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Are humans the only species who drink milk as adults?
I was drinking a glass of milk the other day and that got me thinking that no other animal to my knowledge drinks milk past their infant stages. One could argue that cats might but it isn't good for them to do.
Are humans the only animal that are able to drink milk as adults and not have it cause issues?
Of course, I know some people do have lactose intolerance too.

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

I'm not going to give a full answer, but our pets get dairy from their owners all the time.

My cat seems OK.

Good observation!
Gene coding for the lactase
Gene LCT
Mammals have a gene (called LCT C/T-13910) coding for the lactase enzyme, a protein able to digest lactose. Lactose is a disaccharide sugar found in milk.
Expression of LCT
In mammals, the gene LCT is normally expressed (see gene expression) only early in development, when the baby feeds on his/her mother's milk. Some human lineages have evolved the ability to express LCT all life long, allowing them to drink milk and digest lactose at any age.
Today, the inability to digest lactose at all ages in humans is called lactose intolerance.
Evolution of lactose tolerance in human
Three independent mutations
Tishkoff et al. 2007 found that the ability to express LCT at an old age has evolved at least three times independently. Indeed, they found three different SNPs (stands for Single Nucleotide Polymorphism; it is a common type of mutation), two of them having high prevalence in Africa (and people of African descent) and one having high prevalence in Europe (and people of European descent). The three SNPs are G/C-14010, T/G-13915 and C/G-13907.
Pastoralist populations
Lactose tolerance is much more common in people descending from pastoralist populations than in people descending from non-pastoralist populations, suggesting a strong selection for lactose tolerance Durham 1991.
Selective sweep
On top of that, Tishkoff et al. 2007 focusing on the locus 14010 (one of the three SNP's mentioned above) showed that there is a clear selective sweep (which is a signature of past and present selection) around this locus.
They estimated the age of the allele allowing lactose tolerance at this locus (allele C is derived, the ancestral being G; see nucleotide) at around 3,000 to 7,000 years (with a 95% confidence interval ranging from 1,200 to 23,200 years) and a selection coefficient of 0.04 - 0.097 (with a 95% confidence interval ranging from 0.01 to 0.15).
I recommend reading Tishkoff et al. 2007. It is a classic, is short and is relatively easy to read, even for someone with only basic knowledge in evolutionary biology.
Are humans the only animal that is able to drink milk as adults?
I don't really know... but I would think so, yes!
Drink vs digest thoroughly
As @anongoodnurse rightly said in his/her answer

"Drink" and "digest thoroughly" are two different things

Pets
According to many dog health websites (such this one for example) claim that there is also variance among dogs where some dogs are lactose tolerant and others are lactose intolerant. I could not find any paper on the underlying genetics of lactose intolerance in dogs or other pets. It is not impossible our pets have also been under selection to be able to digest lactose as we humans could have given milk to them. It is also possible that pets do not actually produce any lactase at adult age but rather that some pets are just able to deal with having indigestible lactose in their guts! But then again, "Drink" and "digest thoroughly" are two different things.
Tits and robins in 20th century England
A funny and famous case is the case of blue tits and robins in the 20th century, in England. At that time, in England, the milkman was bringing the milk at home in the morning and would leave glass bottles with a simple aluminum cap in front of people's home. At some point, blue tits and robins learnt that by pecking through the aluminum they can get access to the milk. See this (non-peer-reviewed) article that tells the story.
Somewhat related
There are already a number of good posts on milk digestion in humans on Biology.SE. Consider having a look at:

What inactivates pepsin in infants? and Seriously, do humans produce rennin?
Are there any non-mammalian species known that lactate?
Can an adult without genetic lactase persistence still develop a tolerance for dairy foods?

My cats and dogs all drink milk when it's given to them. What about that?

Can confirm the anecdote about small birds pecking a hole in milk bottle tops (around the mid-90s for me). Happened to us every so often.

Milk is a limited access food, and I believe that's the only reason adult animals can't drink it in nature. Suckling well is not a skill adult animals retain. Given the opportunity, though, many adult animals drink milk. Even chickens love milk! (I sometimes fed excess goat's milk to my chickens. It seemed to be a holiday gift to them.) :)

@ZzZombo Exactly so. My friend's father's dog used to be given a cup of hot tea every day, with milk, and somehow they had figured out that he liked it with one sugar.

@Remi.b You're confused about who said what, and I don't know what 'typically' is doing in the sentence, but the dog concerned lived to a ripe old age. I could never figure out how they knew the dog liked tea, let alone milk and sugar in it. Just an amusing anecdote.

@EJP Oops indeed. I removed my comment.

I just read that fascinating article about the tits & robins.  The most interesting part to me was that milk used to be delivered with no cap at all, just open bottles.  Really???  Cats, flies, birds, dogs, raccoons, possums, beetles... ahhhh.  Yes animals will drink milk whenever they get the chance!  Yes my biggest problem with it is that I don't want to drink ANYTHING after ANY of them!

@BillK It is not so easy to reach the milk in a standing glass (let's assume the bottle would remain standing because of some sort of wooden box in which it stands). I don't think flies would be attracted to milk but I am not sure. Most insects can't climb on glass. There are no raccoons or possums in England (you North American fellow $\ddot \smile$). Squirrel sounds like a potential threat. I suppose that if they used to do so, it is because it worked!

@Remi.b: Just remembered another instance of animals learning to drink milk.  When I was a kid growing up in dairy farming country (small farms, not the massive ones of today), the barn cats would wait patiently while the farmer was milking, hoping he'd squirt a stream of milk into their mouths.

@BillK That took me aback too, and frankly I don't believe it. This page on the history of milk packaging in the U.K. says that originally cardboard caps were used.

As a non-native speaker of english that wasn't aware of the bird called "tit", the last section of this answer had a very weird albeit amusing meaning.

Can confirm - I witnessed my dog recently trying to consume poop. Milk seems a lot better than that :P

@T.Sar you may enjoy https://www.youtube.com/watch?v=ueuA-9pqRok then.

It was actually cream rather than milk that the tits would take. This was in the days of unhomogenised milk where cream would rise to the top.

"A strong selection for ... in pastoral population" most likely means that if you could not digest milk, you died.

@Thorbjørn Ravn Andersen: As far as I can tell, lactose intolerance is merely unpleasant, not fatal.  So if the choice is between eating dairy products or dying of starvation, I expect few people would choose the latter.

@jamesqf Lactose intolerance mean that you do not digest the milk sugar, which contains energy.   I do not know how much, but apparently enough to make it a strong selection factor.

There's quite an interesting contemporaneous discussion of this, and other tit behaviour, in John Barnes' Titmice of the British Isles which was published in 1975. As the image in the linked article shows, it wasn't just blue tits but also great tits.

@Thorbjørn Ravn Andersen: Sure, you don't digest the lactose, but that's far from being the only nutritious substance contained in milk.  Over time, it would create a selection pressure, but one far from a universal "digest this or die" elimination.

@jamesqf Perhaps.  What would you then suggest could cause said strong selection pressure?  If it is merely inconvenient and you don't die, you still reproduce.

@Thorbjørn Ravn Andersen: Just like any other selection pressure.  They're very seldom binary logic.  Just for instance, people might not want to mate with someone whose gut is rumbling all the time.

The problem with this question is 1) wording and 2) access.
"Drink" and "digest thoroughly" are two different things. The latter does not prohibit the former. It is only lactose that is not tolerated; Calcium and other minerals, proteins, fats, etc. are also present in milk and are beneficial to the consumers if the lactose intolerance is not incapacitating.

One could argue that cats might but it isn't good for them to do.

I don't know about this. My barn cats drank milk all the time without diarrhea or other untoward consequences; so did my dogs. Furthermore, feral cats steal milk, as do sea birds!

While censusing, satellite tagging adult males and rototag tagging weaned pups of northern elephant seals (Mirounga angustirostris) at Playa Norte, Isla de Guadalupe (14 - 19 February, 2003), we opportunistically observed the stealing of elephant seal’s milk by feral cats (Felis catus) and western gulls (Larus occidentalis). Western gulls have been previously  reported  stealing milk from female northern elephant seals in several elephant seal colonies... and this behavior has also been observed in other seabirds such as the Pale-faced sheathbill (Chionis alba),  feeding  on southern elephant seal (M. leonina) milk (Favero 1996). However, this is the first report that focuses on feral cats stealing milk from elephant seals.

Regarding access, how would most adults go about getting milk? If offered, though, many adult animals will drink milk preferentially over water if offered at the same time. When I had dairy goats, excess milk was fed to adult dogs, adult cats, and many adult birds (e.g. chickens, guinea hens, peacocks, etc.) The chickens acted like it they were children and the milk was free candy! (I never had pigs, but my uncle and grandfather did, and fed excess milk to the adult pigs.)
As noted above, wild birds will also steal milk when the opportunity arises. Cows will sometimes suck their own teats.
Humans only appear to be isolated in drinking milk as adults by their ability to obtain milk through farming.
http://www.scielo.org.mx/pdf/therya/v1n3/v1n3a5.pdf

That is an interesting point, one that a comment on the OP left me wondering how would other animals get milk since they lack the farming abilities that we have in general.  So really it seems that it isn't that they don't, but comes down to availability and if they can get it from a source.

I think access is the key.  Animals evolve to get nutrition from whatever source is available.  If there was "Milk" available some animal would have evolved to drink it.  This would be very bad for the milk providers so the access to milk is limited (General "Milk Providers" would die out quickly and be removed from the gene pool).  If we created a "Milk Lake" and kept it stocked I bet we'd evolve an entire new local milk-based ecosystem in no time.. this would actually make an awesome biology experiment.

Piglets apparently can reach cow udders... http://www.independent.co.uk/news/world/europe/pigs-drink-cows-milk-austrian-farm-a7198756.html Not to mention orphans of many species will nurse from a surrogate, if available. But one of the triggers for weening is the adult teeth coming in (painful for mom!), so even if a succession of lactating surrogates was available, that might stop them.

