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Why can ATP not be stored in excess?
I just learned that ATP can not be stored in excess and is only made by the body when it is needed. What makes ATP, like glucose and fat is what is stored under the skin or wherever. Now why cant the body just produce ATP and store it for heavy, heavy exercise when it would advantageous for it to be ready rather than it going through the production phase and then used. When I say ATP storage I mean in large amounts.

Let's compare ATP, glucose and fatty acids in terms of energy storage.

ATP has a molecular weight of 507 Da
Glucose has a molecular weight of 180 Da, and contains the same amount of energy as 31 ATP molecules
Fatty acids vary in size, but a gram of fat contains about twice as much energy as a gram of glucose (or glycogen)

The difference in energy density is huge, you would need enormous amounts of ATP to replace glucose/glycogen as energy storage mechanism, not to speak of fat. You can't put an arbitrary amount of ATP molecules into a cell, you 'll get into problems due to the osmotic pressure lots of molecules inside the cell would cause. Glucose is stored as glycogen in cells due to this effect, which makes one large glycogen molecule out of lots of glucose molecules.
The energy density difference is even larger if you take into account that ATP and glucose bind water, while fat is stored without surrounding water. The actual difference in energy density of glycogen and fat is around 6 times.
ATP is also not as stable as fat, it can get hydrolized in water. This would be a problem for long-term storage of energy.
You'll find some more details in Albert's "Molecular Biology of the Cell"

I think @AlanBoyd and @MadScientist have touched on the answer, fat is better suited by density for storing energy than ATP; ATP is optimal for quick conversion to bioenergy.  Look at the question in another way: ATP in bioenergy cycle is dynamic - its an energy flux from food and breath to bioenergy.
Biological energy is used at essentially the same rate at which we take it in.   The vast majority is used as soon as its available. If we were to try to store enough ATP for say an hour the costs would be large.
This back of the envelope calculation (see section 3.8) shows that 1 day of ATP is 64.5kg for a 2800 kcal a day energy intake.  Approximately equal to body weight.
Of course ATP is stored in excess - just a few seconds worth though, 8 if you believe competitive cyclists.  ATP is a pretty small quantum of energy... Even an hour storage would add 12 pounds to an adult body weight.  That's a lot. And what advantage would this give us?  We might be able to engage in high energy activities (which use ATP faster than we can make it) for longer.  But up to now it looks as if improvements in efficiency in generating ATP have been adequate for animals to stay competitive.
Look at how evolution has dealt with the other component of bioenergy: oxygen. We can't hold our breath for more than a few minutes. 22 minutes is the current human record; impressive but still not that long.  Oxygen is in plentiful supply brought in from outside and the adaptive costs to storing oxygen internally would simply not justify building up such a capacity for most of us. It seems even that aquatic mammals only hold their breath for a similar amount of time as we can if we practice.  20 minutes for Orcas. Penguins too.  This isn't meant to be a survey of all animals ability to store oxygen, the point being that storage of oxygen has an adaptive cost that is not trivial.

The Weddell seal can manage 80 min.

ATP is also signficantly less stable than other forms of biological storage molecules, such as fat and glycogen. ATP will also slowly hydrolyze by itself when placed in water. The other methods of storage are likely simply more efficient.

Efficiency depends on the purpose.  ATP is for fast transactions, fat is slow.  carbohydrates are in between.  you wouldn't want to have to metabolize sugar to do the 100 meter dash...

Not a complete answer, but a few random thoughts to start off the conversation:
1) There is another molecule that is used as a fast access store, and that is phosphocreatine which can be used to very rapidly rephosphorylate ADP in muscle. In resting muscle it is present at about 5x the level of ATP.
2) Levels of ATP are also used by cells as a regulatory input - in other words the fall in ATP levels with the onset of exercise triggers a response to replenish ATP through e.g. the breakdown of glycogen. In this view it is useful to have a final stage "energy currency" which can act directly as an enzyme substrate and whose level is a sensitive indicator of current energy demand.
3) ATP is also a substrate for RNA polymerase. If ATP was present at vastly higher levels than UTP, CTP and GTP it would probably cause errors in transcription, and might also interfere with the regulatory role of GTP binding proteins, since it would act as a competitor for binding at the GTP binding site.
4) In any case, if ATP was to be maintained at a much higher concentration for rapid use, presumably as soon as it began to be used the ATP generating systems would have to start up to try to replenish the pool. In other words things would really be no different from the way they are, but would simply operate at a higher resting level of ATP.

