce when you are born, while you don't have the knowledge to make fire. Kids even try to touch fire, because they don't know that it burns. Even if preferences are instincts, it does not mean that they are not learned. For example I prefer blue over pink, because pink is a color for girls at least I learned that when I was a kid and now it is an instinct. My English is not good enough, but I guess reproduction is more than a simple instinct, it is a strong urge. So probably that is a better word for what I was talking about.

@inf3rno you prefer, not basically all great apes on the planet prefer, which is true of cooked food. language is a great example a human needs other humans to develop language, (if you don't learn at least language by puberty you will never have syntaxed language) but every human caries an instinct for language, and if two children with no language are put together for a while they will develop a complete language from nothing. Instinct is not just fixed action loops.

@inf3rno, touching fire may actually be evidence for it being instinctual most animals  instinctually avoid and fear fire. Not true for humans. Also learned and instinct are not mutually exclusive, plenty of instinctual behavior have learned components. not knowing how to do something does not mean you do not instinctually desire to do it.

@John "language is a great example a human needs other humans to develop language" - Sure and normally it is granted, because people live in families and groups. Afaik. the brain structure for languages are genetically coded just as the organs to make sounds.

@John Still it does not make sense to think that it is inherited to cook stuff. Without the capability to make fire all you can do is collect all your meat and pray for a wildfire. Maybe you get it maybe you starve to death. Not a solid strategy to survive. The first humans just ate what they found after a wildfire and learned that it is good. After a while they learned that they can make fire. And that's all. It is something easy to learn from others, no need to code it genetically. Maybe the digestive system changed because they started to eat cooked food instead of raw.

@inf3rno cooking predates Homo sapien by a wide margin, it may very well be the thing that allowed us to evolve, Again I don't think you understand what instinctual behavior is, just because something requires learning does not mean it is not instinctual, there are plenty of instinctual behaviors that have to be learned. There is no human society that does not cook their food. also yes the human digestive system is adapted to eating cooked food, as are our taste buds.

The headline of this question says "eating cooked food" but the text says "cooking food", which is a different question.  Human ancestors in an environment like the Okavango Delta would have encountered carcasses killed by seasonal wildfires.  I suspect intelligence would have permitted early humans to scavenge in fire-prone areas successfully where many other genera would suffer unacceptable risk.

Cooked food is a learnt trait rather than an evolutionary one. On a certain psychological level its a society norm so you would be hard pressed to find an individual who wouldn't mind eating completely raw meat/steak.
But, say if you chuck a few humans into the wilderness at an early age and not teach them how to cook meat they may not actually cook their food. As early prehistoric humans discovered fire they eventually noticed/learnt to cook food and passed on the knowledge . You would have to research the history of that since I don't actually know the details.
Cooking food makes more sense on a psychological level as we cook food based on our cultural upbringing, and our memories and knowledge. A human would prefer cooked meat based on his upbringing or understanding that eating processed meat is safer as it means food contains less pathogens. The way we cook food depends on where we are from (eg.An Indian would cook meat differently from, lets say an Italian because their environment provides them with different ingredients and/or devices, pans/pots)
I hope that wasn't too confusing.

If you just put people in the woods at an early age they'd die. Tool use and hunting are also learned behaviors that affected our evolutionary outcome, similar to cooking.

well yes you are right sorry, I meant it in a more elaborate format. As in raised with no social norms or inhibitions kind of way.

humans have been eating cooked food since before we were human, it is hard to argue something is cultural if we were doing it even before we were homo sapiens. especially considering there is no human culture that does not cook food. Use language as an example what language you learn may be cultural but language itself is an instinct.

