text:
Does conjugation support gene selection?
I have already posted this on chat but haven't got any response. A recent question on group selection stimulated me to ask this here.
QUESTIONS: Why should bacteria conjugate? If we consider that a bacterium is another bacterium's rival (in terms of obtaining resources) why should a bacterium "share" it's antibiotic resistance gene, for example, with another bacterium? I can think of 2 reasons. One is group selection, and the other is "Gene Selection". Group selection has been highly criticized in recent years, and individual selection has dominated thinking, but here my support goes for gene selection rather than individual selection.
Gene selection seems to me the easier explanation over individual selection. Even if we consider the fact that a colony is made from divisions of single cells and the cells are extremely similar and also that conjugation is more probable between cells of a colony, we should also consider that conjugation can happen between very different bacterial species.

I would love to discuss this in chat with anyone interested as I think this question is more of a question to be discussed.

Does it make any difference, for the purpose of your question, if we speak of bacterial conjugaison or of any sexual reproduction? Isn't you question rather something like "Why would sex evolve?" Such question would require a very long answer that presents many different models!

@Remi.b The biggest difference between conjugation and sexual reproduction is - that there is no reproduction of an organism in conjugation. I don't understand why you think the questions are same. I don't want to know the advantages of having " recombination " events in life of an organism. Here, I want to know whether this is  an example of selection at individual level or at gene level ?

As I understand it: In order to answer to your question, one should think about the Muller's ratchet, the advantage of recombination for the group, how a selfish gene causing recombination might spread, about the speed of adaptation, effect on genetic variance, resistance to parasites, DNA repair, libertine bubble theory, etc…

It is roughly the same hypotheses than for recombination through sexual reproduction. But it does not mean I find your question uninteresting. I just wanted to say that there are certainly lots of different models to compare and that you might find your answer in the standard discussions about evolution of sexual reproduction. I might be mistaken though!

@Remi.b I have finally found the perfect words to ask this - Do you think antibiotic resistance gene(for example) spreads because the bacteria wants to protect the whole genome of other bacteria(which will often have the same genome) or it happens because that little plasmid likes to spread it's own genes ? I think the 2nd explanation is better because it can explain conjugation between different species

let us continue this discussion in chat

Interesting Question (glad the "group selection" post got you thinking!)
Me and two friends thought about your question during our Biology BSc at ICL (in fact we also thought about an even more puzzling phenomenon called "bacterial transformation" which is like conjugation, but they incorporate genes from dead bacteria!!) our first year course convener recognized our answers as "most likely candidates" so here they are:
1. Stress-induced Experimentation Hypothesis
The likelihood of conjugation/transformation occurring may change for a bacterial population as a whole depending on how stressed it is (or perhaps how unfamiliar the environment is?). Stress signals could cause the population to be more "risky" and take up the DNA from surrounding living/dead bacteria and incorporate it with its own genome: "the hell, we're out of options.. lets transform into something that resembles the indigenous species of this strange ecosystem!". Indeed Bacteria have memory (see: chemotaxis) this means that perhaps they can be able to tell whether they have been receiving more stress now as opposed to before, meaning they can "trial and error" with various genes that have been imported within their plasmids! — "Let's try this gene, oh wait... I'm dying, hmm let's kill off this plasmid and take some more genes!".
In reply to this my course convener said:

"ah yes, a switch from asexual to sexual reproduction occurs in
  many organisms under stress. The genes that cause the
  sex/transformation to occur may gain a net benefit from recombination
  with genes taken from other organisms/the environment."

2. Diversity Plagarism Hypothesis
If we look at the entire population of conjugating bacteria as a single competitive unit itself (e.g. like a tissue is a coordinated group of specialized cells) that can compete with other populations of bacteria who cannot conjugate the conjugating population will "win". This is because a conjugating population will always have much higher phenotypical diversity as it can mix traits between the individuals. This means a conjugating population is much more efficient at undergoing natural selection for beneficial traits or trait combinations.
Think of natural selection (coupled with mutation) as an inventor... something that helps you invent much "fitter bacteria" is the ability to pull things apart from this bacterium and that bacterium and glue them together, this is essentially what conjugation/transformation does!! it allows you to pull bits from this bacterium and stick it to bits from that bacterium to get a "super-bacterium". It's like open source technology (free to share) as opposed to patented technology!! Conjugation is immediately a good thing because it means you can "steal" cool technology from living/dead bacteria and incorporate it into your population's gene pool!
Hope this was helpful!

An  idea- What if the bacteria who is going to get the plasmid actually "compels" the other to give it the plasmid. We can think of it as "asking" by bacteria 2 rather than giving by bacteria 1.

I think  I said in the comment prety much the same thing as the last para  but with a slightly different perspective.

Awesome, well I have to say I know quite little about the mechanisms and mechanics of the conjugation process. But it would be interesting to know whether conjugation is "consensual". At least for transformation it is clear that there is no need for "compelling", the bacterium merely steals the DNA from the "corpse". A really interesting alternative answer is that the genes themselves are selfish genetic elements that can express some mechanism that allows them to infiltrate the bacterial genome.

Check out the Homing Endonuclease Genes (HEGs) http://bit.ly/puyHda  - HEGs literally make cuts in DNA and insert themselves into the genome.

Oh yes..I think The alternative will definitely be advocated by Dawkins. And yes, I thought of that too and I have written that in the question and in the comments. (It isn't an original idea as I have read the selfish gene !)

The other link seems pretty cool ! And i understand that it is difficult to prove that the other bacteria "compells" the 1st one. But thinking wild things is my hobby :)

I really need to finish that book (logs into amazon) but yes, if you are interested in the mind bending but beautiful collection of selfish elements you should read http://bit.ly/182xVzh, im working on research that uses HEGs to genetically engineer malarial mosquito populations!

Yes I accessed your website yesterday (got the link from your profile) and it definitely sounds amazing. Best luck !

Ah cheers, wild thinking is the best.. hope I didn't sound like I was disagreeing - I genuinely am interested in whether conjugation is either: a mutual agreement, a "giving", a "taking" (stealing). If it is the mutual agreement, then your suggestion comes into play! that you can "compel" or persuade or trick the other bacterium into giving the "blueprints to their technology" (DNA)


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By what mechanism can hypoglycemia induce fainting?
Hypoglycemia (Low blood sugar) is said to be among the potential causes of human-faintings. I was wondering by which mechanism this happens. Google search results are abundant; there are lists of various causes and solutions, but I couldn't find a direct answer to my question.
Is it a controlled reduction of heart function to save energy? Is it an uncontrolled shock reaction (malfunction)? I'm looking for an answer along those lines.
Thanks.

The following article may be of relevance: http://www.ncbi.nlm.nih.gov/pubmed/1437055

There are regulatory mechanisms that may prevent moderate hypoglycemia to progress to a more severe state, however these mechanisms act before lack of conciousness sets in. The progression of hypoglycemia may depend on overall health and medical status and vary between healthy and diabetic persons, for example.
Rosenthal et al. (1) write that

The brain is normally dependent on glucose for oxidative metabolism
  and function. Acute iatrogenic hypoglycemia, occurring as a result of
  insulin excess during the treatment of type 1 diabetes, can cause
  clinically significant cognitive impairment. In health, such
  hypoglycemic cognitive dysfunction does not occur. Endogenous
  counterregulatory mechanisms are activated in response to a small
  reduction in circulating glucose, preventing more profound
  hypoglycemia. In diabetes, the inability to reduce circulating insulin
  levels (1), the failure of glucagon responses (2), sometimes
  accompanied by defective autonomic and adrenergic responses (3), can
  allow plasma glucose levels to fall low enough to result in detectable
  disturbance of cognitive function, ranging from a subtle slowing of
  reaction times (3) to coma (4).

In short, the brain malfunctions due to lack of glucose (the sole energy source for the brain). Note that cognitive impairment and unconciousness can also occur in otherwise healthy persons, for example in the case of prolonged exercise combined with lack of nutrition. The exact cause of cortical dysfunction is not known:

Impairment of brain function is a recognized consequence of acute
  hypoglycemia. It is known that different brain functions have
  different susceptibilities to acute hypoglycemia; for example, the
  triggering of autonomic activation, a hypothalamic function, occurs in
  response to quite modest decrements in circulating glucose
  concentrations (5,6,7), whereas significant cortical dysfunction
  requires more profound glucose deprivation (3). Even within different
  cortical functions, there is variation in hypoglycemia susceptibility
  (26). The mechanisms of cortical dysfunction during hypoglycemia are
  not known.

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/

sort: votes


text:
Can anyone identify this caterpillar / cocoon?
This insect is about 0.5 mm in length, so it is very small. It doesn't have legs I don't believe, I am not too good at this but I don't know if it's a worm or more like a cocoon for something.
I do find this alarming because I found this one underneath my bed sheet on the mattress. Now I do recall seeing something similar on the crack of the shaky tile floor, so I can't tell if it's just an apartment pest or it actually lives in mattresses.
Location: Toronto, Canada

It's carpet beetle larvae.
It's a serious pest, right behind the bedbug. The larvae were found on an old mattress.
I found about 4 more afterwards.

This could probably be many different species in the family Dermestidae, which often have fairly similar looking larvae. The carpet beetle is a good bet thought since many of the other common species feed on animal materials (food, insect collections, fur, leather etc.)

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

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


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Calculation of saturation of carbon in surface waters
I've been looking at some journals lately that look at carbon emission from lakes where some lakes act as sources and other act as sinks. The paper that I have been looking at is
http://www3.nd.edu/~underc/east/publications/documents/Cole_94Science.pdf
where they show that lakes are sources of CO2 to the atmosphere. What are the equations that are used to determine the saturation of CO2 in surface waters?
The recent IPCC report also mentions that lakes act as sources of CO2 but does not give any indication of the equations used to come up with these values. Presumably, to determine the concentration of carbon in the surface water you need to use other measured variables such as temperature. Can anyone suggest a method for estimating this concentration ?