There is a high rate of ATP dependent processes in the cell such that ATP is immediately used up just after it has been synthesized.
ATP is very unstable in a water environment. It is easily hydrolyzed thus it is not ideal for storage in the very aqueous cellular environment. This makes it ideal instead to have storage sourced of carbon for ATP production.

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Basic question about multiplex PCR
Let's say I have a DNA sequence with the following structure:
$$ 5' - N_n - S_1 - N_{1000} - S_2 - N_{1000} - S_3 - N_n - 3' $$
Here, the $N$s represent stretches of arbitrary sequence of the indicated length. $S_1$, $S_2$ and $S_3$ are all unique sequences 20 bp in length.
I design a forward primer PF that anneals to the positive strand at $S_1$. I design two reverse primers PR1 and PR2 that anneal to the negative strand at $S_2$ and $S_3$ respectively. Their annealing temperatures are reasonably close.
Clearly, PF and PR1 together will produce a 1040 bp PCR product, and PF with PR2 will produce a 2060 bp product.
Now let's say I add 0.2 μM PF (standard concentration), 0.1 μM PR1 and 0.1 μM PR2 all in the same reaction. I then run a PCR, with extension time sufficient for the 2 kb product.
I can see the following possible outcomes:

I get a 50/50 mix of 1 kb and 2 kb products.
PR1 competes aggressively and I get hardly any 2 kb product and a lot of 1 kb product.
After a few cycles, the 1 kb product that has accumulated serves as an efficient forward primer for PR2, and I end up getting mostly 2 kb product and little 1 kb product.

Which one will happen? If it depends, what are the major factors on which it depends? Primer concentrations, extension time, annealing temperature, dNTP amount, number of cycles?
This question is basically a very simplified multiplex PCR. While much has been written about practical applications of multiplex PCR, I am hoping that answers will help me understand the considerations that go into deducing optimal multiplex PCR conditions without doing any empirical calibration. This isn't to circumvent the calibration, but to understand the process conceptually.

I haven't done this exact experiment. I am just deducing from the known facts about PCR.
The product of PF and PR2 will serve as a template for both 1kb product (P1) and 2kb product (P2).
Lets assume that after 2nd cycle there is 1 copy each of P1 and P2 (Delay of 1 cycle to make a smaller length product. See here).
Lets assume that the primer binding affinity is equal (and for just preliminaries consider that only one primer can bind a template — such as in overlapping binding sites). So half of P2 will bind to PR2 and half to PR1.
Number of copies at nth cycle is:
P2(n) = 1.5 × P2(n-1)

P1(n) = 2 × P1(n-1) + 0.5 × P2(n-2)
However this is not really the scenario; the primers are not competing for the template.
Which means that both primers can bind to the substrate simultaneously.

DNA polymerases (except Klenow) will remove any DNA strand bound to the template, ahead of it. In that case P1 will not form. But when PR2 runs out, the unused PR1 can produce P1.
Now there are additional factors, such as the distance between PR1 and PR2 binding sites. If the distance between the primer binding sites is less than the smaller product then the abovementioned case occurs. If the inter-primer distance is larger than smaller product then both products will form (and just like the competing primers case, P2 will serve as a template for both products). In this case the copy numbers will be:
P2(n) = 2 × P2(n-1)

P1(n) = 2 × P1(n-1) + 1 × P2(n-2)
This means that P1 will dominate.
Other assumptions:

No limiting concentrations of dNTP, primers etc
PCR efficiencies are equal for both primers and is equal to 2 (in non-competing cases)
Primer annealing temperatures are same i.e binding affinities are same.

you say DNA polymerases (except Klenow) will remove any DNA strand bound to the template do you mean DNA Polymerases have 5'-3' exonuclease activity? or helicase activity? if it'S the second, then both products should be preserved, right?