Its almost certainly instinctual, humans along with other great apes (any many other animals) show a preference for cooked foods over raw in testing, the number that prefer it increases drastically if they are have sampled cooked foods before. So it is likely as built in as your desire for sweets and salt.
Just becasue something is instinctual does not mean you don't have to learn HOW to do it. Language is instinctual in humans, but what language you learn is up to your upbringing (the same is true in some birds), and denied another human to interact with until puberty you will not develop language. that does not make language itself cultural, just the particular language you learn.
No one would argue lions do not have an instinct to hunt, but they still have to learn how to be successful at it.
https://evolutionaryanthropology.duke.edu/sites/evolutionaryanthropology.duke.edu/files/site-images/Wobber%20et%20al_%202008_%20Great%20apes%20prefer%20cooked%20food%281%29.pdf

A study found that great apes prefer cooked food, which contradicts the notion that the preference results from human evolution.
Cooking food properly is generally beneficial for nutrient availability and taste, so the cooking itself is not what causes the animal preference: pulverising with a blender would have some similar effects on preference. Animal preference is based on sensation of sugar, fat, salt, aromatics, which generally are higher when the cells of the food matter have disamalgamated and volatilized.

As @John has pointed out above and in their other answer there exist solid biological evidence that humans (and other mammals) are better at digesting cooked food than uncooked one, and likely to prefer cooked food given a choice.
It is however harder to prove a causal relation that humans adapted to eating cooked food. Indeed, this would require that humans are exposed to cooked food during a reasonably long period of time (on an evolutionary time scale), and that those who are less adapted to digesting cooked food become less fit and gradually elimited from the population. It is more plausible to assume that cooking was discovered as a way of getting more benefits from food, and thus being more fit in respect to the human groups that were not cooking or were being uncapable of digesting cooked food. In other words, it is more likely learned than adapted behavior. But plausibility is not a hardcore scientific argument.
What further complciates this question is that our gut microbiota has certainly adapted to the cooked food. The gut microbiome is not encoded in human genome, but it is partially inherited during birth, and its further changes are mainly determined by the living conditions. So, it is safe to claim that this microbiome has adapted to humans eating cooked food, and it has certainly undergone genetic selection in this direction.


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How to recognise the type of allele by pedigree analysis diagrams?

It was said that this interference pattern is due to dominant allele. I fail to see that.
In general how to recognise the type of allele by pedigree analysis diagrams?

This question is a bit broad. You have to understand a lot of concepts to figure out the nature of the allele. I'll just point out some basics:

If an allele is dominant it should affect both males and females equally (not X-linked)
If one of the parents shows the trait (while other does not) then at least one offspring should show the trait (basic Mendelian segregation)
If both parents show the trait and one of the offspring does not then it means that the parents are heterozygous and the allele is dominant.


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R nought calculation ( SIR model)
1 person gets bitten by 9vectors /night, the vector transmits the pathogen to 0.035 new hosts. Duration of infection: 9.5 months.What is R0?
I am struggling with this question for ages as I would  just multiply 9*0.035*9.5 to get R nought. However I was given a formula to use R0= βS0/v+µ+γ  but I don't know how to use because I don't get what I should.
Thanks for the help!

With $R_0$, you get $R_0$ and it looks better than "R nought"

"I don't get what I should" - what do you get? This sounds like a 'homework' question - which is fine, but you have to explain what you've attempted better so we can work out where you're going wrong.

$\newcommand{\rzero}{\cal R_0}$
If this is a vector-borne disease we don't really have enough information to compute the full $\rzero$ value (i.e. expected number of infected vectors caused by a single infected vector in an otherwise disease-free population), but we can compute a "vector-to-host" $\rzero$ (expected number of hosts infected by a single infected vector). The biting rate seems to be superfluous information unless your "vector transmits the pathogen to 0.035 new hosts" is supposed to be "infected vector has a probability of 0.035 of transmitting disease to a host it has bitten".
What are you "supposed to get"?
The formula you've given, $\rzero = \beta S(0)/(v + \mu + \gamma)$, is more generally applied to directly transmitted diseases, where

$\beta$ is the transmission rate (number of effective contacts per susceptible host per infected host per unit time) $\times$ probability of transmission
$S(0)$ is the population density
$v$ is the recovery rate
$\mu$ is the natural mortality rate
$\gamma$ is the disease-induced mortality rate

The 9.5 months is likely to be a host infection time (most biting vectors don't live that long).
Notation does vary somewhat, though.
For a vector-borne disease I would write $\rzero$ as
$$
\frac{m a^2 bc}{r \mu}
$$
where $m$=number of mosquitos/host; $a$=bites/time on host; $b$=mosquito to human transmission probability; $c$=human to mosquito transmission probability; $r$=human recovery rate (disease duration=$1/r$); $\mu$=mosquito mortality rate (mosquito lifespan=$1/\mu$).
Google Books link


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What kind of small insect is this?
Found in central florida in the bath tub. Its about the size of a pencil marking, very small. What is it?