I imagine this would get a better response on the chemistry SE

Paragraph 2 describes their methods in detail.  If I have time I can outline it, but it might not be today... i think this is a fair biology/ecology question.  These days a fair number of biologists need to know their environmental/bio chemistry

second paragraph reads: Data were obtained from the literature and direct measurements. The value for PCO2 was calculated from ph and DIC or ANC with corrections for other variables. I am looking for the equation used for calculating PCO2 from these variables.

I agree with @shigeta this is still a biology question (I recommend asking on both biology and chemistry SE)

Take a look at Paragraph 2.
I'll outline it in more or less plain english (I hope).
for 37 lakes they used this method:
1) they took a sample of water from 0.1 to 0.25 m below the surface.  Using a thermos bottle.  This would minimize change of the gas composition of the water with a change of temperature.  The bottle was not sealed, but left out for a while in the air there at the lake (it was "equilibrated with ambient air").  If you were looking for issues you might or might not like this.
2) a sample of air 1m above the lake was taken.
3) they got a gas chromatograph to measure the CO2 in the air above the water sample, as well as in the air from above the lake.  They might have taken the readings right there at the sampling point, or not its not clear. They may have also sealed bottles up and taken them to the lab.  It sort of sounds like a point of sample measurement.
If the air above the water samples had more CO2 than the air above the lake, they called the water supersaturated as the water was emitting CO2.
This method does its best to simplify the question of whether fresh water bodies are saturated with CO2 and emitting it or if they might be absorbing it.  By not outgassing the CO2 in the water and trying to get an absolute content of CO2, they are able to get around the various organisms and minerals in the water and pH which would vary the amount of CO2 the lakes can hold.  they are just focusing on whether the water is giving off CO2.


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Gradual slowing breath, its effect on health
I've written a computer program which beeps, then beeps after 10 sec, then beeps after 11 sec, then beeps after 12 sec, etc.
I tried the following "experiment" on myself: do only one breath between the beeps, so slowing breath until I can't do it.
After finishing this "training" and starting to breath normally again, I felt enormous "freshness".
Is this experiment safe for health? How does it influence health?

Whether or not it is safe is a discussion perhaps best to have with your doctor - personal health will determine the safety of this, and it will also depend on how far you push yourself, obviously at some point your program will be beeping once a week... As for health effects we could speculate - perhaps it is similar to some meditation techniques - but this is a very unusual small experiment.

@rg255 It would get to the "once a week" stage after more than 5,000 years.

You can try as much to slow down your breathing but the body will speed it up if it requires. What you've probably done is relaxed and just basically meditated. It's not the breathing but the relaxing yourself to slow your breathing and the focus which has refreshed you. I say conduct some experiments, like listen to calming music and relax and don't monitor your breathing and see if you feel the same.
//updating answer
Slowing your breathing builds up the carbon dioxide in your body. This is bad for the body so it forces you to breathe. In fact our breathing is seriously tightly controlled so that our body tightly controls the carbon dioxide (or more correctly the pH) in our blood. There are some groups of patients in which permanent slow breathing exists. In these people their carbon dioxide climbs and the kidneys have to compensate.


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Could murder be modeled as an infectious disease?
Background

"When swine flu hit the population it spiked in certain areas and
  tapered off in neighboring regions, it hits hardest where people have least protection and this pattern is more pronounced (here)"

Apparently incidences of murder spreads in a similar pattern to infectious diseases such as swine flu according to a 26-year study of the city of Newark, New Jersey (summary).
Questions
It would be interesting to hear your opinions, but some interesting questions I would like to ask are:

To what extent could murder and the epidemiology infectious disease
patterns resemble each other?
What factors could you suggest may lead to their apparent
similarities?
Given that murder could be modeled as an infectious disease could we
apply epidemiological interventions to murder?

Seems like murder would be a weird disease. maybe its like cancer,  everyone is a carrier for murder- we all have it.  It would break out at a rate modulated by environmental conditions.  some might claim you wouldn't have to actually model the individual experiences, but others would expect it.

Interesting! I was thinking along the lines of "if you kill my gang-member I will kill yours" and it spreads like that, coupled with desensitization to murder as more of it occurs nearby - but these kind of discussions are what I was hoping to spark :)

maybe in very small circles you could model it as a meme like disease, but I'm not sure it would model a statistical number of murders. Sociological and policy factors are still probably more likely to model crime in general -  just my opinion... but not without its proponents.  http://www.telegraph.co.uk/news/worldnews/northamerica/usa/10320691/US-crime-murders-and-manslaughters-by-state.html

While it's probably possible to create an epidemiological model that mimics the spread of murders, it would be ethically dangerous territory to study in a controlled way to get a dataset that points to causes (and not correlations).

@ThomasIngalls That objection is also true for infectious diseases, which is why we model in the first place.

@Fomite Good point. Also, nice answer.

Here's a very interesting TED talk for you, regarding violence instead of murder https://www.ted.com/talks/gary_slutkin_let_s_treat_violence_like_a_contagious_disease?language=en

Disclaimer: I'm an infectious disease modeler, and generally pretty skeptical of "We modeled X like an outbreak!" claims, because many are just an exercise in curve fitting.
Given that, the answer is both "Yes" and "No".
"No": Murder as an act really isn't transmissible, and if its not transmissible, it can't be modeled as an infectious disease.
"Yes": It is probably possible to model some things in the same way we model infectious diseases, because the underlying causes of murder may be somewhat 'transmissible'. Certain behaviors, cascading effects (if one family member is incarcerated it increases the likelihood that other members of that family will be incarcerated) etc. might give crime "disease-like" properties.
That's probably largely driven by underlying social networks and the like, which are also important to infectious diseases. But then you have a problem in reasoning. For example, did murder "spread" along a social network, or did we merely sample a group of people with a shared underlying cause (for example, poverty, membership in gangs, etc.)
It's probably useful to model some of these things, but it's more useful, in my mind, to model them as their own process, rather than trying to shoehorn them into being like a disease.

Also, pretty much all areas of modeling borrow heavily from each other such that it is quite possible to have components of a model that look very like components of another, but for very different reasons.


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Is there a maximum pain threshold?

Is there a maximum threshold of pain a Human can experience, beyond which point there is no noticeable difference?

I ask this question in part to better understand the definition of pain and its different facets, e.g. Is there a quantitative measure of pain? Are there various types of pain, or are they all part of the same fundamental experience?
It would also be interesting to know since I could perhaps be allowed to claim:

"well at least I know I cannot feel more pain than X"

Thank you for your opinions.

it only goes to 10. http://en.wikipedia.org/wiki/Pain_scale  ha ha just a little levity

"But this one goes to 11!"

Haha! Interesting how many scales there are, cheers

When the pain receptors are fully loaded then it's not possible to excite these receptor greater. However the perception of pain has a large psychological component and is not well understood. Your brain could modulate your perception of pain naturally or due to illness.


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How is deviated nasal septum related to cold
I have a deviated  nasal septum and I always suffer from  common cold I was just wondering how a deviated nasal septum can be the cause for chronic common cold

Question: What makes you think it's the deviated septum instead of different cold strains?

I am not sure but I was told by a doctor that I have deviated nasal septum and he suggested for and operation

Nasal septum deviation is a condition where the cartilage which divides the nasal cavity into two nasal passages isn't centrally aligned, making one of the nostrils smaller and thus obstructed. Now, in our nose we have something called mucociliary clearance and that is the mechanism getting rid of unwanted particles and pathogens that get into contact with the mucous membranes in the nose.
Studies show that in individuals with a deviated septum the nasal mucociliary clearance time is slower than in individuals whose nasal passages are symmetrical. From this information one can conclude that the particles and pathogens that you inhale are getting to spend more time inside your nasal passages, thus giving the pathogens a better chance at striving and giving you sinusitis.
By looking at the information above you could think that the connection between nasal septum deviation and chronic sinusitis is clear. This literary review however states that the correlation between a deviated nasal septum and having chronic sinusitis is still unclear.


text:
What are the differences between HPRD and BIOGRID databases?
What are the differences between HPRD and BIOGRID protein-protein interactions databases?

What are their purposes? Why do we need two different databases?
How is data collected into each one?
How different are they in the interactions they contain?
Is one considered more reliable than the other?
Which one is more commonly used when benchmarking models?
Are there any other commonly used PPI databases?

Do you mean in funding or functionality? Your question is very general. Both projects have different purposes. The latter seems to be more specific, interaction repository with data compiled through comprehensive curation efforts, while the former more general about proteins. In some cases HPRD is better, while BIOGRID in other depending on the situation. Reliability again depends on your issue. It is often the case that BIOGRID can be more reliable in its specific cases, while HPRD can provide some overview well.

I've added some details to my question. I'm not sure what you mean by more general/specific.

i've covered major differences in my answer, but most importantly HPRD focusses on high-quality manually curated Human data and BIOGRID is for multiple species

Short Answer
In a nutshell, there are two major differences:

Species range: BioGRID integrates multiple species' protein-protein interaction (PPI) data, whereas HPRD focuses mainly on Human data.
Functionality: HPRD has some GUI tools that can interact directly with it's database (e.g. BLAST - for searching proteins and their binding partners via sequence alignment) whereas BioGRID is mostly just a database.