I don't know how true this is, but my understanding about cats, and how lactose intolerance works for most mammals is that the animal will become lactose intolerant after the phase where they're feeding from the mother, but  can remain lactose tolerant if they are still fed milk occasionally. If they go without milk from the time they're done weening to adult hood, they will be lactose intolerant, but will still attempt to drink milk when given the opportunity.

Just to point out an exception, adult cows sucking other cows' milk are not uncommon. At least, it's common enough to be a concern in dairy farms and for simple fixes to have been developed. The usual fix is just a piece of plastic pinned to the offending cow's nose that makes the suckled cow walk away.
I'm not sure of how much of this behaviour is feeding related, but concerns about direct impact on production make me suppose that inter-sucking cows are actually drinking a sizeable amount of milk - of course, there are also concerns about indirect impact on production by affecting the involved cows' health.

My uncle had a dairy farm. Self-suck(l)ing cows were... sold. A cow that drinks her most important asset wasn't anything but a large, feed consuming animal. (I don't believe that, but he did.)

Is this behavior found in nature too, or only when all the cows produce milk?

Here is a bit of a tangential example, because it isn't milk from cows. There are some varieties of ants (Primarily the Leaf-cutter ant, if memory serves) which will collect, breed, feed, protect and "milk" aphids for the honeydew they produce. It is generally classified as a mutually beneficial symbiotic relationship, though one could argue that it is closer to domestication. The adult ants will eat the honeydew secretion.
Source: https://en.wikipedia.org/wiki/Aphid#Ant_mutualism
The reason I bring this up is because one argument against raising cows in a "factory environment" is because humans are the only species that drinks milk after adolescence. While this was not hinted in the original question post, the wording made me think of this.

Lots of speciellt of ants do this  (not only leaf-cutter ants) - "herding" aphids to collect honey dew is very common in ants.

So humans are not the only domesticators!  :)

Pigs can. At least one milk, and milk derivates, producer around here used/uses their own pig farms to dispose of all byproducts of production, overdue products returned from stores, same day unused milk, etc. As they owned the pigs, that should not cause too many problems.
I also remember a photo of depression era USA where a farmer is giving milk to pigs. The caption said that the price was so low that they used it for animal feeding instead of selling for human comsumption. I can't find it now.
At some times and places, butter was the primary reason for dairies. After the cream was skimmed off, the remaining milk had a much lower sale value. In some cases, it wasn't worth the effort of trying to sell it, or no one wanted it, and so it was fed to the hogs.

Milk (or food prepared with milk) is used to feed various domesticated animals like pigs or cats, also when they are adult.

That is correct, but this doesn't happen naturally.

The question does not say must happen naturally.

The way the question is asked, I see this as implied.

@Chris Yes sorry I guess it seems I may need to note that.  Yes I am looking for NATURAL ability as in a normal part of their diet/food chain, though with today's food chain all messed up, who can say what is natural anymore for anyone.  But yes, you are correct.


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How do marine mammals stay hydrated?
This is a question that has always bothered me. A quick internet search yields "metabolic processes" as the reason for how marine mammals obtain water, but what are those processes and why don't land mammals have them? In other words, what are the specific differences between marine and non-marine mammals in how they stay hydrated?

@Charles correct me if I'm wrong, but isn't marine biology (and the word marine) referring directly to the ocean and therefore salt water?

"For most whales and dolphins, however, we simply do not know how they get their water, because it is difficult to observe these animals." That is a troubling line :( The article seemed to conclude that some marine mammals have more efficient kidneys?

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Is there logic in this sentence? "Authors discovered a gene as one of the genes evolved through natural selection"
From a news report:

PhD candidate Daiki Sato and Professor Masakado Kawata have discovered SLC18A1 (VMAT1), which encodes vesicular monoamine transporter 1, as one of the genes evolved through natural selection in the human lineage.

Didn't all genes evolve through natural selection?
I'm self-training myself in translation into Russian, and this sentence stumped me. How do I translate it and avoid an absurdity? I thought that all genes have evolved. That's what genetics is about, isn't it?

I think if you can read that sentence a bit differently and then it makes much more sense: if you put (more) emphasis on the last part [natural selection in the human lineage] it becomes clear that in this case we are talking about natural selection (or like iayrok clarified in his answer, positive selection) respective to the evolution of humans. And here obliviously not all genes are equally affected since, we share a lot with out animal ancestors.

Yes, the statement in the news article is not correct; however, it (probably accidentally) isn't quite as nonsensical as it sounds.
The actual paper that the news article is trying to describe is unsurprisingly more accurate.

Here, we found a gene, SLC18A1 (VMAT1: Vesicular monoamine transporter 1), as a positively selected gene in the human lineage. This gene has a human‐unique variant (Thr136Ile; different from other mammals (136Asn)) whose association with several psychotic symptoms has been repeatedly indicated. Moreover, our analysis showed that this variant has been maintained in non‐African populations by balancing selection and had originated around 100,000 years ago, typically regarded as the timing of Out‐of‐Africa migration.

--Positive and balancing selection on SLC18A1 gene associated with psychiatric disorders and human‐unique personality traits
Here instead of talking about "natural selection", the authors refer to "positive selection" and "balancing selection", two sub-categories of natural selection. Since much of the genome is under negative selection, it's worth noting alleles that are not.

Didn't all genes evolve through natural selection?

The reason the news article is not nonsensical is that natural selection is not the only force that acts on genomes.  We've known for 50 years that drift is an important factor that influences genetic evolution (wikipedia: Neutral theory of molecular evolution, Nearly neutral theory of molecular evolution).  However, it's pretty clear from the article that the author is unaware of these concepts and probably doesn't understand the significance of the paper.

Every time I see how badly journalists misunderstand the scientific news they report on, I wonder how accurate is their understanding of, e.g., the political news they report on.

@DavidRicherby "Gell-Mann amnesia"

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Why don't McDonald's fries decompose?
So I was cleaning out my car and found a McDonalds French fry. as I don't eat anything in my car I know exactly who and when this fry is a result of. The when is + 10 months old and it could pass off as one just prepared. How could this be?

Dehydration prevents decomposition. Frying stuff basically replaces water with fat. Your once-upon-a-time potato was basically mummified at maccers.

Although arguably not the most ordinary question, this question is not opinion-based.

Thank you @ChrisStronks I wasn't expecting the initial  down votes here this is pretty much day one biology. I guess we have to shove it down peoples throats. McDonald's french fries are soaked in hydrogenated oil. Saturated fat's which are entirely hydrogenated have a very linear structure thus making a molecule stack one on ...

top of another, sealing off all moisture. Decomposition occurs from the inside out. At the time the french fry was fried it was essentially sterilized on the inside and then as it cools it is sealed by the hardening saturated fat. I had to start taking Lipitor yesterday so I thought i would post this question. Good choice with the mummification analogy :-) i'll give it to t. Abrams and less you want to post something

Is this straight out of 'Supersize Me?'

@HDE226868 think you might be right I forgot where I learned this from.

I was a little disappointed that the mechanism wasn't discussed in the documentary, so I'm glad you asked here.

French fries and cigarettes will satisfy any dietary need for acrylamide

This controlled experiment of burger decomposition explains in detail why fast food burgers do not decompose easily. The same can be applied to fries, which are smaller and come dehydrated from the frying.
The main take-aways from this experiment are:
1: Dehydration is the main reason why fast food fries/burgers do not decompose easily. Placing the burgers in a ziplock bag, preventing dehydration, causes the burgers to decompose.
2: Since an unsalted, home-made burger did not decompose, preservatives, chemicals, saturated fats, and other components are unlikely to be the case of the fast food burgers not rotting.

+1 for using "take-aways" - even though I suspect it was not a deliberate pun seeing as we are talking about fast food, it tickled me. Good clear answer with references too.

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Is the Michael Jackson skin pigmentation disease realistic?
Quoting wikipedia:

Jackson's skin had been a medium-brown color for the entire duration
  of his youth, but starting in the mid-1980s, it gradually grew paler.
  The change gained widespread media coverage, including rumors that he
  might be bleaching his skin. According to J. Randy Taraborrelli's
  biography, in 1986, Jackson was diagnosed with vitiligo and lupus; the
  vitiligo partially lightened his skin, and the lupus was in remission;
  both illnesses made him sensitive to sunlight. The treatments he used
  for his condition further lightened his skin tone, and, with the
  application of pancake makeup to even out blotches, he could appear
  very pale. Jackson was also diagnosed with vitiligo in his
  autopsy.

1) Is this plausible?
2) Is it likely to be an actual disease, or would there be so many mitigating factors that it is unlikely a person would suffer to the extent he did?

Vitiligo is a real disease, and can absolutely have the effects it did on MJ. I've known people with skin that looked like patchwork quilts, and others where there was more generalized loss of pigmentation. I've met sub-Saharan Africans with skin much lighter than mine (my ancestors are from Northern Europe). I see absolutely no reason to question his appearance from a medical standpoint.

1) Is this plausible?

It is absolutely plausible. His particular condition was called Vitiligo
 (as stated in your quote) and isn't that uncommon, albeit not usually as severe.
Skin pigmentation expression changes over time, sometimes dramatically.

2) Is it likely to be an actual disease, or would there be so many mitigating factors that it is unlikely a person would suffer to the extent he did?

Vitiligo is a very well-documented disease, and like every disease, there's a broad range of affectation. Treatments options are very limited, and so makeup or other methods are often used to disguise the affected skin.
Here's some more pictures of people with Vitiligo at varying stages:


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At what temperature does DNA re-anneal?
If primers weren't present in PCR at what temperature would DNA re-anneal? I am wondering how primers manage to bind on DNA strands before DNA manages to anneal back together.