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What is this fuzzy, black fungus that grew on my plates in the 4⁰C room?
I often find the fungus below growing on my (ostensibly) sterile plates in the 4⁰C room. Presumably it takes a few days to reach this size.
The colony looks puffy and dimpled in the middle, like a chocolate cake. The colony is actually black, but looks grey because of what I assume are hyphae and/or spores on top.
It looks like if I disturb the colony physically spores will be released (I haven't tried this because I don't want to contaminate the whole lab with aggressive spores). I notice that the center of the mass curves upward over time, and after a few more days of growth this colony will probably tear itself apart, leaving a gaping hole in the middle (based observation of similar contaminants on other plates, not pictured).
I suspect this is a very common lab contaminant. It grew to this size in less than 2 weeks, and was at 4C the entire time. I noticed many plates in the same batch/sleeve were contaminated, but each plate had only one colony, so it somehow spreads from plate to plate but not within the plate. What is it?

If anyone has any suggestions for simple but informative, classical microbiological techniques that would help identification (common stains, inexpensive selective media) I would be happy to try them - although it would be hard to justify very involved experiments since this doesn't pertain to my main research (in other words, if this was bacteria, sequencing the 16S would probably be out but a Gram stain is fine - this is very likely not bacteria, but I don't know the equivalents of those methods for fungi). Since identifying species is not really my strong suit, I'd appreciate if you link to a protocol when suggesting methods.
Update: I have found 4 more plates, all LB-Ampicillin, with what I suspect to be the same contaminant. With regard to Alan Boyd's comments, the colony morphology seems to be uniform in several aspects. It is not necessarily flower-shaped as I have claimed, but on the other hand, it never has a halo of satellites (dots) around it either.
Photos of the plates:

View from the top (agar side close to the benchtop) - shows round colony morphology and various stages of growth. Bottom left colony shows small dimple as the mass begins to swell. Top right shows cracks (actually tears) appearing as the mass is distorted by growth. Note that there is never two colonies on the same plate. The plates all came from the same sleeve in a cold room storage.
View of same colonies from the bottom - note star-shaped inward creases which form as the colonies grow and distort the surface.

Aspergillus niger?

@AlanBoyd According to the Wikipedia photo, A. niger colonies have a halo of dots around the main disc. In contrast, mine have very tidy edges (even after the middle bursts), and they are flower-like rather than circular. I don't know if this is significant.

Yes I saw that. However fungal colony morphology is very dependent upon the composition of the agar. But if I was more confident I would have answered, not comented.

@AlanBoyd Perhaps relevant: Besides the LB, I saw this grow on an LB-spectinomycin plate and a YPD plate. Colony morphology was indistinguishable.

I am far from an expert, but looking at similar pictures around the net I would guess for some Cladosporium species.

@skymninge Some photos of Cladosporium appear similar, but none are exactly like this. I think it's a promising possibility, but I'm not sure if it's really Cladosporium.

Just take a sample and do deep sequencing on it. Then compare the results with the genome database.

Sounds like a plan, @StefanGruenwald !

@Superbest, http://synapse.koreamed.org/DOIx.php?id=10.4489/MYCO.2008.36.4.211&vmode=PUBREADER#!po=7.14286. The picture in this study, esp the one from the bottom view, looks very similar to yours. Did you find out what the mold was?

Cladosporium sphaerospermum

I'm voting to close this question because more details are necessary to answer this question accurately, however, this mould seems like Cladosporium.

@WYSIWYG Actually Cladosporium sounds pretty good. I was planning to provide the additional details (eg. microscopy) but haven't gotten around to it yet.