Long Answer
In bold are the unique features of each database.
About HPRD:

The Human Protein Reference Database represents a
  centralized platform to visually depict and integrate information
  pertaining to domain architecture, post-translational modifications,
  interaction networks and disease association for each protein in the
  human proteome. All the information in HPRD has been manually
  extracted from the literature by expert biologists who read, interpret
  and analyze the published data. HPRD has been created using an object
  oriented database in Zope, an open source web application server, that
  provides versatility in query functions and allows data to be
  displayed dynamically.
FAQ HPRD: Why did you decide to develop yet another database instead of integrating other existing databases?"
  We believe that biological databases are still in their early stages
  and no protein database can be considered as an established standard.
  We feel that a variety of databases trying to solve problems in
  diverse ways provide the biologists the possibility of choosing their
  favorite. Our approach is radically different from existing databases
  and we want to offer biologists the possibility of choosing instead of
  imposing one database by default. Besides, most of the databases are
  automated and ours is manually curated to avoid errors. We are also
  trying to provide information that few other databases provide.

About Biogrid:

The Biological General Repository for Interaction Datasets (BioGRID)
  is a public database that archives and disseminates genetic and
  protein interaction data from model organisms and humans
  (thebiogrid.org). BioGRID currently holds over 720,000 interactions
  curated from both high-throughput datasets and individual focused
  studies, as derived from over 41,000 publications in the primary
  literature. Complete coverage of the entire literature is maintained
  for budding yeast (S. cerevisiae), fission yeast (S. pombe) and thale
  cress (A. thaliana), and efforts to expand curation across multiple
  metazoan species are underway. Current curation drives are focused on
  particular areas of biology to enable insights into conserved networks
and pathways that are relevant to human health. The BioGRID 3.2 web
  interface contains new search and display features that enable rapid
  queries across multiple data types and sources. BioGRID provides
  interaction data to several model organism databases, resources such
  as Entrez-Gene, SGD, TAIR, FlyBase and other interaction
  meta-databases. The entire BioGRID 3.2 data collection may be
  downloaded in multiple file formats, including IMEx compatible PSI MI
  XML. For developers, BioGRID interactions are also available via a
  REST based Web Service and Cytoscape plugin. All BioGRID documentation
  is available online in the BioGRID Wiki.


text:
Modern immunology textbooks
I am looking for recommendations to good textbooks introducing modern immunology. Review articles, preferably modern (post 2000) would also be useful.
Please, include a brief comment with each book recommendation.
About book listing questions on SE: I understand that SE sites in general have adopted in the last year a policy against book listing questions. Instead, book lists should be moved to tag wikis. However, since BiologySE is still beta and young and the tag-wiki for immunology is mostly empty, I believe we would benefit from a question listing good introductory books to modern immunology, at least temporarily. Eventually, when Biology.SE matures, this question should be closed or locked, and the book recommendations herein moved to the tag-wiki for immunology. Moreover, for most other SE sites I have seen, the tag-wikis usually gather information that first appeared in questions like this, even if the question is eventually closed or locked. That's why I think this question will be useful to the community, at least temporarily.

I am surprised Janeway's Immunobiology is not listed here:
Murphy K. Janeway's Immunobiology. 8th ed. New York: Garland Science; 2011.
It is very comprehensive, accessible and goes beyond any graduate course I know. Most immunology researchers I know have a copy of this handy somewhere in their office. A particular highlight are the very clear illustration.
I would suspect that a new edition is currently in the works, so I recommend checking if a new edition is due to come out before you buy.

Cellular and Molecular Immunology
 Abul K. Abbas MBBS (Author), Andrew H. H. Lichtman MD PhD (Author), Shiv Pillai MD (Author)
This was my Fall 2011 Basic Immunology text for a hybrid med-school/undergrad class at my University.
I have not read others, but every time the topic of Immune responses comes up in other Undergrad courses, I have been well or exceedingly informed because of it.

Given @becko's note on putting references in tag-wikis, maybe we should put this listing in the tag wiki for immunology

@A.Kennard But, as I said in the note, the question should remain open until it accumulates more answers.

The MCM's book is good one.
I recommend the book BRS Microbiology and Immunology, because then you can see the thing in the real context and have good exercises too.
First Aid for the USMLES Step 1 then explains you how to read for immunology and gives you rather good summary about the topic and some mnemonics.

I took an undergraduate immunology class for fun a few years ago while I was working at a university (taught by a Ph.D. from MIT).
"The Immune System" by Peter Parham (3rd ed. 2009) was really enjoyable and seems to have taught me well. So well that although I had very little background in biology, after taking that class I was able to discuss and sometimes even help my (then)girlfriend in her graduate level immunology class. I praise the book highly.
https://www.amazon.com/Immune-System-4th-Peter-Parham/dp/081534466X
edit: Apparently there is a 4th edition now, 2014.

If you actually read the link you provided, you'll see that there's a new edition of that book, from 2014. Answering a request for "modern" immunology texts with a book from 2009 is not helpful at all - a lot has changed and been discovered since then.

Then take the time you spent writing that comment and edit the answer with the new link. Yes, immunology is changing wonderfully fast. However, the asker qualified post-2000, so 4th ed. is even better.
Instead, @MCM and Rob Hall both suggested books two years older, which apparently is your threshold (perhaps more likely, reputation bias is acting). Content-wise, they provided similar information.
But not to worry for you, it is very likely I will not attempt further contributions to stack biology. The integrity of your stack is safe another day.


text:
How to get conservation of vaccine candidates between hundreds of bacterial strains?
We have identified vaccine candidates via an ex-vivo RNA-seq approach. Next step would be to perform conservation of these candidates (about 20) between multiple bacterial strains (about 200). I would like to know your suggestions to perform this step.
From my bioinformatic experience, it could be possible to start with a first rough screening using blastp or blastx against a multiple strain database, and more accurate approaches would be then performed to validate this results.
Please let me know your suggestions and possible references you might consider helpful to answer this question.
Thanks for your help. Best regards, Bernardo

It may help to specify how sophisticated your computational techniques are. The answer will be very different depending on whether you want to use websites and black-box software, or if you are able to do this on your own computer using custom-made scripts/programs.

Hi adam, I prefer command-line tools, I have medium programming experience. I would like to combine already available tools with possible on-the-go scripts if needed.

This website will allow you to blast all sequenced microbial genomes:
http://www.ncbi.nlm.nih.gov/sutils/genom_table.cgi
Recovering the full gene sequence might be a bit of a hassle, since BLAST will only allow you to recover the region that matched your query. You may need to set up your own pipeline for this. You may also be able to identify a "protein family" or "cluster of orthologous genes" using the BLAST results.
Once you have the full sequence, you can perform a multiple sequence alignment with CLUSTAL, Muscle, or another program. This will help you to identify the conserved regions.

Hi adam. The 200 genomes have not been published yet, so I would have to use local BLAST in any case. I will avoid to recover full gene sequence going through BLASTP. Thanks for the CLUSTAL, Muscle tools, they will be useful for a latter step. I think the question now is to think how to get yes/no table, that is, presence/absence of each vaccine candidate in each of the 200 bacterial strains.


text:
Blast a sequence against multiple databases
I would like to BLASTP a list of protein sequences in fasta format against multiple protein databases. Since I'm only interested in the first hit of each database, it is possible that BLAST result would need to be parsed.
Do you know if this strategy is a good one, or you suggest me others?
Thanks for your help. Best regards, Bernardo

"Good" for what? If you're asking whether your approach with parsing is good, I'd say parsing should be performed for most of purposes any-case. If you want just one hit, there is a parameter 'max_target_seqs': see manual

We have identified vaccine candidates via an ex-vivo RNA-seq approach. Next step would be to perform conservation of these candidates (about 20) between multiple bacterial strains (about 200). I would like to know if it's a good idea to start with a BLASTP or go to more advanced strategies.

Are you willing to set up standalone blast on your computer, and run a script on it? It's actually pretty straight-forward once you get to that level (using BioPython or BioPerl)

I do this all the time if you use stand alone blast. It's a simple flag you need to pass.

To scan multiple databases:-

Download all the databases that you intend to match against (all databases will have a download option)
Download standalone BLAST executables from NCBI
Pool all the sequences from the different databases and make a BLAST database using the program makeblastdb (it is better to check for redundant sequences and remove them for improved performance)
Run blastp with desired parameters against this database
The first hit wont mean much. Use cutoffs on E-value or Bit-Scores or precentage identity

Now, if you vaccine targets a protein it is good to study the protein sequence conservation. BLAST isn't a really good option for studying conservation by comparing different orthologs. Use tools for multiple sequence alignment like ClustalW or T-COFFEE. In my opinion it is also better to use BLOSUM for scoring the alignments compared to PAM.
It might also be important to look at the protein structures. You can try VAST if possible.

Hi, maybe I didn't explained myself well. I already know that my vaccine targets a protein. My question is how to get yes/no table for 200 bacterial strains. ClustalW, T-COFFEE and VAST seem to be a latter step, but thanks for this. :) If I merge all the 200 bacterial genomes in the same database, would it be easier to parse later? that is, when checking presence/absence for each bacterial strain?

If it's a species with already sequenced genome and you use a genome mapping approach, you probably get gene id's "automatically" during transcriptome assembly.
If it's a de novo approach, and all you get is a list of sequences, KAAS would help you to identify orthologous genes already known in other bacterial genomes (there you'll find even predefined subsets of genomes to blast against, 'for Prokaryotes' being one of them).

They bacterial genomes have not been published yet. I've been  used a genome-based RNA-seq approach.


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The reason why researchers usually use cell lines from "blast cells"?
What's the reason why researchers usually use cell lines from "blast cells" (so, immature, like lymphoblastoid cells) for measuring gene expression data? Is that they are growing up, which would make their expression data higher and more significant?

It's probably because those are the cells they have access too, or they're trying to figure out expression levels in some differentiated lineage. I've seen lots of expression kinetic experiments done in bacteria, yeast, and all sorts of standard mammalian cell lines.

Some of the reasons why immature blast cells are studied:

They have self renewal ability
Can be differentiated to different types of cells
Serve as model for studying development: this is quite pertinent to the gene expression studies. Because it is important to know what changes take place during differentiation and simply looking at the differentiated state won't explain that process.