To answer your second question, one of the main reasons primers anneal before your target re-anneals to itself is not because it binds stronger, but because you add primers in large molar excess to their targets.  The primers will find your template faster than your template will find another matching template, and once the primer is annealed the template cant bind onto another template even if that reaction is more energetically favorable.  This molar excess is a requirement for the exponential amplification in PCR, and when you start to lose the excess primer concentration you lose exponential increase due to your targets re-annealing (and you get the production of unwanted PCR artifacts like chimeras).  As for the temperature, it depends on your template, but I guess it has to be somewhere between the primer annealing temp and the temp of your melting step.


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Assembly reconciliation
We have some bacterial genomes that were assembled using Spades, they were sequenced with and IonTorrent PGM.
There are many assemblers and they give different results. I was interested in a tool that can merge the results from different assemblers but there are not many. I found only 2 : GARM and GAM-NGS.
Are there other tools to do merges? Does this improves the genome seq quality?

I think, you might lose quality they have their own error system which is only partially considered.

do the different assemblers five very different results with similar parameters ?

This is an old question but it seems relevant to answer now given current state of art. See also this related thread on biostars.
There are now many tools that perform this function, which is somewhat routine. A partial list:

quickmerge
metassembler (older)
MAC
RagTag (successor of RagOO)
CAMSA

I don't know which is best. Quickmerge is the one that I remember seeing the most. I believe that it is more common with eukaryotic genomes than microbial, as microbial genomes are now often getting closed with long reads.
In general we should expect that the regions that are agreed-upon by the assemblers will be fairly trustworthy, e.g. "improved" potentially. Artifacts are more likely to be found by using this kind of comparison as well.
The strategies used in each case will depend upon which tool you use. I haven't used them enough to say for sure.

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Designing genes with DNAWorks: Maximum nonzero score?
I'm designing a gene in DNAWorks, and I'm unable to find a set of conditions that gives an "overall score" of zero (which is what I normally insist on). People that have used DNAWorks: what's the highest nonzero score you've been able to successfully assemble?

Can you give us more information on what you are trying to assemble (size, length of overlap, length of oligos) and how you plan to assemble it?

The gene is ~600 bp in size. I'm flexible on the oligo length and overlap length, but I was thinking something like 50-60 bp oligos and 15 bp overlaps. I'll assemble it by Gibson assembly directly into the vector backbone, but the part is designed so that I can also assemble it the standard way: first assembling the gene by PCR and then ligating it into the vector. Thanks!

@GerganaVandova, I think that the question is trying to  get at the design portion and not the actual building portion of gene assembly.

@bobthejoe I am trying to say that the design portion is not the bottleneck.

You might want to read Gibson's paper on the step-wise assembly of the mouse mitochondrial genome (1):

He started with 60b long oligos with 20b overlap, as he assembled 5 of those 60-mers into a backbone, obtaining 384b fragments. On the next step, he joined 5 of those 384mers, obtaining 1.2kb constructs. You can do the same, but on the second step use 2x 384mers to get you ~600bp gene. Gibson didn't use DNAWorks to chop up the sequence. He just started from base 1, so that his fragments were F1 [1:60], F2[41:100], F3[81:140], etc.
I think that 15b homology is pretty low (Gibson used 20b for assembling the 60mers in the first step, and 40bp homology for the next assemblies). 60b oligo length is standard.
You can also try one step assembly with all of your oligos (via PCA) as you planned, but I think that the two step assembly might be more efficient.
Let me know if you need more help.
1. Gibson et al, 2009. Chemical synthesis of the mouse mitochondrial genome


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Can a cell culture insert plate be used with a vacuum manifold?
There exists 96 well plate setups for use with vacuum manifolds. Is it possible to use 6/12/24 plate inserts with the same setup?

This company sells a vacuum manifold for 24, 48 and 96 well plate formats.


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How does DNA resolve on size exclusion resin?
We generally have a good idea of how DNA separates using agarose gel electrophoresis, how well does DNA resolve on a SEC resin like superose? I get the impression that salt influences where it elutes.
Is it possible to compare the molecular weight of DNA and where it elutes to the molecular weight of proteins and peptides and where that elutes?

It works pretty well and can be used to desalt DNA. The DNA runs a bit different than proteins since it is more a long stretched molecule while a lot of proteins are globular. See this references (the first is about the behaviour of DNA on superose):

Size-exclusion chromatography of DNA restriction fragments. Fragment
length determinations and a comparison with the behaviour of proteins
in size-exclusion chromatography.
Size exclusion chromatography of DNA and viruses: properties of
spherical and asymmetric molecules in porous networks
Size exclusion chromatography of plasmid DNA isoforms


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What is correct MVM vs. MMV?
I'm writing up a report and I see conflicts everywhere on the internet. Should it be Murine Minute Virus (MMV) or Minute Virus of Mice (MVM).
The followup question is does it really matter.

i would say no, but just an opinion

According to the International Committee on Taxonomy of Viruses, it has had several official variations of that name over the years:

Minute mouse virus
Minute of mice virus
MVM Virus
Minute virus of mice
Mice minute virus

The current (2014) accepted name is: Rodent protoparvovirus 1
"Does it really matter?" As long as you write in full the name you're using the first time you use it, people will know what you're talking about. However, for consistency amongst current literature, perhaps we should all strive to keep up with current taxonomy.

Given the wide variety of academic sources using each abbreviation, it's fairly clear that there is no standardised usage; as such, as long as you state the full phrase the first time you use it and use whichever form you pick consistently throughout your report, it doesn't really matter which you use.
To avoid confusion, I would recommend mentioning that both are used to refer to the same thing the first time you introduce the term.


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Would current-day human-initiated panspermia be effective?
With current technology, we are able to easily send a probe to the Alpha Centauri star system at a speed of about 20 km/s (velocity of voyager probe), which means it would take about 65000 years to get there.

In light of this, suppose we sent a probe capable of delivering 100g of biological material to an Earth-like planet in α-Centauri.

Are there organisms that:
1) Could survive the journey, perhaps frozen or in a dormant state;
2) Would have a fair probability of surviving in the barren oceans (or land if preferred);
3) Eventually have a change of evolving to more complex lifeforms?

If possible, give a rough estimate of how likely you think that would be -- would we need to send 10 probes for a good chance, or billions of probes?
The lifeless environment seems to necessitate either photosynthesis or chemosynthesis to survive. But what about the necessary food (organic matter)? Would any of those restriction make it virtually impossible to achieve long term life with current goals?

Do you have a source for the "easily send a probe to AC" statement?

@arboviral By easy I meant feasible for a large space agency. According to NASA the voyager program cost around $865m USD ( from May 1972 through the Neptune encounter), which I assume includes cost of all systems, personnel and communications. Each probe had about 815 kg launch mass.

The technical problems with delivery to a specific planet seems outside the scope of a biology specific site - launching something that will pass within watery planet's distance of a star, eventually, may be "easy" but delivery to the planet's surface will be lots harder.

How this might affect any existing life - including a life detection/abort mechanism is a space tech question but whether to include it would be an ethical question.

@KenFabian Agreed but actually I've posted a question on this to Space.SE; it's linked in my answer. If I get anything pertinent in the answers I'll add it.

Rather than relying on shipping (few) organisms, one may prefer to ship chemicals and a ribonucleotide synthesizer that could be programmatically instructed (as commented in a recent book by Craig Venter)

Okay, there are technically four questions here, but I'm willing to have a stab anyway.

[Are there organisms that c]ould survive [65,000 years], perhaps
  frozen or in a dormant state;

Probably/possibly (prossibly?). There are claims of the recovery of viable bacteria from samples that have been frozen for millions of years, and viable green algae have been growth from permafrost samples at least 5,000-7,000 years old. Dormant bacteria have also been  reportedly recovered from 25-40 million year-old amber and salt crystals formed 250 million years ago. Several of these results are controversial, since in some cases the organisms's genomes are suspiciously modern, and it's not clear whether they could represent sample contamination, but confidence in several of the ones in the range of 10-100,000 years seems to be fairly high (for example, this Carnobacterium recovered from 32,000-year-old permafrost . Using freezing methods optimised for viability, it should be possible to achieve better viability levels than occur naturally (but you'd have to test your samples after 65,000 years to make sure!).
It's also (with a fairly high degree of confidence) probably possible to create micro-environments containing viable bacterial communities that can survive for thousands of years without light or nutrients, but this looks like it would require liquid water, and the maximum lifespan of most radioisotope thermal generators (RTGs), which would be the lowest-maintenance form of heat generation, is only a few thousand years (I am not a physicist though - you might want to post this on Space.SE).

[are there organisms that w]ould have a fair probability of surviving
  in the barren oceans (or land if preferred)

Yes, if you have liquid water and CO2. If you don't, you might need to engineer something. There are various currently-available technologies for inferring the atmosphere of exoplanets.
I'd recommend sending as many species as possible to encourage the formation of a complex ecosystem (and increasing the chance that one of them survives!). The gypsum-crystal samples mentioned above contained around 40 strains of bacteria plus several viruses, so that's a start. Maybe try freeze-thawing that first. Happily (pretty much by definition) any crystals proven to contain bacteria are water-soluble, so if the planet has an ocean of water then they'll eventually dissolve, releasing their (hopefully) highly invasive payload.

[Are there organisms that would e]ventually have a change of evolving
  to more complex lifeforms?

This is the easiest one to answer: an unqualified yes. Any organism relying on error-prone information storage (so DNA, RNA, or pretty much anything else) is capable of evolution.

If possible, give a rough estimate of how likely you think that would
  be -- would we need to send 10 probes for a good chance, or billions
  of probes?