This small hexapod appears to be a species of Springtail (or Collembola).  It is similar to the one below, with slightly different markings.

From the University of Florida:

Springtails are minute insects without wings in the Order Collembola. They occur in large numbers in moist soil and can be found in homes with high humidity, organic debris, or mold. Homeowners sometimes discover these insects occurring in large numbers in swimming pools, potted plants, or in moist soil and mulch. They feed on fungi, fungal spores, and decaying, damp vegetation, causing organic material and other nutrients to return to the soil; these nutrients are later used by plants. Occasionally, springtails attack young seedlings and may damage the roots and stems.

More information can also be found at NC State University Entomology Website:
http://www.cals.ncsu.edu/course/ent425/library/compendium/collembola.html
It is hard to say what species it could be, but it looks most similar to:
Isotomurus plumosus:

or Isotomurus tricolour from Rick Cowen:

It is hard to tell but it seems to be part of this genera, or is at least in the family Isotomidae, if not the exact species.
Their taxonomy is actually under debate, and they are in a group of hexapods that are no longer considered insects.


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Identification of Unknown Insects found in landfill (spider like)
Could someone help me to identify the following spider-like insects? They are very small, so I used a macro lens to capture them. I have tried to capture them as clearly as possible.
They are about 2-3mm long with a black hairy head/belly.

They were collected from a closed section of Tseung Kwan O Landfill and Clear Water Bay Country Park of Hong Kong. This area is revegetated so the ecology is much like an area which contains many kind of trees.

Spiders for sure (4 pairs of legs, two body parts), but very hard to tell from their condition and the quality of the photos.


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How did the largest/longest dinosaurs hold their head and necks up?
After seeing the images in the articles shown below, I am having a tough time understanding the mechanics of how these incredibly long and heavy necks can be supported outstretched like this. A rigid beam or tube would remain fairly straight through compression on the bottom and tension on the top, and since there is muscle, tendon, ligament and bone, I know the necessary mechanical functions are there somehow.
Is there one "neck muscle" along the top that holds the neck "up", or many short muscles between vertebra? Where is the origin of the tension, the shoulders or the pelvis, or is it all the tension distributed along the whole spine from neck to tail?
How does this work??

above: Titanosauria of Chubut from here.

above: A reconstructed Patagotitan mayorum, a 70-ton dinosaur discovered in Argentina. (Courtesy of José Luis Carballido) from The Washington Post article Which dinosaur is the biggest? There’s a new contender — and it’s alarmingly large.

above: A reconstruction of the newly named titanosaur Patagotitan mayorum. from The National Geographic article New Dinosaur Species Was Largest Animal Ever to Walk the Earth.

There are lots of papers on this. A good summary article is Why sauropods had long necks; and why giraffes have short necks, by Taylor and Wedel.  They list a number of anatomical features that allowed sauropods to support such long necks:

Several anatomical features enabled this extreme elongation, including: absolutely large body size and quadrupedal stance providing a stable platform for a long neck; a small, light head that did not orally process food; cervical vertebrae that were both numerous and individually elongate; an efficient air-sac-based respiratory system; and distinctive cervical architecture. Relevant features of sauropod cervical vertebrae include: pneumatic chambers that enabled the bone to be positioned in a mechanically efficient way within the envelope; and muscular attachments of varying importance to the neural spines, epipophyses and cervical ribs.

Let's take these one by one.

A stable platform for a long neck. Large, heavy quadrupedal bodies, so the long neck didn't unbalance the animal when it stretched out.
"A small, light head." Sauropods didn't chew their food, so didn't need large muscles or heavy bones in their head, so they didn't have a heavy weight at the far end of the long neck.
Numerous small, elongate cervical verterbrae. Sauropods had 12-19 vertebrae in their necks. By contrast, giraffes have seven, each of which needs to be large and heavy, limiting how long the neck can be.
Efficient respiratory system. Sauropods, like modern dinosaurs (birds) have a more efficient respiratory system than mammals, so they could tolerate the inefficiency of a long trachea.
Pneumaticity of cervical vertebrae Sauropod vertebrae had air sacs (i.e. hollow pockets of air) in them, making them much lighter than mammalian vertebrae of the same size and strength.