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Why do we need deep sequencing?
Why do we need deep sequencing? Why cannot the sequencing technologies read all the nucleotides correctly at the first read? Sorry since this question is too trivial, I don't have a biological background at all, and I have just started doing research in CompBio. Thanks.

Short Answer
In a nutshell, DNA sequencing technology has a limit to how long a stretch of DNA it can read in one go.
Long Answer
So what most commonly occurs is the length of DNA you wish to sequence needs to be (almost randomly) chopped up into given lengths (depending on the technology) and each length or read is sequenced in parallel. But now you don't know which lengths to stick together! i.e. the ordering of these chopped up lengths. So you sequence it many times over (deeper) and this way you can align contiguous ends of these lengths together like a jigsaw puzzle. The more times you sequence the more accurately the 'contigs' will be aligned.
DNA Assembly Diagram

Comment if you want more details, but the technical term you want to google is "sequencing assembly".
Here's the wiki
:)

Thanks, this helps a lot! One more trivial question, and I will get it completely :) The sources I checked on "sequencing assembly" usually assume some background which I don't have, so they don't answer my following question: Why the lengths that would be read are chopped almost randomly which would require this alignment stuff, and not chopped in sequential order of the DNA stretch and just augmented to each other after being read in parallel? I am sure you are smiling at this question right now :) But thanks in advance!

Actually it is a good question because I must have been quite ignorant in my past lectures since I do not "know" the answer but I can make a good guess: It is because you cannot handle the DNA like that, remember it is a chemical! You put it in a solution and you cant just "grab it" with a tweezer, snip it here and there with scissors. You chop it with enzymes that make cuts at highly repeating regions along the sequence - the pieces that result just diffuse around and boom you have a broken jigsaw to solve

If comments or answers have helped don't forget to "up vote" to help the community :)

Thanks! This helps a lot, too. I accepted the answer, but cannot vote up yet because I am new here so I need 3 more reputations for that :)

^^ restrictions... what field is it you are from? and why the Bioinformatics question?

I have Computer Science major and started PhD in CompBio.

@user5054. I just re-read this now, if you find Bioinformatics terminology tricky, then you would benefit from reading the "Glossary" sections of well-established Bioinformatics resources. Example: https://www.vectorbase.org/glossary

Deep sequencing is naturally error prone.  Sequencing will never be perfect, because no enzyme will ever perform 100.00000% perfectly.
In Illumina sequencing, you put your starting molecule down on the flowcell, then the polymerase makes a cluster of copies around it.  But at each step of building each copy, there's a chance the polymerase will make a mistake.  Then at sequencing, a single complementary labeled dideoxynucleotide is added to the complementary chain.  But there is always a chance the enzyme will make a mistake.  Then after the base is read, the label needs to be cleaved.  Another step where the enzyme might make a mistake.  Then the base is converted to deoxy, another possible error.  Even if each step is very unlikely to fail, after a lot of steps, there will be enough problems that the cluster won't show the correct color uniformly.  The software tries to compensate, but the result is that you will have reads with inaccuracies.  That's why you have to have depth.

Another important point is that we almost always sequence a population of cells, not just a single cell. Cancer cell populations, for example, can have multiple sub-populations of cells with different genetics (subclones). Deep read sequencing allows us to see this heterogeneity, and also measure the abundance of each sub-clone. Even with a single cell, we can see the abundance of different alleles... Usually 50-50 in normal cells, but can get pretty crazy in cancer.


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Body size, what are the evolutionary trade-offs?
Background
Considering just the "Kingdom Animalia" branch of organisms. It is clear that bigger does not necessarily mean better - there is large variation in body size...
From the 94 µm long Tantulocarid arthropod (Stygotantulus stocki)

To the 25.5 m long Blue Whale (Balaenoptera musculus)

Questions

What trade-offs exist between having a particular body size (very large, very small) to other traits and factors?
Alternatively, what evolutionary/ecological advantages/disadvantages are there to having a large or small body size?

Thank you!

I saw something recently that claimed that, in general, lineages evolved to become larger more often / more consistently then to become smaller. It seems like it might be relevant to this question, but I can't seem to find the citation - maybe someone else can?

Ah, apparently it's Cope's Rule, and it's still a pretty hot topic of debate for and against.

You should quote or summarize this rule as an answer!

Somewhat related questions include: How does natural selection favour large body mass and size (or so it seems), Do large animals often evolve into smaller animals?, and What was the reason for some plant and animals to become giant in course of evolution?

Have you read the book WHY SIZE MATTERS by Bonner? It's an excellent book covering every aspect of size in an easy to read manner.

There is the classic essay "On Being the Right Size", J. B. S. Haldane

I don't think one can fully answer to such a broad question. It depends on the population, the environment (presence of predators for example), the genetic background (having a big stomach is good but only if the intestin is big too), the population's social relations, .. Many traits are correlated and one might want to say that a given trait is beneficial but it is not because this trait is correlated (because of genetic, physical or social constraints).
Trade-offs
Here is a list of possible advantages/disadvantages.

visibility to predators
ability to hunt bigger preys or to manipulate smaller preys
running faster
be more impressive
fighting ability
energy consumption for maintaining a body
Quantity/quality of food to be found
homothermy (heat loss)
sustaining its own weight
Rooms for the organs
Attractiveness to the other sex
being more able to move freely (in viscous environment (water))
mechansisms for bringing nutrients and air to the tissues
density of the body (water)
excretion of wastes
moving in small habitats
Hiding in small areas
bearing big and complex structures
Parental care
flying better
acceleration in each movement
etc...

Allometric relations
You might be interested in life-history traits, and in allometric relations. You might be interested by this article as well. The reason for allometric relations can be found here:

If an animal were isometrically scaled up by a considerable amount, its relative muscular strength would be severely reduced, since the cross section of its muscles would increase by the square of the scaling factor while its mass would increase by the cube of the scaling factor. As a result of this, cardiovascular and respiratory functions would be severely burdened.
In the case of flying animals, the wing loading would be increased if they were isometrically scaled up, and they would therefore have to fly faster to gain the same amount of lift. Air resistance per unit mass is also higher for smaller animals, which is why a small animal like an ant cannot be seriously injured from impact with the ground after being dropped from any height.
As was elucidated by J. B. S. Haldane, large animals do not look like small animals: an elephant cannot be mistaken for a mouse scaled up in size. This is due to allometric scaling: the bones of an elephant are necessarily proportionately much larger than the bones of a mouse, because they must carry proportionately higher weight. To quote from Haldane's seminal essay On Being the Right Size, "...consider a man 60 feet high...Giant Pope and Giant Pagan in the illustrated Pilgrim's Progress.... These monsters...weighed 1000 times as much as Christian. Every square inch of a giant bone had to support 10 times the weight borne by a square inch of human bone. As the human thigh-bone breaks under about 10 times the human weight, Pope and Pagan would have broken their thighs every time they took a step." Consequently, most animals show allometric scaling with increased size, both among species and within a species.
The giant monsters seen in horror movies (e.g., Godzilla or King Kong) are also unrealistic, as their sheer size would force them to collapse. However, the buoyancy of water negates to some extent the effects of gravity. Therefore, sea creatures can grow to very large sizes without the same musculoskeletal structures that would be required of similarly sized land creatures, and it is no coincidence that the largest animals to ever exist on earth are aquatic animals.

This post talks about the reasons for the allometric relations between animal size and speed of movements.
Concerning the relation between heat loss and size, you might be willing to have a look to the Kleiber's law. This law has been extensively debated and is today thought (or known) to be wrong.

Just a philosophical note
You might also be interested in the philosophical discussion of adaptation, optimality, cost and benefit like this book (which I haven't read!) for example.

cheers for this, I now realize the issues you've raised. What do you think of me re-wording it so that I ask for "general and commonly observed" advantages/disadvantages? E.g. there may be some evolutionary reasons that hold true to all clades? E.g. the surface area to volume ratio effect for heat retention.


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Do animals suffer from "Human" mental disorders?
It is tragic, but apparently Killer whales and Dolphins can commit suicide too (e.g. here)...
This suggests they can become depressed. I wondered whether they were "clinically" depressed like many people are, and what other mental illnesses have been observed in animals in general.
Questions

Which mental disorders have been observed in animals? Which animals?
What is the prevalence of these mental disorders in those animals?
Are the causes and treatments of these disorders similar to Humans?

Strange thought
Organisms that have not evolved the ability to make "conscious choices" cannot decide to end their life.

We had a similar question, relating to suicide, before. The http://biology.stackexchange.com/questions/3478/is-there-any-documented-evidence-for-suicide-among-vertebrates-other-than-humans/8931#8931

You will be hard-pressed to find any scientific data on this question. Psychology in humans is already a difficult study, at times failing to demonstrate results with real scientific rigor. When studying animal psychology, you face another substantial barrier - language. Although some primates have been taught to communicate with sign language, the best of them are still far from the level of proficiency of a human. We can measure brain activity and observe behavior, which can lead us to strong suspicions about what is going on in an animal's mind, but very little can actually be proven.
Mostly, all we can do is speculate about such questions. You will find some veterinarians out there who treat pets for mental conditions, but you will find at least as many people calling them quacks as those who believe in the validity of their work. And certainly, they can't prove to you that a treatment has helped an animal. It's subjective.
If we see an animal do something which in a human might reliably be interpreted as a sign of depression, it's possible that this interpretation is appropriate for the animal as well. It's also possible that there is some totally foreign unrelated explanation. The problem we find when trying to scientifically discuss matters which cannot be proven scientifically is that scientists must be careful to state what they know and nothing more. So they might say "We cannot prove that the porpoise is depressed", or "Science cannot prove the existence of a God." This is often misinterpreted as evidence against the finding - that the porpoise is not depressed; that there is no God. This is a fallacy. Rather, we should recognize that we have different ways of exploring questions like these.
I can't prove it to you, but I know that my Beagle had a rich emotional life. I know this because I spent huge amounts of time with him. He was a close friend of mine. I would just as soon question whether my wife has real emotions as my dog. I can't prove that my wife's emotions are real either, but I don't have to. It would be silly to assume that everything she shares with me is some sort of evolutionary programming, and not real emotion. Now, when I extend this to cetaceans, I must admit that I don't have any friends in those circles. So I can only guess.