This is the problem. The reasons go rather beyond this SE (again, maybe try Space.SE) but literally any machine you can conceive based on anything more complex than chemistry or melting points is going to fail after 65,000 years in space. Forget computers, moving parts, rockets, etc. So how do you do it? You really want something that starts to melt as it approaches the other star and releases tens of thousands of packets, each containing copies of everything you're trying to seed the planet with and capable of surviving re-entry (for this, you should post another question on Space.SE - those guys are going to love you). Even so, I don't have the figures for this (again, Space.SE) but I have a very, very strong suspicion that since you're basically throwing darts at a pinhead millions of miles away you'd need to build a moon-based factory or something and fire synthetic comets/meteors containing your payload every few minutes for thousands of years. But since that's trivial compared to the travel time, and that in turn is miniscule compared to the time it'd take for the arrivals to evolve into anything worth visiting, I imagine that's fine. Launch early, launch often.
(I have posted a related question on Space.SE)

Regarding actually getting the payload to the new planet, orbital mechanics is relatively easy; doing the math to get the payload to Alpha Centauri is fairly simple. The bigger issues are:

Fuel required to push the payload to the velocities required and
Fine-tuning the approach once in the AC solar system to target the preferred planet
#2 is the real kicker because, as @arboviral and I have mentioned, spacecraft don't do that well in a vacuum, and most propulsion systems (and guidance systems, for that matter) would almost certainly fail by the time the craft reached AC.

Nice answer, thanks. Concerning the estimate of likelihood, I'd actually prefer you simply assumed the payloads could be delivered to the surface intact -- because we're indeed on a biology SE and because this allows isolating different fields, such that you can assemble a systemic estimate a-posteriori (i.e. combining engineering and biology knowledge).

There are many organisms capable of surviving in extreme environments. While 65,000 years is a long time for any organism, it is possible for some, or even all, of a 100g sample to survive long enough to reach it's destination, especially if the spacecraft were capable of keeping the sample's temperature high enough above absolute zero. I would argue that the extreme cold of space, especially interstellar space, is the most difficult obstacle to overcome in a situation such as this.
TL;DR If it can survive the journey to another planet, it almost certainly can survive on the planet. Let's assume that our organisms could survive the journey. So now let's consider the planet our little friends will be trying to colonize. Water is absolutely necessary for earth-based life to survive. You are going under the assumption that the planet is Earth-like, so we will assume that there is water. We can also safely assume that the elements required for Earth-based life is available, since these elements have been found on planets in our own solar system, and based on how planets are formed, there is no reason to think differently for another earth-like planet. The organisms' most difficult challenge may be releasing those chemicals from their original state (state at time of arrival) into a usable state. The other major issue that comes to mind is if only one species is sent and there is one major obstacle that that species isn't equipped to deal with, and they die off. There is no good way to predict all of the possibilities in this case, the best bet is to send several species and hope they get along and work well enough together to thrive. I'd say photosynthesis-utilizing organisms would have a better chance of surviving, given that the planet is Earth-like and therefore in the Goldilocks zone. Most planets have atmosphere's (even Pluto has one!), and many of them have carbon dioxide in their atmospheres. Bacteria are very adaptable and some of them are extremely resilient, and given the above assumptions, I see no reason why they couldn't survive.
Given how long it took for multicellular organisms to evolve on Earth, it'd probably take at least as long elsewhere. That being said, life is an amazing thing, and finds ways to do lots of things, so my personal opinion is that if 1 and 2 were successful, 3 is a certainty given enough time.

As for the number of probes we would need to send for this to have a statistically good chance of succeeding, I don't have any hard numbers for you, but I suspect even just one probe has a fairly good chance of working (ignoring possible issues with the spacecraft itself, spacecraft don't exactly have a great track record for longevity), and I think two probes would be sufficient.

Please note that I make several assumptions in my analysis which may or may not be accurate. Additionally, my conclusion that two probes would be sufficient is entirely my opinion, and may  be drastically insufficient in reality.


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If we had children wear an apparatus swapping e.g. Red and Blue colors, would their perception adapt?
In the context of neuroscience and philosophy, one difficult question is what makes colors so peculiar and vivid if they're just signals encoding light intensity coming from certain receptors -- an instance of the "Problem of Qualia". In other words, why do perceived colors take their particular "qualitative" appearance. Experiments like color matching functions and simple mathematical properties clearly cannot fully account for this qualitative appearance -- a mathematical model like the opponent process:

can explain for instance that yellow and blue or red and green should appear to be in opposition, but it cannot explain exactly why we perceive green to be our particular green and not some other qualitatively distinct perception with the same mathematical properties.

1) Are the "appearances" of red, green and blue the only possible
  "appearances" that satisfy the mathematical properties of colors in
  our visual system? Or more generally are those simple mathematical
  properties plus their general relation to objects in nature sufficient
  to explain their subjective appearance? (say we had a propensity to
  like and perceive blue positively because of it's association with
  clear whether)

I suspect not. Intuitively I suspect there are a number of different ways colors could qualitatively appear like that go beyond this simple mathematical model and their association with seen objects, embedded in the structure of our brain's complex neural networks. But I don't have a convincing argument to support this conclusion.
I wonder what kinds of experiments can be done to explore this subject, and what experiments have already been done.
One such (imaginary) experiment that comes to mind is swapping different colors a child sees since birth with an ocular device. If the statistical association of objects and color signals were decisive for qualitative color perception, we might expect that then color preference (the favorite which is usually blue) would shift accordingly if we swapped red and blue -- people should start preferring Red over Blue.

2) Do we have any evidence suggesting the outcome of this kind of experiment (and the nature of perception in general)?

Your first question needs re-phrasing. Can you define "appearances" and "mathematical properties of colors in our visual system" more clearly? You insinuate that "appearances" are associated with preference, but surely that's not all there is to it, is it? The experiment you are suggesting sounds a lot like Mary the neuroscientist.

@vkehayas I'll think about it. Indeed my experiment is in the same vein of Mary the neuroscientist, but it has a big difference. I'm not questioning that physical processing gives rise to experiences with a phenomenal character (I'm assuming it -- I dismiss 'Mary the nsc.' since Mary). I'm questioning mostly why our phenomenal qualities are thus-and-so. Is the particular character of our experiences explainable solely by the visual system and what we see, or do we have to dive further into the brain for a complete explanation?

@vkehayas Also I associate "appearance" with preference, but I mostly mean that "appearance" should (weakly) imply preference: that Blue appears the particular way it appears to us would imply that most people like the color Blue the most -- which is empirically true; and not that preference fully describes "appearance". If preference changes when swapping colors (subjects prefer Red over Blue), that would be evidence that the appearance of colors is a function of the statistics of what we see -- that perhaps the "appearance" or "look" of nature has remained unchanged even with the swap.

But if preference remains the same, then it seems safe to conclude the appearance of isolated colors is independent of the statistics of our observations. That we don't like and perceive Blue in a particular way just because the sky is blue, or that we don't have a particular sensation associated with green just because trees and leaves are green.

"...or do we have to dive further into the brain for a complete explanation?": I think that this sentence, and the spirit behind it, is useful to include in the question. Your comments make what you are asking much clearer to me, so please consider editing the question to reflect those. I am unclear on the data concerning the preference to blue and would like to see a reference if you can provide it. Regarding the statistics of the environment and the preference to blue color:https://biology.stackexchange.com/questions/24481


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How does one calculate the resolution of a crystal structure?
Considering that I have a diffraction pattern of a crystal, how would I calculate the resolution of a structure in Angstroms? How does that value differ from the information that I would get from the beta-factor?
I'm aware that the resolution can be calculated by Bragg's law but how does that provide details for the entire structure?

Excellent question for the upcoming Chemistry beta. This should be moved once the proposal reaches beta.

I guess the answer is very different for NMR then. Time for a new question.

Hi sorry i missed this one - not too hard for "biology"
If you look at a protein crystal (or any crystal really) in an x-ray beam, it scatters lots of spots (diffraction reflections).  If you look at a picture of crystalline diffraction, at larger angles from the center of the x-ray beam, the reflections get weaker and weaker and basically just stop, if the wavelength is short enough (in all crystallography labs its plenty short - from 1.5 to 0.9 Angstroms).
The resolution is marked by the angle of scattering to the last measurable spot (aesthetics can vary here, but there is little variance from personal judgement here).  Once you have the angle of scattering, you can calculate the resolution from the Bragg scattering equation:
lambda = 2d sin(theta)
which is rearranged to solve for 'd'
d = lambda / 2 * sin (theta)
where lambda is the wavelength of the incident radiation and theta is the scattering angle.
d = the apparent width of the 'slit' which caused this highest resolution reflection is called the 'resolution' of the X-ray scattering experiment.
There is one part that's a bit tricky as in the typical diagram, depicting Bragg reflection/scattering, you would take the incident x-ray beam as first beam and the scattered angle as the beam of the high resolution scattering, which is more easily measured as 180 - 2* theta.

Does this mean that the resolution is an ensemble average?

Yes- The resolution is a result of the mean coherence of the crystal; if its disordered on the 2 angstroms, then the resolution peters out at that diffraction angle.  There are cases where diffraction in one direction is stronger or weaker than in other directions.  Such anisotropic resolution is not unusual and is described pretty literally "crystal diffracts to 4Angstroms along the a axis and 3Angstoms otherwise.

Resolution is a general metric, the quality of the x-ray structure, describing the amount of data collected for the structure.  The quality of the structure depends on how well the structure reproduces the data collected.


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First pass protein structure prediction
I'm working with a protein that doesn't have any homology to other proteins so it will likely require ab initio structure prediction. However, since I don't work for a structure prediction lab and I don't have a stringent requirement to have a high resolution structure, I'm fine with a 6-10 angstrom resolution prediction to help me visualize the protein.
I'm imagining I-TASSER to get an initial idea of the topology. SWISS-MODEL doesn't find any homologs to template against. I'm trying to avoid using Robetta since it will probably take a month. What other low-resolution webservers should I test?
Alternatively, you could just tell me to suck it up and submit it to a month-long prediction.