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Cloning and Telomeres
I read that the length of telomeres in Dolly was shorter, because the DNA was taken from an old sheep. Shorter telomeres may lead to early aging. What is happening now with cloning? Do we use a telomerase to restore the length in a donor cell?

No, it doesn't seem to be common practice. A telomerase treatment would probably do more harm than good, and may be completely unnecessary in the first place.
Betts and coworkers published a study in which they examined telomere length in cloned cattle. They found that while telomere length in cloned embryos does start out somewhat shorter than in naturally produced embryos, by the time that the normal processes of embryonic development were in full swing telomere length in cloned and natural embryos was equivalent.
Betts' results make sense in light of the fact that telomerase activity (and the activity of many, many related proteins) is normally upregulated in embryonic cells.
As for Dolly, while it is true that her telomeres were shorter than those of an average age-matched sheep at the time of her death, it's far from clear that those short telomeres had anything to do with her decline. Also keep in mind that she didn't just keel over suddenly in the night, she was euthanized. A subsequent autopsy showed that she had a form of lung cancer caused by a retrovirus common in sheep.
Edit: why were Dolly's telomeres shortened?
This is a good question, as the findings of shortened telomeres in Dolly's case do contradict the findings in the Betts paper. Clearly we need more citations:
-"Analysis of telomere lengths in cloned sheep." Shiels et al, 1999
This is the original citation for the claim that Dolly's telomeres were shortened. There isn't too much extra information to be had as it's a very short paper (1 page letter). They did look at other cloned sheep created from types of cells other than skin cells (as Dolly was) and saw the same kind of telomere shortening relative to controls. They also make a point of mentioning that Dolly's telomere length may be within the normal variation for sheep.
-"Remarkable differences in telomere lengths among cloned cattle derived from different cell types." Miyashita et al, 2002
The investigators found that telomere length in cloned cattle was strongly dependent on the type of cell from which the clone was derived. For example, clones made from mammary cells tended to have shortened telomeres, whereas those derived from muscle cells had normal length telomeres.
-"The analysis of telomere length and telomerase activity in cloned pigs and cows.", Jeon, 2005
This group found that cloned cattle had normal length telomeres, whereas cloned pigs had elongated telomeres. By way of explaining these results, they found that telomerase activity was upregulated in cloned pigs relative to control pigs, whereas telomerase activity in cloned cattle matched that of control cattle.
How should we take all of this information? At the very least we can say that telomere length in clones is highly dependent on species and on source tissue, and that telomere length can increase, decrease, or stay the same in cloned animals relative to control animals. Clearly telomere length in cloned animals is a fiddly property. It is very likely that it also depends on the exact details of the cloning protocol as it was carried out (i.e. how much did the experimenter's hands shake when they inserted the needle to suck out the nucleus?, etc.).
So I would say not to read too much into Dolly's shortened telomeres. They may have been a result of her being a clone, or they may have been a result of natural variation. In either case the shortened telomeres were not linked to her ill-health, and it's likely that small tweaks to the cloning protocol would eliminate any telomere length discrepancies in future clones.

Somatic cells (used in SCNT) are also prone to recombinations and other somatic mutations.

@tel. Thank you for the answer. But then why Dolly had shorter telomeres, what was different?

@Barbos I posted an edit with some follow-up about Dolly's short telomeres. It's surprisingly involved!


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Do bacteria with multiple flagella move faster than bacteria with a single flagella?
Do bacteria with multiple flagella move faster than bacteria with a single flagella? Assuming the flagella are at the same length.