"You will be hard-pressed to find any scientific data on this question." This is untrue. There is a whole field of study on animal psychology and cognition called Ethology with a lot of high quality literature. You don't have to guess if your beagle has a rich emotional life; fMRI's can prove it thanks in part to Dr. Gregory Burns (human and animal neurobiologist).

@anongoodnurse I've seen the summaries and reports on some of these studies. While it's nice that someone is making these attempts, I find it very pale evidence next to the experience of having a pet. The point I'm making in this answer is that I am NOT guessing about my beagle's rich emotional life. I know it for certain. These studies' results did not add to my certainty. Science was never intended to be the only source of true knowledge. Mistake that, and you will find that for all the PhDs you can collect, your still an idiot.

You're the one making a mistake, not me. I take it you're not a scientist, nor have you ever been. Experience is subjective; research, while still limited, is much less so. You can believe with all your heart that your pet snake has a rich emotional life; that doesn't make it so. It really doesn't matter (to truth or fact) what you believe. It only matters to you, and maybe those who love you, work for you, etc.

@anongoodnurse I apologize for any offense taken. The statement was intended more generally, not personally. Nevertheless, I stand by it (other than the misspelling of "you're"). Science is one of many lenses through which truth can be observed. Refusal to look through any other lens is tantamount to willful blindness. On questions of emotion, science is not of zero worth, but it's a little bit like - I don't know - trying to use a thermometer to determine color. That's fine, but I hope you don't mind if I'm more interested in what I'm seeing with an optical spectrometer.

A functional MRI can tell you a lot more than your eyes can about your own feelings. People rationalixe, suppress, dissemble. FMRIs don't. Just the facts m'am. I was a person before I became a scientist, which was before I became a doctor. It's not that I don't use my eyes or my mind; it's that I know which is less subjective.

I know of at least one case, some social primates develop maladaptive behaviors similar to sociopathy if raised in isolation without the social contact with others of their species as they grow up. It appears they need to be socialized as children just like we do.

Source 1
Source 2

Good question: We know that prion diseases affect the psychology of animals (Scrapie, Mad Cow). But without a doubt genetic regulation of endocrine and neurotransmitter pathways is subject to the same folly as in Homo sapiens. Sorry I can't support that with links to publications...
update: There are many animal models: http://www.ncbi.nlm.nih.gov/pubmed/746371

Having an animal model of a disease does not prove that animals can have the same symptoms. An animal model will have the same chemical imbalances, that does not, however, necessarily mean that it will have the same psychological manifestations of said imbalances. It might, but there is no proof.

@terdon, I would still advocate Gent's answer, though, some users may not have realised the significance of a parasite/pathogen's ability to affect the cognate brain physiology of some organism. Deviations from normal decision-making, are often exploited by such parasites, towards their own fitness gains... quite an interesting angle of an answer IMHO.

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


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Chemoautotrophy in large organisms?
The major nutritional mechanisms include chemoautotrophy, heterotrophy (including parasitism and saprotrophy) and photoautotrophy. All of these modes of nutrition developed first in prokaryotic ancestors, and gradually, through the course of evolution, these prokaryotes formed complex eukaryotic, multicellular organisms. Some of these complex descendants (the majority of Kingdom Plantae) possessed the photoautotrophic mode and some (the majority of Kingdom Animalia, some of Kingdom Protista & Kingdom Fungi) possessed the heterotrophic mode.
My question is, since all the three modes developed quite early in evolutionary history, why didn't any chemoautotrophic multicellular, eukaryotic organism develop? (Or, if they did, why did they not form a wide-diverse group as the organisms with other two modes of nutrition did.)
(One possible reason could be lesser availability of chemoautotrophic substrates, but I have no proof, nor any argument to support this.)

i think its because organisms with more genes to regulate are not as competitive as organisms with many many genes and phenotypes. i.e. If there's a lot of sugar available from eating plants, making your own slows you down.

@shigeta There's also an advantage to ingesting and internally digesting biotic material - once you've eaten, you're no longer in competition with your neighbors those nutrients, so your meal can't be cut short by crowding.

@satwik-pasani While they would still probably be considered heterotrophs, there are a variety of insects that spit gastric(-like) juices onto prey and externally digest them, then suck up what's left.

I've been thinking about this question for a few days and along the lines of @ThomasIngalls comment, the simple answer is that cooperation between organisms has such a huge advantage in selection that any chance a eukaryote would become a chemautotroph would simply not adapt fast enough to compete with those that are already holding these niches.
The chemautotrophs I'm aware of are usually archaeabacteria.  They are optimized to grow slowly and have a large number of genes that can break down the unusual chemical compounds to grow in an inorganic often anoxic environment.  These bacteria have genes evolved from the chemautotrophic earliest days of life on earth.  They live deep within the earth, under ground, in volcanic vents.  There are animals that live in some of these environments, but its simply too easy for these to use the bacteria that are already growing here readily rather then re-evolve the genes to do it by themselves.
Eukaryotes are already symbiotes - they used bacteria to create ATP and photosynthetically fix carbon to the extent that they absorbed them as mitochondria and chloroplasts respectively.  If eukaryotes were under a tremendous amount of selective pressure, some of them might absorb symbiotic chemautotrophs, but without such pressure, it doesn't happen when you are competing against plants with roots and animals that eat for their energy.
Forming systems of organisms is much more stable than having individual species that can do it all.  This question is actually similar to other questions that ask why we don't have metal armor, run as fast as cheetahs, etc.  Evolution doesn't actually create super animals that are completely self contained.  The ones that reproduce the best are the ones that can actually spread out the risk of survival and contribute to an ecosystem.
It kind of makes me think of human beings - the only superorganism on the planet in this regard.  We don't really need to compete against any organism - we are in fact killing most of them out there without really thinking about it.  That might now turn out to be good for us long term.


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Definition and example of Gene Variant
Could someone clearly define what a gene variant is with an example. I am totally confusing myself with SNPs, alleles, variants and how the major and minor allele are defined. An example with gene names would be really helpful.

I have condensed your title so that only the key features remain, making it easier for people scanning the list to see what it's about. You don't need "Could someone..." in a title. Trust this is OK.

A fairly easy-to-understand example is that of the ABO blood group system. In this case, there is a single gene involved - ABO, which codes for an enzyme that modifies sugar groups on the surface of red blood cells. This ABO gene has three variants or alleles — i, IA, and IB. i (coding for Type O blood) is recessive, which means that its phenotype can only be observed if there are two copies of it – ii – one from the mother and one from the father. IA and IB are co-dominant, meaning that both can be expressed at the same time, and their phenotypes can be observed even if there is only one copy of that allele — for example, IAi would give Type A blood (as would IAIA), IAIB would give Type AB, and so on.
Major and minor alleles (at least in my mind) simply refer to the frequency with which an allele is found in a given population: a minor allele is one that is expressed less-often than a major one. The term minor allele frequency is sometimes used as a numerical representation of expression — a certain allele is only expressed in 3% of the population, for example.
These terms are all from classical genetics — talking about genes and variants without really knowing (or needing to know) what exactly the gene was made up of. Of course, we now know that genes are composed of sequences of DNA nucleotide base pairs (A, T, C, and G), which are then translated by 3bp-codons into proteins, where each codon corresponds to one of 20 amino acids, plus START and STOP sequences. It is in this context of DNA sequence analysis that terms like SNP or Single Nucleotide Polymorphism are used. If you were to compare two alleles, say IA and IB, any single-nucleotide difference between the two could be termed a SNP. Frequently, SNPs are often notated based on the changes the difference would bring to the translated protein sequence — for example, a AAG codon codes for the amino acid lysine, while GAG encodes glutamatic acid. In other cases, a SNP would make no difference to the protein sequence — for example, TTA, TTG, CTC, CTA, CTG, and CTT all encode leucine. You can find the DNA codon table here.
You should keep in mind that SNPs are not the only source of variation in genetic sequences — deletions, translocations, repetitions, inversions, frame shifts, and other mechanisms can all alter the DNA sequence at a particular locus or site. Taken together, all of these differences are often referred to as mutations, which simply means "changes."
I hope this was helpful, please let us know if you still have questions.


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Do we actually get more sick (flu/cold) during winter?
The word flu derives from the Italian phrase "influenza de freddo" meaning "influence of the cold".
Indeed it is that time of the year when my colleagues seem to have the flu/cold more often than not. I remember during university, winter lectures would be riddled with people coughing and sneezing - the so called "freshers flu"
Questions

Is there statistical evidence for this claim?
If so, what are the causes/factors involved?
Another post asks why our noses get runnier during cold whether, is this related?

As a sidenote: looking at the kind of questions you ask, you might be interested in this book

Cheers, I think so far you, @GriffinEvo and biogirl have suggested too many books for my wallet to handle. Will keep this in mind until i progress through them :)

@Remi.b Oh yes, I read about that book in the book "the blind watchmaker" and Dawkins says it's nice too. :)

The combination of these two reports from the CDC give information about the comparative prevalence of flu infection in the winter (September '12- May '13) and summer (May '13 - September '13). I'm going to assume that 2012-2013 was a fairly representative year as far as the level of detail of "do we get sick more in the winter" goes. Particularly striking are the graphs linked to in both documents of the number of flu-infected respiratory specimens per week:
Winter (infected specimens out of 311,000 tested):

Summer (infected specimens out of 52,000 tested):

Together these two figures cover data Sept '12 - Sept '13. Note the difference in scale on the vertical axis. Forgive me if I don't run any statistical tests, but I think you can spot the trend.
The sum of all the Winter cases represents 23% of the 311,333 specimens tested from Sept '12 to May '13, and the sum of all the bars in the Summer figure represents 3.9% of the 52,150 respiratory specimens tested from May '13-Sept '13.
Still left to answer: Why is this the case? In my preliminary research it seems like we still don't fully know the answer to this one; I'll leave someone else to speculate.