Have you used hhpred to search for homologues? What was your criteria for defining there was no homologues? You could potentially go down to around 30% sequence identity to model.
I would submit the the query sequence to both I-Tasser and Rosetta and see if both of the servers agree on the topology. I-Tasser will always provide 5 models of your query sequence (even if they are rubbish) ranked by a confidence score.
While you wait for the above servers to finish, I would submit the sequence to a number of secondary structure prediction servers to come to a general consensus for the secondary structure of your protein. Some servers you could use are:

Predict Protein
Phyre2
Raptor X
Jpred
Psi-Pred

If the servers come to a consensus, compare the secondary structure prediction with that of the secondary strucutre of the models, to see if the ab initio modelling concurs with that of the secondary strucutre prediction. This will give you more reason to be confident in your model.
I would then validate your models using:

Prosa - This calculates a Z-score, and plots where it fits with structures with a similar amino acid length, from the PDB.
DOPE Score - This is employed in Modeller and measures the "nativeness" of your model, the lower the score the better. But you will need to install Python and have some knowledge of how to use the command line. I can provide the code to Run Dope with modeller.

Finally, are there any constraints you could introduce such a oligomerisation site or a protein-protein interaction site, to help with the modelling?


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How does sodium in one's diet affect blood pressure?
Due to high blood pressure, my doctor has recommended I go on a low-sodium diet.  So, that got me wondering what it is about sodium that drives this recommendation?
What does sodium do to a body that, by its presence or absence, affects blood pressure in humans?

Don't have the time to write a proper answer, but maybe you want to check out this review (and if someone wants to write an answer starting from it he/she is very welcome to do it!). Dietary Sodium and Blood Pressure

The basic reason is osmosis, the tendency of solutes to move from an area of high concentration to one of low concentration across a permeable barrier. So, ingesting large amounts of salt results in a high sodium concentration in the blood stream. This in turn causes water to enter the blood vessels by osmosis. More water in the blood means a greater volume of liquid and, therefore, higher blood pressure.
This process occurs primarily in the kidneys, specifically in the part of the nephron called the loop of henle (the image below was taken from wikipedia and is originally from Grey's Anatomy):

With low salt concentrations, water exits the loop and is retained by the body. When sodium concentration is high, the opposite occurs, water enters the blood stream by osmosis and increases blood pressure.

Great answer! I read that there may be variations in the blood pressure over the course of the day, and that the renal function itself has a circadian rhythm. Is there anything circadian in this loop that may alter how Sodium affects the blood pressure based on the time of day?

Salt will cause high blood pressure, but only under certain circumstance.
physiologic hormonal compensations for increased blood volume:

Atrial natriuretic peptide -- increases sodium excretion, hence this is INCREASED with high blood volume
Antidiuretic horomone -- ADH increases water reabsorption in the kidney, hence this will be DECREASED with high blood volume
Renin/Aldosterone -- increases sodium reabsorption from ultrafiltrate back into blood, hence it will be DECREASED

these explainations are a bit reverse (saying that these horomones have these effects and that is why they are released) for the sake of simplicity, and I'm not discussing the mechanism of release of these horomones (aka under what circumstances they are released in the place where they are released from)...
while these horomones help with the kidney regulation of sodium balance and blood volume, this still depends on the kidneys being given the circumstance where they can be effective.
Pathologic circumstances, when elimination of excess sodium fails:
Some people simply have a higher sodium sensitivity and there are a variety of factors that have been statistically correlated to sodium sensitivity, but often the mechanism is unknown. Here are various factors statistically correlated to affect salt sensitivity:
http://physrev.physiology.org/content/85/2/679
the above article shows that no organ systems need be compromised for excess sodium to raise blood pressure, but just for the sake of discussing more macroscopic things I want to discuss these organ systems based reasons for the kidney being unable to compensate for excess sodium in the diet=

The kidney:
A patient with renal disease may not be able to regulate the excretion of sodium. Even in normal humans, the kidney's capacity to excrete sodium declines with age, and smaller increases in salt intake induce a rise in arterial pressure, as GFR (the renal filtration of the blood sent to the kidney) falls by about 40%, though individual variations are wide and some people lose less.

Other than the kidney:
Other diseases can also interfere with renal excretion of sodium. A problem with maintaining blood volume will cause constriction of the renal artery. This would occur before a drop in blood pressure would occur, as this is a way of preventing a drop in blood pressure. This occurs in congestive heart failure and liver cirrhosis.

A patient with congestive heart failure may not have adequate renal
perfusion.  Hence, to maintain adequate blood pressure the renal artery is constricted.
Also, liver cirrhosis may decrease renal perfusion
because of the lack of blood proteins (proteins found inside the
blood vessels that keep water in the blood vessels via osmosis)
holding fluids in the intravascular space and having them escape into
the extra-vascular (outside the blood vessels but still outside the
cells of the body) space. Again, to maintain adequate blood pressure the renal artery is constricted.
burns, also because of loss of blood proteins--> leakage of intravascular fluid to extravascular space--> decreased blood volume and increased sympathetic nervous system output--> reduction of renal blood flow... same as for cirrhosis

In addition to reduction of salt in the diet, diuretics (ex. loop and thiazide) can help the body excrete even more sodium into the urine than what your body can do on it's own.
this article describes the renal handling of excess salt in the diet:
http://booksite.elsevier.com/brochures/thekidney/PDFs/TheKidneyCh36_P088488.pdf


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Orientations of codon and anticodon
So 5'-AUG-3' is the start codon on an mRNA transcript
Does that mean that the tRNA anticodon is 5'-CAU-3'?
Here, I see that the tRNA anticodon for methionine is UAC, and the chart doesn't specify which end is 5' and which end is 3', but I'm guessing it's 3'-UAC-5'. I thought nucleotides are supposed to be written 5' to 3', and that's a norm, but apparently it isn't the case here? Am I missing something?

That page you linked to is, shall we say, unconventional, in its depiction of the code. I'm not surprised that you were confused.

The tRNA anticodons are both complementary and anti-parallel. That means for $5'-\text{AUG}-3'$, the tRNA anticodon would be $3'-\text{UAC}-5'$.

The image has the mRNA oriented with the $5'$ end on the right end. It shows both, complementarity and anti-parallel configuration. The reference you cite might have cited the anticodons $3'\rightarrow 5'$ and mRNA codons $5'\rightarrow 3'$. In general, we usually cite the codes from $5'\rightarrow 3'$ but it doesn't matter until it is explicitly specified or unambiguous.

Pasan did you draw this tRNA? May I know what tool you used ?http://tex.stackexchange.com/questions/164206/draw-a-trna-diagram?noredirect=1#comment377038_164206

@Mariya I wish. But this is one picture I found online. But if I had to draw, I would have preferred Corel Draw.


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Are human disease-causing organisms living in other creatures helpful to them?
There are many examples of this.
How is rabies helpful to a dog?
How are Zika virus & Malaria helpful to a Mosquito?

"Disease causing organisms" do not necessarily benefit the host; more commonly they do nothing or actively harm the host somehow. A good example is malaria; it can only be carried by a specific mosquito because it causes death in some and in others can't fulfill its mosquito-required part of the cycle. Dogs die of rabies.


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Does the Spinoreticular Tract end in Brainstem?
According to this book on Springer spinoreticular tract is :

As the name implies, the tract originates in the spinal cord and terminates in the reticular formation (RF) in the brainstem. While most of the fibers appear to terminate in the RF of the medulla and lower pons, some may ascend as far as the midbrain.

But according to Wikipedia :

The spinoreticular tract is an ascending pathway in the white matter of the spinal cord, positioned closely to the lateral spinothalamic tract. The tract is from spinal cord—to reticular formation— to thalamus.

What I am unable to understand is if Wikipedia is true then why do we consider this tract as ending in the brainstem rather than ending in the thalamus?
Also I am getting different information about the location of the origin of spinoreticular fibres,
My Textbook says:

The spinoreticular fibres begin from the spinal neurons mainly in lamina VII (also V and VIII).

But this site says:

The term spinoreticular tract refers to a fiber bundle that arises largely from lamina I, lamina IV and lamina V of the spinal cord.

Which source is correct?

I'm curious... the Wiki article is identified as needing more citations, so I'm wondering why you are weighing an admittedly incomplete Wiki article against your textbook.

Sometimes my textbook too gets wrong. Also who is correct in the second part?

Depends on who you read. One reputable source stated the spinoreticular tract originates from neurons located mainly in contralateral laminae 7–8, the lateral reticulated part of lamina 5. They are also located more sparsely in lamina 1, area 10, and the lateral spinal nucleus. Its axons are myelinated, and the majority cross the midline to ascend in the ventrolateral funiculus, intermingled with spinothalamic fibers. Some spinoreticular tract axons are collateral branches of the spinothalamic tract neurons. Another stated something slightly - very slightly - different.

Could you please cite the source for further reading?

In the top 5 f hits on google.

When will you answer the question about chassignac's tubercle?

From my previous answer/comment, it should seen obvious when I will answer it. The answer is nowhere written in stone.


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Why replication collapse but not stall leads to DNA break?
I have been looking into the concept of replication dynamics and was wondering why collapsing but not stalling leads to a DNA break.

I recommend improving this post by explaining to us what "collapsing" and "stalling" mean. What context are you talking about? How do you know that collapsing but not stalling leads to a DNA break?


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Difference in multicellularity between prokaryotic and eukaryotic organisms
As most prokaryotic organisms are single-celled, and in eukaryotic organisms this is the reverse, is there some evolutionary advantage that led to these features evolving? Or is it purely the fact that features of eukaryotic cells allow functions (i.e. enabling multicellular organisms) not possible in prokaryotic cells?

What matters is how many times multicellularity evolve and not so much how many species are multicellular. Have a look at this answer section How many times did multicellularity evolve independently?

Your title question does not match with you content question. Are you interested in the evolution of size or of multicellularity?