Note: in the following I'm going to focus on E. coli, which is the best understood system for bacterial flagellar movement. It would be interesting to compare uniflagellate bacteria and bacteria that have a fixed number of flagella. However, I know about E. coli and I think there is something interesting to be learned just from them, so I'll continue.
You're in luck that you asked this question when you did: a very cool paper (1) was published just last year addressing your question. They find that the number of flagella has only a small effect on bacterial motion, but to understand why requires some background (A lot of the following background comes from this paper, which summarizes it pretty well).
I would argue that E. coli movement is one of the best-understood examples of cell movement we have, with excellent, high-resolution, quantitative data being generated for over 40 years now (the king in this field is Howard Berg at Harvard, if you want to learn more just read a recent review from him).
E. coli have a variable number of flagella, from one to ten or so. They operate in a bundle, but this bundle is highly dynamic due to the way E. coli moves. Rather than proceeding continually a straight line like a car, E. coli moves by a series of starts and stops called a run-and-tumble: the bacteria moves in a straight line for a short amount of time (a run), and then it stops in its tracks and changes direction (a tumble) before starting off again (2). At a first pass this run-and-tumble behavior is essentially diffusion, the bacteria covers a lot of ground without going anywhere on average unless there's some food nearby, in which case the run-and-tumble is slightly biased so that the bacteria drifts toward the food.
As I said, during runs the flagella are bundled together and all turning counter-clockwise. A tumble happens when the bacteria sends a signal to the flagella to start turning clockwise. This breaks apart the flagellar bundle and sends all the flagella in different directions. Up until the paper I mention above, it was still not clear exactly how many flagella need to start turning clockwise before the bundle breaks up and a tumble commences.
Now you can see why having more flagella might not necessarily be a good thing: you might be able to move faster during the run (though this is not obvious to me, given the sometimes unintuitive nature (3) of low-Reynolds number fluid dynamics) but at the same time the flagellar bundle will be more sensitive to break-up because with more flagella come more opportunities for one to start moving counter-clockwise and mess things up.
As the authors of the above paper (1) find, it turns out that there are correlations between the actions of different flagella in a bundle, so that a bacteria with many flagella effectively acts like a bacteria with fewer flagella. The result is that the overall pattern of run-and-tumble is not much affected by the number of flagella; you might argue that number of flagella has a minor effect on bacterial movement.
On the other hand, you might be interested not in the net movement of a bacteria, but just on its speed when it's moving forward, in the run phase. Unfortunately I wasn't able to find any good measurements of the run velocity of a bacterial cell as a function of number of flagella. But hopefully given this recent paper, maybe such measurements are on the horizon!

(1) Mears PJ et al. (2014) Escherichia coli swimming is robust against variations in flagellar number. eLife 3:e01916.
(2) Turner L et al. (2000). Real-time imaging of fluorescent flagellar filaments. J. Bacteriol. 182(10): 2793-2801
(3) Purcell EM. (1977). Life at low Reynolds number. Am. J. Phys. 45: 3-11.


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What is going on in these cells?
Here are some pictures of human iPS cells in culture. After several passages, some cells look really weird, can you help me understand what is going on? What am I looking at? What are those blastocyst-like structures? (bluish picture) and what about that cell full of vacuole-like thing?
P.S. do not pay attention to the scale bar, it's incorrect.

Extra info:
I did not induce them, I got them already dedifferentiated so I can't be specific on that part of the protocol. However, I am growing them in Essential 8 Flex Medium (with supplements as specified from the kit protocol), I add rock inhibitor 4h before passaging them. Passages are done by dissociating colonies using EDTA only (no enzymes). Most of the expanded cultures look normal, some showed the formation of embryonic bodies (the last picture added) but the blastocysts are very different and not really expected.

I am not entirely sure but there is some vacuole formation so maybe they are going towards the apoptosis. However to see clear phase contrast between Feeder layer and iPS cells the light diffraction may give you hallow formation around the radius of the cells. (Source: Dad)

This question would be easier to give an answer to if you provided specifics on your protocol for inducing and culturing iPS cells, any variations from typical protocols, any experimental treatments, etc. The greatly elevated vacuole formation suggests cytotoxic stress. Elevated autophagy can be cytoprotective if the cell is moderately stressed, but it is a precursor to apoptosis when the stress cannot be alleviated by autophagy. Depending on the scale (please clarify), the blue picture may depict an "embryoid body" (essentially a blastocyst) - see "identity" section in your own wiki link.