Edit: Some tentative answers to why is there a seasonal flu outbreak:
This review (1) does a nice job of laying out some of the current ideas about the cause of the seasonal flu. One interesting note is that seasonal flu is a phenomenon of temperate climates: in tropical regions flu outbreaks occur on a much less regular periodic schedule. Some possible causes mentioned by the authors (paraphrased from the article):

It takes time for virus to mutate enough to be infectious again to people who were already infected with it.
The efficacy of the immune system may vary seasonally, say, due to changes in daylight hours/vitamin D and melatonin levels (which have been shown to affect immune system function in hamsters)
Flu is transmitted better in more crowded conditions + in winter people are more crowded together. This is a popular explanation, but the authors claim that it has not been satisfactorily tested. It has been argued convincingly that the 1918 flu epidemic was exacerbated by the crowded condition of army barracks in WWI (see citation in paper).
Indoor heating encourages air recirculation, which allows virus to persist in the air around you longer.
Viruses survive/persist better in cold, dry conditions. This may allow them to spread in the atmosphere longer during the winter, and be more easily transmitted from person to person via "bioaerosols" (sneezes).

Ultimately, as I said before, we don't really know yet. Reading that list you can imagine several ways in which a few of those factors are not at all causal and are rather just strongly correlated with the "true" cause of flu seasonality.
(1): Lofgren et al. Influenza Seasonality: Underlying Causes and Modeling Theories. (2007). J. Virol. 81(11): 5429-5436. doi:10.1128/JVI.01680-06

nice find and summary! I'll wait a bit to see other people's answers before ticking, but upvoted of course

As this answer cites my paper, it is clearly correct ;). I would note that it's true for influenza, and a few other winter-circulating diseases (Norovirus comes to mind). Other infections are more prevalent in the summer (many bacterial GI infections for example) and some don't care at all.

"Viruses survive/persist better in cold" -
Could you provide proof links on that?

@ctapobep, I am mostly just paraphrasing the open-access article cited here. In that article they make the claim several times that viruses are more stable in cold, dry environments. They cite this paper: Hemmes et al. (1960). Virus Survival as a Seasonal Factor in Influenza and Poliomyelitis. Nature 188: 430-431, which appears to investigate the stability of certain viruses in cold, dry environments.

@ctapobep, furthermore, This result isn't surprising: viruses are inert particles made of proteins in a relatively ordered/low entropy configuration. If you increase the temperature, you make it more thermodynamically favorable for the protein making up the viral particle to loosen from their ordered configuration and move freely, which effectively destroys the particle.

Has anyone investigated the possibility of migrant birds carrying new strains?


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Clarification of the procedures to amplify cDNA needed
The typical procedure to obtain cDNA from genomic extracted DNA is the following:
RNA is extracted from desired tissue, RNA/DNA hybrid is obtained by virtue of reverse transcriptase RNA dependent DNA polymerase, H RNAse creates gaps in RNA of DNA/RNA hybrid and with the aid of a typical DNA polymerase dsDNA is transcribed, right?
Then, the newly synthesized cDNA is linear (like a "small chromosome")?
How is it protected from the nucleolytic activity?
Is the procedure really like I described or does the reverse transcriptase already give a dsDNA from single stranded mRNA?

Here is the rough procedure that I've used to prepare cDNA before

Extract RNA from desired tissue (select for mRNA using the polyA tail of mRNA)
Conduct reverse transcription. This requires a primer complementary to the polyA tail to get the reverse transcriptase started (Edit:You could also use random primers to prime reverse transcription. This eliminates the redundant polyT sequence from the cDNA. This is the method used in the Illumina TruSeq high throughput sequencing library prep kit). Now you have a collection hybrid RNA/DNA double strands
Digest the RNA strand specifically. This can be accomplished with RNAse H as you mention, or by introducing basic conditions, which degrade RNA much more rapidly than DNA due to the 2'OH of RNA. Now you have linear ssDNA complementary to the inital mRNA templates.
From this point your applications may differ. If you are doing microarrays, all you need is ssDNA, since you want to hybridize the cDNA to the array. If your downstream use of the cDNA requires dsDNA, then you need to synthesize a complementary strand to the cDNA (and potentially amplify the product). This can be accomplished through PCR random primers, or some more complicated PCR that will incorporate extra sequences on either side of your cDNA (e.g. bar-codes and adapters in RNA-Seq).

How is [the cDNA] protected from the nucleolytic activity?

If you are digesting the product of reverse transcription with RNAse H, that enzyme digests RNA specifically, so your DNA is unharmed. If you are going with an alkaline conditions treatment, then the RNA will be degraded in those conditions much more quickly than the DNA due to the presence of the 2' OH group in RNA which can act as a nucleophile for a self-cleavage reaction.

so the cDNA will have a poliT tail?

It depends. If you just have one strand and you prime with polyA tails, then yes. If you synthesize a second strand, however, then you will have a double strand with one side polyA and one side polyT. I also looked up how the Illumina TruSeq library prep kit does this, and they use random primers to prime the reverse transcriptase, so if you did that then you wouldn't necessarily have a polyT tail on your first strand cDNA. This makes sense if you want to maximize the amount of informative (i.e. non polyA/T) cDNA, say, for RNA-Seq.


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Can you "spam" bird sounds so that birds no longer interpret them right?
Is it possible to make birds confused by repeating recorded chirping or singing? Or do they always perceive them as usual, even if the situation is clearly not as described by those sounds?
For example:

mating song when there's no mate
danger/alarm cries when nothing's going on

Specifically, I'm interested in public placed with a lot of traffic using looping speakers to scare off birds that like to dump upon almost unsuspecting citizens. Like underground entrances and city malls. Does the effectiveness decrease over time because of that?

No idea, but have you thought of the fact that this might scare away those unsuspecting citizens, too?

Yeah, that's quite annoying too. I'm thinking it's not the best solution against birds. But even if I don't have a say in that matter, I want to know more about how it works.

This is entirely anecdotal, but the birdwatching community tends to ask people not to overuse calls (played via a smartphone or similar) to attract birds. Apparently, this can cause birds to stop responding to actual calls in the long run.

This is at least doing some confusion, probably also harm. A lot of wildlife conservationists warn about using smartphone apps which replay bird songs, as they are confusing the animals. An example is the Dorset Wildlifetrust.
This phenomenon has even be analyzed scientifically, and the results show that birds are irritated. Territorial birds seem to be affected more and it has been shown that, when a fake call was replayed to them, they sang more often and longer. In the first paper they speculate that this will drain too much energy and prevent the birds from doing other important things.
The second paper looks at zebra finches, which are not territorial. Here they find that birds pay less attention, the more often the song is replayed.
The articles:

Simulated Birdwatchers’ Playback Affects the Behavior of Two Tropical
Birds
Habituation in songbirds.


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Cell life: division for immortality or reproduction with aging
Are the two cells that are derived from one cell, ‘twin sisters’ or a ‘mother and a daughter’?  In other words, can a cell really be divided to live an "immortal" life or is cell reproduction the reality of cell life that accounts cell age difference between two successive generations, cell aging-associated senescence in cell reproduction, and cell line survival after the death of old cells.

First of all, in eukaryotes (as far as I'm aware), older cells can be distinguished from younger cells due to telomere shortening, so there is an ageing process. HeLa cells mentioned by @Gary Chou have a more active telomerase which mitigates telomere shortening, allowing cells to continue to divide indefinitely. I think it's a very interesting question whether this immortality eliminates any sense of "older" and "younger" cells from in HeLa cell culture. I suspect not, but I am not sure on the specifics.
In general this question will depend on how an organism divides (we're going to talk single-celled organisms from now on). For example, the yeast Saccharomyces cerevisiae is a budding yeast, which means that it divides by budding a smaller cell off of the larger cell. This clearly allows for an interpretation of "mother cells" and smaller "daughter cells." Indeed, as lots of research on ageing in S. cerevisiae has shown, beyond being larger, the mother cell undergoes replicative ageing: over time the mother cell is less capable of growth and division--she gets old!
Perhaps the most interesting case of all (and maybe the one you had in mind) is when the organism divides symmetrically, like the bacteria, which undergo binary fission. For decades, as far as scientists could tell, the two cells that were the product of one bacterium dividing looked identical, and all measurements seemed to indicate that the cells were "sisters," i.e. exactly the same, both newborn. So if in the right conditions bacteria could continue to divide indefinitely, it seemed that bacteria were immortal, since each division reset the ageing clock for each bacterium.
However, a seminal study in 2005 (1) changed this view. The researchers took time-lapse microscope movies of a colony of Escherichia coli from a single cell. E. coli is rod-shaped, so when it divides it has to synthesize two new ends or poles, one for each cell, so just after division each cell has a "new pole" that was made in the process of that division and an "old pole" which had originated before. In this study Stewart et al. kept track of the old poles in the growing colony, and they defined the age of a cell as the age of its old pole. They found that older cells (i.e. cells with older poles) displayed replicative ageing, just like yeast! They grew more slowly and were less capable of dividing. This was examined rigorously by Wang et al. (2) in a "mother machine" in which bacteria were able to grow in constant nutrient conditions (by flowing fresh media across them) in dead-end channels. The cell at the dead-end of the channel always inherited the old pole, and so was a "mother" to all future cells. They found that, while a cell line was able to grow for very long periods of time completely stably, after hundreds of generations there was an increased likelihood for the cells to display signs of stress. They attributed to the accumulation of toxic factors in the mother cell over time. So even in cells dividing by binary fission, there appears to be some difference between the two cells arising from the division, depending on how old the pole that they inherit is.
These effects in bacteria are small, and require watching many generations to reveal. Even in light of these results many researchers will still call the "mother" cell the cell about to divide and the "daughter cells" the cells that result from division, implying that there is no difference between "daughters." Stewart et al. claim that on the basis of their work this conception of bacterial division must be revised, and that instead of division producing two identical daughters,

the old pole cell should be considered an aging parent repeatedly producing rejuvenated offspring.