Multicellularity - apologies, I thought the terms were almost synonymous


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How to check if a population density obeys replicator dynamics
Say we have a probability vector or population density $p = (p_1,...,p_n)$ with $p_i \geq 0$ and $\sum_i p_i =1$. Also assume we know the functions $g=(g_1,...,g_n)$ such that:
$$p_i(t+1) = g_i(p(t))$$
where $t$ is a discrete time index. Is there a way to check whether $g$ implements a discrete time replicator equation? I.e. whether there is a function $f=(f_1,...,f_n)$, called the fitness landscape, such that:
$$p_i(t+1)= \frac{f_i(p(t))}{\langle f \rangle_{p(t)}} p_i(t).$$
where $\langle f \rangle_{p(t)}:=\sum_j p_j(t) f_j(p(t))$ is the average fitness of the population density.
Pluggin in $g_i(p(t))$ gives an equation that we could try to solve for $f$ but I don't know how:
$$g_i(p(t)) = \frac{f_i(p(t))}{\langle f \rangle_{p(t)}} p_i(t)$$
or equivalently:
$$\frac{g_i(p(t))}{p_i(t)} = \frac{f_i(p(t))}{\langle f \rangle_{p(t)}}.$$
We can of course also drop the time dependency and write:
$$\frac{g_i(p)}{p_i} = \frac{f_i(p)}{\langle f \rangle_{p}}.$$
Is there a (in the best case necessary and sufficient) criterion that has to be satisfied for this equation to have a solution?
I am also grateful for tips how to tackle this problem in a principled way, including numerically.

For discrete time replicator dynamics, fitness is defined only up to a multiplicative factor. I.e. if you pick some number $k$ then $(f_1, ..., f_n)$ defines the same fitness function as $\hat{f} = (f_1/k, ..., f_n/k)$. In particular, this mean for any $p$ you can always pick a $k$ such that $\langle \hat{f} \rangle_p$ = 1.
So using your final equation, just let $\hat{f}_i(p) = g_i(p)/p_i$.
Note that the resulting landscape $\hat{f}$ will be a relative fitness landscape and not an absolute fitness landscape. But there is no way to recover an absolute fitness landscape from the data you have. You would need information on how the population size, not just frequencies evolved for that.
As a final note: if you're trying to match this to experimental data, the discrete time approach might not always be necessary. In that case, you can try the method that I describe in this post or depending on your experimental system, you might be able to just do the game assay as we defined in this paper.


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Valence electrons in DNA nucleotide addition
Can anyone explain the movement of valence electrons during the nucleophilic attack that occurs during DNA synthesis? The 3' oxygen starts with two lone pairs of electrons but what happens during the formation of the phosphodiester bond?


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What is a concussion?
When I was a kid and someone got a concussion, I seem to remember people telling me that it was when your brain impacts the side of your skull, accelerating fast enough to do so despite the cerebrospinal fluid buffer.
But wikipedia doesn't mention this explicitly. Is this just one possible cause for concussions? Is it possible to generalize about them? How much don't we know?

Concussion generally refers to the set of clinical symptoms that are secondary to the head injury and are characteristic by altered state of consciousness like instant onset of transient neurologic dysfunction, lack of consciousness or temporary respiratory arrest and loss of reflexes.
Since it's connected to the head trauma by definition, there is in principium no other cause of it.
The patophysiologic mechanism of concussion is not well understood yet, it's thought it results from two main sources:

the acceleration of brain causes increase of pressure
the impact of brain on the hard shell causes deformation and sheer stress in brain tissue (probably stronger cause of cytologic changes discussed later on)

These two mechanisms might lead to changes in the tissue structure and also trigger cytologic changes in the astrocytes and neurons such as:

Astrocytes respond to a focal mechanical stimulation by propagating intercellular waves through their network. Mechanically stimulated astrocyte networks show changes in the cytoskeleton, organelle function, and biochemical cascades over time.

The changes in neurons detected in vitro include microstructural changes, direct membrane permeability change and change in the receptor abundance, structure of subunits and

Early evidence showed that these physical insults can affect the properties of important synaptic glutamate receptors that can regulate neurotransmission and plasticity in networks. Moreover, inhibitory synaptic receptor functions can be altered with a physical force, showing that the balance of excitation/inhibition coupling is important to consider when assessing the effects of these physical forces. Perhaps equally important is the alteration in the receptor composition and intracellular signaling that occurs after a microinjury.

Microinjury is also linked to triggering of cell death pathways in brain cells.
The importance of these mechanisms are not yet clearly understood though and there probably are many more playing their role.
Sources:

Overview study
Robbins and Cotran pathologic basis of disease

Does "concussion" imply "brain impacted the side of the skull"?

The brain doesn't have to impact the skull. Acceleration itself and the rise of pressure it causes if big enough can according to the article cause enough stress for some of these changes to occur.
Morover the impact is always hindered by the cerebro-spinal fluid, but the thing that matters is how much of the energy is absorbed by the fluid and how much by brain tissue. If impact is small, much of the energy is absorbed by the fluid and little damage is done to the neural tissue. If it's big, proportionally less is absorbed by the fluid and the rest can cause the damage to the brain.

The CDC has a nice webpage about concussions and traumatic brain injury, as does the Mayo Clinic. The brain and head move rapidly back and forth due to impact or sudden acceleration or deceleration, in spite of the cerebral spinal fluid bathing the brain cavity. This causes chemical changes in the brain and/or damage to brain cells, affecting brain function.
Symptoms are not always instantaneous; sometimes it can take hours or days for symptoms to arise. There are multiple diagnostic tools that exist, including graded symptom checklists, the Standardized Assessment of Concussion, neuropsychological assessments, and the Balance Error Scoring System. These are summarized in this American Academy of Neurology (AAN) article from 2013.

"...sometimes it can take hours or days for symptoms to arise." I think that is true of some symptoms perhaps, but all people diagnosed with a concussion show one of a number of symptoms immediately after impact. I've never, ever heard of a concussion diagnosed without any symptomatology - even relatively minor, such as dizziness or cognitive impairment - post impact, and as an ED doc, I've assessed many, many head injuries. Diagnosis may be delayed because people think the symptoms are minor.

Also, just checked your references, which do not support your statement. The closest it comes is in the Neurology article, which states "...many of whom do not obtain immediate medical attention."

The note about symptoms taking time to arise might be referring to symptoms caused by bleeding in the brain, which could be caused by trauma but is separate from concussion.


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Modulating the level of acetyl CoA

Describe what might happen if there were no mechanisms for modulating the level of acetyl CoA.

I am not sure what is meant by "modulating the level of acetyl CoA", or what mechanisms contribute to this. Presumably the citric acid cycle would be affected in some way because acetyl CoA enters it, but I'm not sure what exactly would happen.

What type of organism are we considering? Respiring or fermentating?

Probably respiring, but there is no additional detail in the question.


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Why do ladybugs have a different number of points on their backs
Everytime I see a ladybug I ask myself this question.
Why does every ladybug have a different amount of points on its back? Is it because of its age? Or because of its genes? Is it inheritable?

It is unclear if you are asking about variation in the number of spots within or between ladybug species (so intra- or interspecific variation).

I am working on a children's book with a group of friends about a bug named Willow. For this book, we have needed to do research on ladybugs and how they get their spots. Ladybug spots do not tell you the age of a ladybug, but they can tell you the species. Some ladybugs don't even have spots. The most common ladybug is the Coccinella septempunctata or seven-spotted ladybug.

The spots on the back of Ladybugs over the surface is defense mechanism to avoid predators. The spots come in different shapes and different numbers. Some say that those dots tell us their age. Since some ladybugs have 24 spots which means its age would be 24 years and that is not at all possible. So this is a popular misconception running around us.
But the real truth about the number of spots on the ladybugs' back is:

The number of spots on a ladybug does have significance. The spots and other markings do help you identify the species of ladybug. Some species have no spots at all. The record-holder for most spots is the 24-spot ladybug ( Subcoccinella 24-punctata), which has 24 spots, of course. Ladybugs aren't always red with black spots, either. The twice-stabbed ladybug ( Chilocorus stigma) is black with two red spots.

So now we know that the number of spots on the back of Ladybugs will help us to identify what species it belongs to. To give an insight into different species of them you can refer to this Identifying Ladybugs.

The above image shows different species of Ladybugs where you can see the varying number of spots in each bugs' back. More information can be found here Stripes on Ladybugs.

If I am not mistaken there is also intra-species variation in the number and mainly shape of the points.

Though this is a good answer describing how we can use spots for ladybug ID, it doesn't actually answer the OP's question: "WHY do they have multiple spots?" I'm surprised the OP accepted this answer...

Yes, some species like the harlequin ladybeetle (Harmonia axyridis) can have dozens of different morphs, with different number of points.

It is because of genes, and is completely inheritable!   First I want point out that there spots, or points, do not change over time.  Rather the spot number and location is fixed when Coccinellidae are pupa (tween aged insects).
You will notice I said Coccinellidae instead of ladybug.  That is because "ladybugs" are actually several different species of insect.  Thus we refer to the whole family of ladybugs, Coccinellidae.  The spot number, shape, and color is different for different species, which gives you the variation in the number of points.


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What is the purpose of co-transport?
My current understanding of co-transport is that, first, a substance is actively transported across a membrane, establishing a concentration gradient across said membrane. This same substance then diffuses down the established concentration gradient, effectively travelling back to where it began, but this time travelling via a transmembrane protein that transports another substance also, regardless of its concentration gradient. Thus, this second substance is transported to wherever it is necessary.
Would it not then make more sense for the latter substance to simply be actively transported to its destination, as opposed to involving another substance which has no net movement at the end of the process? What is the advantage of co-transport?

This is a useful question and I have upvoted it, but there is no reason to talk about evolution. Keep it simple and just talk about the rationale of a process, or its advantage over some alternative, or why it is used in some situations and another process is used in other situations. Leave talking about evolution for situations where you are considering this — comparing the biochemistry of different organisms, for example.