Edit to add Figure 4 from Taylor & Wedel, illustrating how relatively light sauropod necks must have been for their size:

Figure 4: Extent of soft tissue on ostrich and sauropod necks.
  1, Ostrich neck in cross section from Wedel (2003, figure 2). Bone is white, air-spaces are black, and soft tissue is grey. 2, Hypothetical sauropod neck with similarly proportioned soft-tissue. (Diplodocus vertebra silhouette modified from Paul, 1997, figure 4A). The extent of soft tissue depicted greatly exceeds that shown in any published life restoration of a sauropod, and is unrealistic. 3, More realistic sauropod neck. It is not that the soft-tissue is reduced but that the vertebra within is enlarged, and mass is reduced by extensive pneumaticity in both the bone and the soft-tissue.

Muscular attachments.  This is the aspect that most directly answers the original question, but it's first important to understand that other sauropod features as noted above allowed them to get away with less neck strength than you'd otherwise expect.  In fact sauropod necks were much less (relatively) muscled than, say, ostriches. They got away with this by improving mechanical advantage:

In effect, sauropods inflated their vertebrae within the muscular envelope of the neck, moving the bone, muscle and ligament away from the centre so that they acted with greater mechanical advantage: higher epaxial tension members, lower hypaxial compression members, and more laterally positioned paraxials.

Taylor and Wedel go into this in much more detail, with many helpful diagrams, and the paper is open-access, so I won't repeat all their points here. They talk about neural spines, epipophyses, cervical ribs, and muscle attachments in various combinations.
The cervical ribs are easily visible on the Patagotitan skeleton image in the question:

There's a long description of cervical rib anatomy and possible functions here:

My favorite hypothesis is that long tendons allow an animal to shift the bulk of the muscle–and therefore the center of gravity–toward the base of the neck, but that long unossified tendons can be distorted through stretching, which wastes muscular energy. Ossifying those long tendons is like putting bony wheelbarrow handles on each vertebra, allowing the muscles to move the vertebra from a distance without so much wasted energy, and probably with finer positional control.

That's just one aspect of the way sauropod necks were structured.
TL;DR: Sauropod necks could afford to be relatively light, because of the small head; their neck bones tended to be relatively hollow and light for their size; their scale and shapes meant that muscles had good mechanical advantage; and different species had other adaptations including ligaments and stiffening bones that also helped.

You know you've stepped up to the big leagues when your paper has to talk about "giraffes hav[ing] short necks"

"modern dinosaurs (birds)" :O Did I miss something? What do dinosaurs have to do with birds?

So, if they compensated the length/weight relation with hollow bone structure... Doesn't it mean that the neck, already a vulnerable part, becomes weaker? I mean, a strong enough bite or ram from the predator, and a spinal cord gets severed, thus rendering the dino immobile.

@Clonkex https://xkcd.com/1211/

@Clonkex Birds are dinosaurs. (and " Birds are descendants of extinct dinosaurs with feathers, making them the only surviving dinosaurs according to cladistics."

@BruceWayne (or should I call you... Batman...?) Oh duh, of course. I totally forgot that was a thing. Sorry, I'm not an evolutionist, I sometimes forget these things that most other people take for granted.

@oleksandr-firsov Since this is how their necks were structured, obviously natural selection determined that the benefits outweighed the costs. We don't know enough about predator/sauropod interactions to know why in detail. The neck was still very strong (look at the meshwork of cervical rib bones supporting it). Maybe most predators couldn't reach the necks (T rex was about 20 feet tall, just up to a full-grown titanosaur's shoulder). Maybe a thicker neck wouldn't have made any difference against a bite. But again, this is how they were, so that tells us a little about predators at the time.

Air sacs mentioned this week in NYTimes' New Clues to How the Biggest Dinosaurs Got So Big

The first sauropod in space!

new dinosaur question: Would anything limit an “invasive species” T. rex introduction now besides running out of food or intervention by humans?