Furthermore, they add a nice philosophical touch to their findings:

These results suggest that no life strategy is immune to the effects of aging, and therefore immortality may be either too costly or mechanistically impossible in natural organisms.

(1): Stewart EJ et al. (2005) Aging and Death in an Organism That Reproduces by Morphologically Symmetric Division. PLoS Biol. 3(2): e45
(2): Wang P et al. (2010) Robust Growth of Escherichia coli. Curr. Biol. 20(12): 1099-1103.

Great answer, and those are the same reference papers I would have referred to. Although the Wang et al. paper suggests that there is no difference between the mother and daughter cell, and that cell death is independent of growth (and that there is not a reduction in division rate with age). The idea being that the result from Stewart et al. was due to the older cells being in the middle of the colony with fewer available nutrients.

Also the website of the Jun group (where the Wang et al. paper came from) is excellent: http://jun.ucsd.edu/ lovely videos showing the mother machine in action!

@StephUnna fair points. I didn't stress the growth-independence of cell age defects in the Wang paper enough; it is probably not accurate to use the term replicative ageing for bacteria, since the ageing effects are not manifested in problems with growth/replication. What I was referring to by "signs of stress" is the increased filamentation rate that Wang et al. observes in older cells. Though they may still grow with the same rate, there is a difference between mother and daughter cells due to accumulation of defects in old-pole cells over long times.

In term of eukaryotic cells, most of them are mortal and will indeed age (the famous telomere sequence for example). However due to mutation some cells do achieve immortality such as HeLa cell line widely used in bio research.

Could you please develop a bit your answer and include in particular the OP's question. When (for what cell types) does the analogy "twin sisters" hold and when does the analogy "mother and daughter" hold?


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Finding RNA Loops
I was rooting through the literature, but there is too much work on the topic of detecting loops in RNA and the RNA helices that go with them.  Can anyone point to a good review on this topic or even better describe some better performing algorithms?

What exactly do you mean by loops? Just unstructured parts of the RNA (= not in any base pairs)?

A loop in this case would be the result of an RNA helix from a single stranded RNA.  The loop would be the result of the strand forming a helix by itself.

So you only need to find the helices, from there identifying  the loops is trivial. Can the loops have interactions with other parts of the RNA, e.g. pseudoknots? If not, any secondary structure prediction program like mfold should suit your purpose.

just looking for helices.  i wasn't aware that was trivial.. is mfold accurate?

as @MadScientist said mfold or RNAfold(Vienna) should work for secondary structure prediction. Anything flanked by a half-stem should be a loop. Both mfold and RNAfold have a limit on the size of the sequence. They don't take large sequences and splitting the sequence is not a great option because the local MFE may be different from the global one. There is also an experimental technique called PARS in which the RNA is digested with different RNAses (V1, S1) and base-paired regions are identified by sequencing

Recently sequencing approach has been extended to obtain RNA secondary structures in-vivo by using a soluble RNA-methylating agent (DMS).

EDIT: Anything flanked by a half-stem (which pair with each other) should be a loop

any reviews?  the last time i looked this was not a completely solved problem.

As an improvement to what @WYSIWYG mentioned, PARS is fairly low resolution since it is still enzyme based. The newer in vivo SHAPE or DMS-seq methods are much better and more informative.

I frankly don't trust Mfold or RNAfold for finding structure. There are just too many false positives and without experimental verification, it's not reliable. For finding hypothetical local structure, it's great. However to find evolutionary conserved structure MSA methods like what has been used with Rfam are a more suitable way.
Since you asked for Reviews, any of Sean Eddy's Rfam updates are good. I also suggest checking out https://www.mendeley.com/groups/545791/rna-structure/.
But for now, I think Revolutions in RNA Secondary Structure Prediction by David Mathews who developed the Turner rules and Mfold is a good start.


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How do birds learn their tunes in isolation from their own species?
I wonder what a bird would sing if it didn't have its parents around (or any other birds for that matter) to learn its chirping sounds from.
I'm interested in how a bird would sing...

in complete isolation from creatures communicating through sound;
in isolation from its own species, but with other birds;
in isolation from all birds (other animals and creatures are there for it)

For example,

Would a bird even feel the need to speak up if there wasn't any other vocalizing creature around?
Would a bird learn other species' signals? Would it only learn from one species, the one which it would think of a fitting mate?
Would a bird try to mimic a non-flying creature's signals?

These are similar questions, but if you think they should be separated, let me know in the comments.

Birds have to learn their song patterns.
They are able to chirp, but the songs with "meaning" are learned from their parents or whatever they learned to be their "parent".
Here is a paper that related bird song learning to human learning (of speech, for example).
Birds brought up by parents from another species learned to sing their songs.
There are many birds that learn to imitate other animals or sounds, so in isolation from all birds they will probably do this.
I can't recall where, but I read a paper once, where little finches brought up by humans developed a song resembling the "Hello there, now there's food", their caretaker always greeted them with. (Not the speech, but the overall sound pattern.) They might not understand the signals, but they try to communicate nevertheless. Some birds use sound from other species to mock others, scare them off or lure them into thinking they might be more powerful than they are.
Birds brought up in total isolation do sing, but not the typical songs you know from their species. Deaf birds who can't hear themselves, though, do not (always) sing.

Nice, thanks for sharing! I was also interested in how birds initially created their species-specific melodies. There probably wasn't someone to teach them, so they must have invented those tunes and then those tunes evolved. Do you know anything about that?

As birds also have regional dialects, the development of their song is part of evolution, like for humans the development of speech, languages and dialects. How that works involves a lot of time and a lot of science I know nothing about. And, I thing the "first development of meaning for a birdsong"-mechanism involves a lot of speculation, too. It might just be similar to development of hindering feathers, that make birds more attractive to their mates. The more elaborate a song, the more effort went into it. So the dads singing songs the mums like got more offspring to teach it to.

this is not true of all birds, yes many birds learn their songs but many birds have completely gene programed instinctual songs. cuckoo's being a classic example. Some will instinctually know a basic song but learn to refine it and make it more complex.  there is a whole spectrum of bird song behavior.


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Why do yeast ferment Equal sweetener
I had my students conduct a fermentation experiment manipulating sugar amounts (number of sugar packets in solution) and measuring CO₂ production via capture in a balloon and measuring circumference (very common HS lab experiment). I also had them conduct a trial with two packets of Equal sweetener. To everyone's surprise two packets of the "zero calorie" sweetener produced as much CO₂ as four packets of sugar. Can anyone shed light on why this would have occurred? Equal contains maltodextrin and dextrose in addition to the aspartame. I'm assuming that yeast are able to metabolize one or more of these substances, but I haven't been able to find a more detailed explanation.

Your sugar substrate was sucrose. Yeast cells metabolise this by secreting an enzyme, invertase, which splits the disaccharide into glucose and fructose both of which can be fermented by yeast to produce CO2.
According to this site

Equal Original (blue packaging)  is a zero calorie sweetener that contains aspartame and acesulfame potassium as its sweetening ingredients along with a bulking agent.
Equal Original PACKETS:
dextrose with maltodextrin, aspartame, acesulfame potassium

This agrees with what you say - that the sweetener that you used contained dextrose - and leaves me very confused. Dextrose is another name for glucose so how can this contain zero calories?
The answer lies in the legal definition of zero calories  = less than 5 calories per serving (presumably per package in this case.) So let's assume that by adding two packs you were adding 8 calories equivalent of glucose.
Calorie content of carbohydrate = 4 calories per gram
Two packs could contain 8 calories = 2 g glucose.
The molecular weight of glucose = 180
therefore 2 g = 2/180 moles
if completely fermented to CO2 each mole -> 6 moles CO2
12/180 moles CO2 = 0.75 litres of CO2.
I conclude that there is enough glucose in two packets of Equal to generate a reasonable amount of CO2.
Yeast cannot ferment maltodextrins. It is possible that aspartame (aspartyl-phenylalanine-methyl ester) could be metabolised, but I think the dextrose/glucose solution is the best explanation.
EDIT:
I meant to say, just to illustrate that this is a significant amount of glucose, standard rich yeast medium is 2 g glucose /100 ml (2 % w/v).
EDIT #2 My back-of-an-envelope calculation has a fundamental error in it, but luckily I am the first to spot it. If glucose is being used fermentatively, then only one third of the carbon will end up in CO2, with the remainder going to ethanol. This means 0.25 litres instead of 0.75 litres. Yeast is so oriented towards fermentation that even in the presence of oxygen the fermentative pathway will dominate.

I agree with all of this, except there is one problem with the data. (Keep in mind this was High School Bio) A packet of equal is far less mass than a packet of sucrose(since aspartame has such a high sweetness profile), and as such a packet contains a very small amount of dextrose compared to the amount of glucose/fructose in the sucrose packets. That said, there was nearly as much CO2 generated by two packets of Equal as four packets of sucrose. Granted, there is an upper limit to the yeast growth curve and metabolism, but there were higher rates as we increased from 2 to 4 packets sucrose.