@Jam is correct — if a little long-winded — in pointing out that one of the benefits of co-transport (no need to involve evolution) is that the concentration gradient of one co-transported molecule can provide the thermodynamic energy for the transport of the other molecule against a concentration gradient. This is dealt with in a quantitative manner in Section 13.1.2 of Berg et al. and in a qualitative manner in Section 13.4.
However, there is another factor to consider. This is the maintenance of electrical neutrality.  Typically it is charged ions that are transported (anions in the examples shown below, taken from Ch. 18 of Berg et al.) so that co-transport of a counter ion is needed to maintain electrical neutrality.

The diagram above also highlights another important point. You need to look at the biochemistry of the co-transporting systems, rather than just considering them in abstract. One of the sites of many co-transporters is the mitochondrial membrane, where transport is part of a co-ordinated process.
Consider for example ATP, ADP and phosphate. ATP is synthesized in the mitochondrion from ADP and phosphate, and then much of it must be transported into the cytoplasm. At the same time ADP and phosphate must enter the mitochondrion as substrates for the generation of more ATP. Active transport is clearly a non-starter here (it would use the ATP that is to be transported!) and co-transport ensures that the influx of ADP is balanced by the efflux of  ATP.  Phosphate influx (which is balanced by hydroxide efflux, to preserve neutrality) must be coupled to this process, although I am not aware of how this achieved (contributions welcome here).
Analogous considerations apply to NAD+ and NADH, but it is the electrons that are transported, rather than these compounds themselves, using surrogate oxidized or reduced compounds. Shuttle systems of this sort integrate the biochemical functions of the mitochondrion with those in the cytoplasm, and need to be studied individually to understand the choice of co-transporters. Section 18.5 of Berg et al. is a convenient starting point.

Would it not then make more sense for the latter substance to simply be actively transported to its destination, as opposed to involving another substance which has no net movement at the end of the process?

But where would the energy for the transport come from! Thermodynamics tells us that the universe tends to increase the amount of disorder (Entropy). If we have active transport of a solute, then by definition, this is going against a concentration gradient. So we could end up with a substance being entirely on one side of a plasma membrane, which wouldn't be disordered at all - clearly thermodynamics wouldn't let this happen by itself since we would be reducing entropy.
This is why energy is needed for active transport. We need to put in the leg-work by using some energy to locally reduce entropy, and ultimately move something to one side of the plasma membrane. Think of the concentration gradient like the pent up energy of a spring. We can release this energy when we want, in order to make it thermodynamically feasible to move a solute against its concentration gradient.

What is the evolutionary advantage of co-transport?

We've established that we need an energy source to drive active transport. But indeed, why would we use a concentration gradient? Couldn't we equivalently use a different energy source? Well yes, we could use ATP (for instance in Na$^+$/K$^+$-ATPase). But a concentration gradient might already be established over a plasma membrane, so its already there as an existing source of energy. Perhaps this is why co-transport evolved with this mechanism.

I follow your answer completely, and had considered your suggestion. However, in companion cells of the xylem for example, a concentration gradient (of H+ ions, I believe) is actively and deliberately established in order to transport sucrose via co-transport. What purpose would you suggest this, then, has?

@ElizabethT It's been many years since I've done any plant biology :) but aren't companion cells in the phloem? I know that phloem companion cells partake in active transport of sucrose from sap (which they can then use to feed themselves). Most cells have some sorts of uptake mechanisms because there are things like amino acids that they want inside, but things like ammonia that they want outside. So cells can use concentration gradients (and co-transport) to control this.

You are completely right. Rookie mistake - I do know some plant biology, I promise! That's an interesting point, thank you :)

@ElizabethT No problem! And I didn't mean to be condescending with that remark about plant biology, I just meant that you should take my answer with a grain of salt :)

That's honestly not the way it came across, you did put forward new ideas that I hadn't considered before. Consider my mind broadened!


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Im trying to find out what type of snail this is
The snail is pretty large and located in texas.

I'm guessing it's an invasive apple snail, popular in fish tanks.
http://texasinvasives.org/animal_database/detail.php?symbol=15
https://www.youtube.com/watch?v=Pi2wcFPPJsI
Some people keep apple snails as pets, they are very interesting to keep for a while.
Your photo doesn't give enough info, location, sea or pond, clear image of shell, underside, soft body, to say for certain. apple snails have a wide variety of colors.

Thank you! My friend and I believe you are correct.... it was about 6 inches long and spotted in a park that has a large pond.


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Do model species evolve away from Batesian mimics?
Batesian mimics - palatable mimics of a poisonous species - are detrimental to the species they imitate. Predators learn which species are unpalatable by tasting some. If Batesian mimics are rare or nonexistent, few if any of these samples will be tasty and predators'll quickly learn to leave this species alone.  But if Batesian mimics are common, predators have good chance of being rewarded for attacking things that resemble the model species.  It would seem that an overabundance of mimics would create a condition for the model species to evolve to visually differenciate itself: is there any evidence that this occurs?

This paper may be interesting, https://academic.oup.com/biolinnean/article/32/4/337/2682777/Individual-selection-kin-selection-and-the

I have found some papers that support the hypothesis that an overabundance of Batesian mimics creates a condition for model species to evolve differentiating characteristics -- in particular,  Franks, D. W., G. D. Ruxton, et al. (2009). "Warning signals evolve to disengage Batesian mimics." Evolution 63(1): 256-267.
The authors argue that new conspicuous traits in unpalatable species evolve in response to mimicry, since a mimic that evolves conspicuousness without being a good-enough match pays full cost of conspicuousness without the benefit of its predator learning advantage.

There is an ongoing discussion in the literature on whether Batesian mimicry is always parasitic or can also be mutualistic. I don't know much about this discussion and won't be able to make a synthesis. I suspect semantics about what Batesian mimicry really will also matter in this debate.
In Parus major (and from the same first author), I could find an evidence supporting that Batesian mimicry is parasitic (Rowland et al. 2010) and another evidence suggesting it is mutualistic (Rowland et al. 2007) depending upon the details of the study system. Franks et al. 2009 suggests that in extreme cases, Batesian mimicry can indeed be parasitic.


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Amino Acid mutation profile for human coronavirus: Why is the mutation from T to I so frequent?
Still watching the emerging lineages of SARS-CoV2 I noticed that the amino acid mutation from threonine to isoleucine seems to be particularly frequent. Counting mutations in a lineage with a lot of mutation (I choose BA.4) kind of confirmed my anecdotal impression: Indeed, T-to-I mutations were the most frequent ones.
They are more frequent than alanine to valine mutations, and the difference in frequency is not explained by a difference in the frequency of the amino acids in the virus proteines (Threonine is somewhat more frequent than alanine, but not that much).
In part this phenomenon can be explained that a T-to-I mutation involves a nucleotide change from C to T which is the most frequent nucleotide mutation of Coronaviruses in humans. However, in order to be fixated in a lineage, the T-to-I mutation needs also to provide some evolutionary advantage. It seems to be a generic advantage of that kind of mutation.
So my question is: What are evolutionary advantages of T-to-I mutations of SARS-CoV2 in humans?

To elucidate an evolutionary advantage, you'd need to consider the structural context each mutation site along with other nearby mutations. The T->I mutation changes the position from polar to non-polar, which can change how that region of the protein folds (if it folds). Thr is also a site for post-translational modifications like phosphorylation or O-linked glycosylation, either of which could be relevant to just about any aspect of infection like receptor binding, cellular entry, regulation of cellular processes, structural stability of the capsid, or immune system evasion.

The change from C to T (or U in the case of RNA) can happen via the oxidation and deamination of the Cytosine (see reference 1 for the explanation of the mechanism).
The mechanisms looks like the following figure (from the reference 1):

The changes the genetic of the codon from AC* to AU* the first coding for Threonine (T) the later for Isoleucine (I) (image from the Wikipedia):

This does not mean that there is any driving mechanism for this mutation or any particular advantage. As the article states there are quite a few oxidative events per day, since a viral infection causes the generation of a lot of viral particles, this reaction will simply happen by chance.
Besides this mutation happening by chance there seems to be a mechanism called the "APOBEC-mediated RNA editing" which seems to edit the RNA of viruses. According the reference 2 this can be observed on other RNA viruses as well, leading to a higher prevalence of this mutation as it should occur naturally. The author speculate about this as a potent driver for diversification and evolution.
In DNA this error is not so problematic since there are two strands and error correction mechanisms but for a single stranded RNA genome every mutation will persist.
Reference:

Oxidized, deaminated cytosines are a source of C → T transitions in
vivo
Extensive C->U transition biases in the genomes of a wide range of
mammalian RNA viruses; potential associations with transcriptional
mutations, damage- or host-mediated editing of viral RNA

This is a great answer (+1) exhibing the mechanism behind the mutations, but it does not explain the prevalence of T-to-I mutations over A-to-V mutations.

@jk-ReinstateMonica I think the prevalence of this mutation comes from the APOBEC-mediated mechanism. Why this is in place is unknown I think. I will try to see if I find some further information on it.


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When and how did the Embecovirus acquire hemagglutinin esterase?
The Embecovirus is different from the rest of Betacoronavirus by possessing an additional protein, a hemagglutinin esterase (HE).
There are known similarities between the HE's of different viruses (Coronavirus, Torovirus, and Influenza C), see e.g. this paper by de Groot (2006).
My questions are: How old is this acquisition?
Where does the hemagglutinin esterase come from?

This is not simply an answer site, but instead a site that promotes self-learning with some expert help. ——— Where have you looked for answers? Either there are papers reporting on investigation of the evolution of this virus and its acquisition of HE or there aren't; it would improve your question if you reported what you have found (with citations) and why you can't answer at least some of these questions yourself. In fact, if you look at the abstract of the first reference for the wikipedia article you linked to you will find at least one answer.