Without knowing the actual contents of one pack of Equal we are at an impasse. However it is noteworthy that the formulation quoted in my answer says "Dextrose with ...". I'm not familiar with US labelling law, but in the EU the first-listed ingredient is present at the highest level. And of course glucose is probably cheaper than aspartame so it would make commercial sense to use the highest amount of glucose possible while remaining "zero calories".

I don't have a definitive answer to this, but a little over a decade ago I was in an undergraduate lab that had a similar thing happen - a small amount of metabolism of a "control" group of bacteria fed artificial, sugar/calorie free sweeteners instead of sugar.
Our running theories at the time were:

Contamination. Always a problem in laboratory experiments, and especially undergraduate lab experiments.
Trace contaminants. "Zero calorie" isn't actually 0, it's just small, and hardy microorganisms may be able to do just fine with small amounts of nutrients. If there's another factor limiting their growth, that may result in the identical CO₂ results.
Some intermediate compound or the like that is useful for metabolism. As you said, possibly the ability to use maltodextrin or dextrose.

Equal is marketed as a "zero calorie" sweetener, with respect to human digestion. The sweetening agents are aspartame (Asp-Phe; a dipeptide) and acesulfame K. The maltodextrin and dextrose are probably bulking agents to give the product a free-flowing, poweder consistence.
The "fermentables" in question are:

Dextrose. This is another name of glucose, and is the most easily metabolized sugar in the Equal packet.
Maltodextrin is an oligomer of D-glucose linked by $\alpha$(1,4) linkages. If this were the disaccharide of glucose-glucose, or maltose, then yeast could readily ferment this. However, yeast cannot hydrolyze maltodextrin and therefore cannot metabolize it.
Aspartame is a dipeptide which can easily be fermented.

Therefore, yeast will happily metabolize dextrose and aspartame, but not the other two agents.

I don't think it is correct that dextrose is linear. Since the two cyclic pyranose forms (alpha and beta) are in equilibrium with the linear form in solution it's not clear how you would be able to isolate pure acyclic glucose (less than 1 % of what is present in solution), and even if you could, as soon as it went into solution it would equilibrate to the pyranose forms again.

Alan, quite right. I made a mistake. The open chain form is in equilibrium with alpha and beta cyclic pyranose and furanose forms. I have corrected myself.


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Cats, Dogs and Bears - how are they related?
What is the ancestral relationship between cats, dogs and bears?
I presume they are more closely related to one another than other paraphyletic clades of mammal.

Which came first?
What did their common ancestors look like?
What are their geographical origins?

You'll like this: http://tolweb.org/tree/

and this: http://www.onezoom.org/mammals.htm

Clades are, by definition, monophyletic.

Cats, dogs and bears all belong to the Carnivora clade of mammals, but they are not the only ones belonging to this clade.
For instance, cats are more closely related to mongoose and hyenas than to dogs or bears, who in turn are more closely related to raccoons, weasels, and walruses.
Their common ancestors likely displayed various adaptations to a carnivorous diet, as the name of the clade suggests, and which are still present in many extant Carnivora (the panda being a well-known exception).
Together with many other groups of mammals, Carnivora are part of a clade named Laurasiatheria thus named because they may have originated in the Laurasia supercontinent, which comprises nowadays north America and Eurasia.


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The number of nipples (breasts) a species has?
Only mammals have mammaries and mammary glands.
What evolutionary factors determines the number of mammaries (nipples/teats/breasts) a species has?
Is it always an even number?

Heh, never thought of that. I would guess the size of the brood is the determining factor.

A bit of terminology - a mammary gland is not necessarily the same as a breast. One breast contains many mammary glands - the tissues which produce milk. These are connected via milk ducts to the nipple.

cheers @MattDMo! i've changed wording now, how does it sound?

@hello_there_andy I think the concept of homeotic genes / Hox genes will fascinate you as much as learning about Symmetry in EvoDevo.

That's the reason that Penguins can't evolve into seal and whale type animals, the child bearing.

The number of mammary glands a species has is related to litter size. The relationship generally follows the "one-half rule," which states that the average litter size is equal to half the number of mammaries. The number of mammaries also tends to put an upper limit on litter size. It's not necessarily a hard limit, but survival tends to drop noticeably when number of offspring being nursed exceeds number of mammaries.
The number of mammaries is almost always even, but a notable exception is the Virginia possum, which has thirteen.
Gilbert, A.N. 1986. Mammary number and litter size in Rodentia: The "one-half rule". Proc. Natl. Acad. Sci. USA. Vol. 83, pp. 4828-4830.

As an addition to the excellent post by Erin.
As a name-giving key feature,mammals have mammary glands.
"Animals that are bilaterally symmetric have mirror symmetry in the sagittal plane", which includes Chordates such as mammals.
Some have seen this iconic picture, showing the bilateral symmetry in chordates:

It is easy to see why most commonly even number of mammary glands are found in mammals, given that they form in pairs, distal from the notochord.
Evolutionary, an uneven number of mammaries may be explained through a subjectively-mild mutation which may be retained as a vestigial-like feature, somewhat-functional or not.
On a molecular level, unilateral mammary glands likely involve key developmental pathways such as hedgehog and likely has underlying polygeneic root causes, - for the termination of gland formation on one side.
See this intersting paper:

Kohei Amakasu, Katsushi Suzuki, Hiroetsu Suzuki* "The Unilateral
  Urogenital Anomalies (UUA) Rat", Comp Med. 2009 June; 59(3): 249–256.
We established an inbred rat strain with unilateral urogenital
  anomalies from an incidentally identified male rat with unilateral
  renal agenesis and an undescended left testis. These rats were
  characterized by unilateral renal agenesis in both sexes, undescended
  testes with agenesis and hypoplasia of the accessory sex organs in
  male rats, and complete and partial agenesis of the uterine horn in
  female rats. All of these urogenital anomalies were unilateral and
  restricted to the left side; we named this phenotype unilateral
  urogenital anomalies (UUA). Breeding tests showed that these
  abnormalities were inherited as polygenic traits

It is noteworthy that the mammary glands in the male human population didn't decrease fitness to such a degree where evolutionary pressure would have lead to cease gland formation altogether, by adding extra information to the sex-chromosome(s). As such human males retain mammary glands, albeit typically never reaching a functional state.
The factors weighting against such additional genes are, that the default formation in most mammals is the female body plan, which conserves functional mammary glands to potentially feed their offspring, chipping away at the chance of genes involved in the cessation of mammary gland formation.
Secondly, selection pressure for information retained on the sex-chromosomes is higher, as opposed to autosomal (non-sex) genes. (See this nice concise post by Danielle Venton,  The Degenerating Y Chromosome,Genome Biol Evol (2011)  3  1338-1339. )
Concluding, naturally, it would be easy for an asymmetric sponge to have an uneven number of protrusions or orifices, less so for humans, unless the orifice is located along an axis of symmetry.
See also:

http://en.wikipedia.org/wiki/Hedgehog

Ad biological symmetry:


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Is tongue rolling genetic?
Is the ability to roll your tongue or not truly inherited or genetic? What I have gathered from school has been contradicting with evidence I found elsewhere.

I could only find fairly old literature on the subject, so take this with caution.
Some papers seem to indicate some sort of genetic component to tongue rolling, although the precise molecular basis are not really described (but, again, these are 30-40 years old papers...)
From: Inheritance of ear wax types, ear lobe attachment and tongue rolling ability. - Cruz-Gonzalez and Lisker - Acta Anthropogenet., 1982

The mode of inheritance of ear wax type, ear lobe attachment and tongue rolling ability were studied in 77 families with a total of 293 children. The results clearly showed that the dry ear wax type and the attached ear lobe type represent the homozygous state for two pairs of autosomal recessive genes. The evidence for the same being true regarding the lack of ability to roll the tongue was less conclusive in our material, but this could be due to difficulties in communication between the examined individuals and the examiners.

Tongue-rolling phenotypes and geographical variation in the United Kingdom

The distribution of tongue-rolling phenotypes in a sample (n = 477) of undergraduate students of the University College of Swansea (U.K.) was studied. The birthplaces of these students were also recorded. England was divided into six areas, and Wales was left as an area on its own. The data suggest that those students who come from north-east are more non-rollers, which may be due to mixture with Scandinavians.

Left-handedness and tongue-rolling ability.

948 undergraduates at The Ohio State University were administered the 10-item Edinburgh Handedness Inventory and asked to indicate the extent to which they could turn up the sides of their tongues. Significantly fewer left-handers than right-handers (62.8% and 74.8%, respectively) reported being able to turn up either or both sides. Sex differences in tongue-rolling ability were also noted. Among the 403 men included in the final sample, 77.4% could roll their tongues, whereas only 69.7% of the 491 women could do so.

This paper, however says (luckily Google finds a PDF here... seriously it should be illegal to have papers from the 70s behind paywalls... but I digress):
No evidence for a genetic basis of tongue rolling or hand clasping - Martin, J Hered., 1975

OCCASIONALLY one still finds in elementary genetics courses and elsewhere, the ability to roll the tongue and the manner of clasping the hands cited as examples of simply inherited human polymorphisms. This is despite extensive evidence to the contrary that has accumulated over several decades. Sturtevant T found that about 65 percent of persons studied were able to tum 1.JP the edges of the tongue and although some people were able to learn the ability, family data indicated that it was inherited as a simple dominant allele. However, Matlock reported 7 out of 33 monozygotic (MZ) twin pairs discordant for the ability, and Sturtevant concluded that there is sufficient nongenetic inftuence to make the character practically useless as a genetic marker. He confessed to being "still embarrassed to see it listed in some current works as an established Mendelian case."

The paper is also cited in the "Myths of Human Genetics" page of the University of Delaware.
So, all in all, it seems that there is evidence against a Mendelian transmission of this character, although these studies are quite old and some further analysis is warranted to exclude non Mendelian (read epigenetic) transmission of tongue rolling.