Did you look at embecovirus NS2a as well "putative cyclic phosphodiesterase" it is interesting because (at the same location just after ORF1b) there is a 40% similar ORF in Lucheng rat alphacov NC_032730

@reuns No, not beyond just noticing its existence in the embecovirus. And I noticed that the placement of HE in the Torovirus genome is different from the one in Embecovirus genome.


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recombinant gametes

Suppose you are able to observe under a microscope the total number
  of meiotic divisions occurring in one gonad of a given individual and to
  outnumber exactly the crossovers between two given loci for which that
  individual is dihybrid. If the frequency of these particular
  crossovers is 100% (that is to say that every meiosis exhibits one
  crossing over between the two loci you consider) you anticipate that
  the total percentage of recombinant gametes would be equal to:

I don't understand how to solve this.

What have you thought of so far?


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Compatibility drugs info
Let's suppose that I take a DrugA for ProblemA and then I got this ProblemB and started to take DrugB. Are there general rules I can look up to figure out whether I can take DrugA & DrugB simultaneously?
I mean drugs can cancel each other or vice versa increase effects of each other (in an extreme extend); or one of drugs has adverse effects that are bad for the other drug.

Can you rephrase your question? I think I understand what you are trying to ask but this is really unclear.

What about now? :)

Much better :-)

Yes.. if you look up drug info then they say which drugs are incompatible with it. I don't know of a standard database but sites like these are helpful. @Chris. are you going to sit in front of your comp on a nice saturday?? :P

@WYSIWYG Unfortunately, yes. bio.sx is nice for breaks inbetween. I got a load of work to be done until the end of next week.

@caseyr547 Actually I was wondering about pharmacology in the first place, so that would be extremely useful.

I think you are referring to drug contraindications, which is a very large consideration and study in drug administration when multiple drugs are taken at a time. Many examples of drug-drug interactions can be found online such as here http://en.wikipedia.org/wiki/Drug_interaction

I would like to start by suggesting you talk to whoever prescribed you the drug or your pharmacist. They should be most up to date with interactions and there are some interactions which may only affect you more seriously because of your medical history or current conditions.
Here are some sites that you can check drug interactions in order of popularity:
Medscape
Drugs.com
Healthline
WebMD
RxList

Drugs.com provides good lists of side effects when combining drugs. Just type (drug) interactions into Google and it should come up. Then you can click on a given drug and see how dangerous the two are together/what they can cause. Of course, your doctor is always the best resource.


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Why doesn't muscle strength depend on its length?
In case of tug of war the more people participate the more strength they represent. And in case of muscles - the longer it is, the greater the number of myosin heads bind to actin when muscles contract. So why doesn't length matter?
UPDATE:
Since I've found multiple answers that compare muscles to ropes, let me comment on why those explanations don't work for me. Ropes don't have "muscle" strength, they have tensile strength. So this analogy can only compare tensile muscle strength to tensile rope strength.
In the end I'm pretty sure I'll find out that tensile strength constraints the muscle strength. And that's probably going to be the reason why muscle strength doesn't grow with length - something does not allow it, otherwise it would get damaged.
But I'd like find out what exactly prevents further contraction. Is it mechanical receptors on the muscle cell which block deploarization? Mechanical receptors in tendons which send nervous signals (but then - do tendons get thicker in proportion with the muscle)? Something else?

Does this answer your question? Why is muscle force more dependent on cross-sectional area than on fiber length?

@kmm, I haven't seen that question, though I tried hard to look for it. Thanks for pointing out. But no, unfortunately there are no satisfying answers there :(

@kmm, I've updated the question to explain why the rope analogy doesn't answer the question.

To those who vote for closing: this site doesn't have an answer to my question. If you close it - someone else in the future will have to ask this question again. Otherwise no one will ever answer it.

The close votes are for this question being a duplicate (which I think it is). Whether or not you find the answers here or on the other question satisfying does not change that this and the other question are basically asking about the same concept.

@kmm, yep, I'm not arguing with that. It's just unfortunately this usually means the question won't be answered at all (unless moderators will bump it up, which they probably won't). So we'll wait for yet another duplicate..

I think you probably just need to take the leap to understanding a muscle pulls more like a rope does than like a spring, and tensile strength is the best way to think about it. That's what the answer on both this question and the target duplicate are saying, and that's why people are considering it a dupe. Dupes are dupes because the question is effectively the same; if there is an old question you want a new answer on you could offer a bounty.

@BryanKrause, this analogy game will bring us only so far :) A motor protein is a motor protein. It doesn't matter if goes in parallel or in a sequence - it will exert a force and therefore the muscle will become stronger. Unless there's an additional complexity hidden somewhere (which is probably the case). Bounty or not it seems like there are simply no people here who work in this field and can give a good answer. Hence we get more and more of "rope" answers.. So maybe you're right - this dupe won't help.

If you put me between two Hafþór Júlíus Björnsson and we all linked hands and pulled on each other, we would not have a pull strength of two Hafþór plus me. Each Hafþór would pull at one Hafþór, but they'd pull me apart. Think of them as two thick muscles and me as one thin muscle. You can make the chain as long as you want, we can never pull with more than my strength, you'd just stretch me until I broke. Even the chain of Hafþórs would only pull at one Hafþór, because if a Hafþór is pulled at 2X their strength they would also lengthen.

@BryanKrause, if we assume that 3 Hafþórs don't break the weakest Hafþór then they do add up to more strength. In fact together they pull 3x as strong as 1 Hafþór. Sure, as we add more and more Hafþórs one of them will break eventually. At that point we reach the max strength. Getting back to muscles: if we add more myosin in a row - they will too pull stronger. But something doesn't let them even though now they can. So it's not that the muscle isn't getting stronger, it's that something limits it. I'd like to find out what that is and how it scales with the muscle length and width.

Myosin pulling is like a rope. It can't pull twice as hard or it breaks. If I can lift a Hafþór I can lift a Hafþór. It doesn't help me if that Hafþór can also lift another Hafþór; to pull them both I'd need to be twice as strong. If I want to double the strength I need them side by side me, not in a chain.

I think you're missing that there is nothing in the middle to pull against. The chains are all pulling each other down the line so the total strength isn't summed. If Hafþór on one end pulls, the next Hafþór has to pull the same just to stay in the same place.

Alternatively maybe it helps to consider Newtons 3rd law?

@BryanKrause, that's because our analogies are imperfect. If we return back to the tug of war.. Hafþór is actually pulling on the rope. Not on another Hafþór. So the more Hafþórs (myosin) we have the harder they pull on the rope (actin). And in your muscles you don't have 1 myosin head per muscle cell - you have many of them in a sequence. And you have many sarcomeres in a sequence. If you remove half of them - you'll have half of Hafþórs (myosin heads) pulling on actin.

Ok then that's what you are missing: you're imaging some central rope of near infinite strength that everything acts on, like people in a tug of war. That's wrong. None of my analogies involved tug of war. Myosin pulls different actins together, like maybe the myosin is the arms and the actins are the bodies in the chain. The only ground points are the tendons at each end of the muscle, in between it's all muscle fibers pulling against each other. Bob drew the scenario reasonably below, besides the tendon/ligament confusion.

No one in the linked duplicate referred to tug of war, either, except someone in the comments with the same confusion as you, and someone else responded to them and explained how this doesn't work.

@BryanKrause, I now realize what was my problem, I've put it in a separate answer. Thanks!

It's simply that the fibers are arranged end-to-end. If you simplify this down and imagine a single muscle fiber you have actin and myosin like this:
ligament-|actin-myosin-actin-myosin-actin-myosin

If you think of this as a strand of cotton pulling on a weight (ligament). Each group only pulls along the length, so the strength is not multiplied, but rather related to the strength of the individual fibre.
In reality muscles are stacked into bundles, which are much stronger as all the fibers can contract pulling with the strength of the multiple ends. Like this:
         |actin-myosin
         |actin-myosin
ligament-|actin-myosin
         |actin-myosin
         |actin-myosin

This is like the multiple strands of cotton making up a rope, the strength comes from having lots of them distributing the load.
This is something called physiological cross-sectional area, which describes the strength of a muscle by estimating the cross-section of the muscle across its thickest part.

The confusion I had is that I thought that myosin pulls on actin with a force which some how isn't the maximum possible. And if we were to add another sarcomere in a series - each myosin would have to work harder and together with the new sarcomere they would exert a greater force.
But this of course isn't how it works. Myosin doesn't have a notion of a varying strength, it's binary: it either attaches to actin or not. If we were to try to pull apart actin or myosin harder by their "tails" (by a neighbouring sarcomere) - actin would've started to "slip" from myosin. Therefore putting more sarcomeres in series would not make the muscle stronger - we'd simply add more "slipping".
The other possibility in a theoretical world would be to make actin and myosin strands longer and add more myosin heads (we'd have to reinforce lots of structures though). This way we could've made the muscle stronger by making it longer. But that's not how it works: a longer muscle cell merely means more sarcomeres in series.
Thanks @Bryan Krause for nudging me into the right direction in the comments.


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Why all negative ssRNA viruses have helical capsids?
You can always say it's a coincidence, but is there particular need to have a helical capsid? Do they need their RNA to be more protected than +ssRNA? Is it better for RdRp attachment?
This paper suggests it is mostly for RNA synthesis https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3993539/:

For negative-strand RNA viruses (NSVs), eight families have been recognized by the International Committee on Taxonomy of Viruses (ICTV). The unique feature that distinguishes NSVs from the rest of the virosphere is that the nucleocapsid, instead of the naked genome, is used as the template for viral nucleotide synthesis. It is indubitable that the assembly of the NSV nucleocapsid is related to the unique mechanism of its viral RNA synthesis.

Also this one: https://www.sciencedirect.com/science/article/pii/S0042682215001543. But I don't know if anyone has tested inserting naked -ssRNA with RdRp and see if it does something.

Can you provide sources that support your assertion that all such viruses have helical capsids?