I did not induce them, I got them already dedifferentiated so I can't be specific on that part of the protocol. However, I am growing them in Essential 8 Flex Medium (with supplements as the kit specified), I add rock inhibitor 4h before passaging them. Passages are done by dissociating colonies using EDTA only (no enzymes). Most of the expanded cultures look normal, some showed the formation of embryonic bodies (the last picture added) but the blastocysts are very different and not really expected.

Also, I did not continue growing the blastocysts, but I have backed up a few aliquots.

@Alec_djinn can you edit that information into the question please? I would also recommend changing the images to thumbnails (as described here) to improve readability.

@arboviral better?

I'm under the impression that primed or differentiated iPSC regularly exhibit membrane blebbing, based on a quick literature search.

@CMosychuk can you link the literature you are referring to? I couldn't find any reference so far.

@alec_djinn Just a couple examples, though I may be mistaken. (ref) (ref)

overgrow them and thrown some dapi on them, then check fluorescence.  I wouldn't be surprised to see mycoplasma in this culture.

they might be embryoid bodies:
https://en.m.wikipedia.org/wiki/Embryoid_body

looks like it, at least in the last picture.

ips cells fascinate me to no end. I wish I could culture them at home.


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Transduction with P1 lysate prepared from strain that is proC::Tn10
If I do a transduction with a P1 lysate prepared from a strain that is pro*C*::Tn10 and the recipient is wild type, will all my recombinants  be ProC- and Tet resistant since the Tn10 is in the proC gene?

Slightly confused by this  - what are you going to plate on after the transduction step?


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Do genes play a role in the athleticism and shape of a person?
I am an Indian with a small thin stature with some deposition of fat around my belly.I was wondering if genes play a role in fat deposition in the body for Indian, Chinese, European or African people. Fat deposition may differ among all these people around the belly, thighs etc.
These people also differ in their stamina and speed naturally.

For example here in India in the game of cricket there has been no
  fast bowler out of 1.2 billion people who can do fast bowling
  because it requires a lot of strength and stamina.Also on field
  athleticism is also very bad compared to Australian or South African
  players.I assume that may be its because of some cultural or genetic
  problem.

possible duplicate http://biology.stackexchange.com/questions/3165/athletes-nature-vs-nurture

Here is a book you might like to read

All these characteristics you observe (speed, ability to play cricket, belly size, height, etc…) are what what we call in biology a list of phenotypic traits. Basically, the phenotype is a characteristic of an organism that we can eventually measure or describe (physiological, behavioural, morphological, and life history are four common classes).
In a given population the phenotypic variance (the variance in height for example) can be expressed as the sum of the genetic variance (=the genetic variance underlying the phenotypic trait of interest), the environmental variance (=the environmental variance underlying the phenotypic trait of interest) and the variance due to the interactions between genes and environment (the variance due to the interaction that is underlying the phenotypic trait of interest).
Mathematically expressed it gives:
$$V_{phenotype} = V_{genetic}+V_{environment} + V_{gen X env}$$
Therefore, for each trait there is a given part of the variance that is explained by the environment and a given part that is explained by the genes. We might go a bit further and defined the concept of heritability (in the narrow sense, see wikipedia article for more info). The heritability (in the narrow sense) is the ratio of the phenotypic variance to the additive genetic variance. Mathematically expressed it gives:
$$h^2 = \frac{V_{additive}}{V_{phenotype}}$$
Each trait has it's given heritability. The heritability can be defined only for a trait in a population (which defines $V_{genetic}$) and its environment (which defines $V_{environment}$).
For example, the heritability of height in human is around 0.8 (non-peer reviewed source). Which means that 80% of the variance in height in the world-wide population is explained by the genetic variance. See this post for more info about the concept of heritability
In your question, you also used (before your question was re-edited!) the word fitness (also it is not really present in your question). The fitness is a very important concept in biology, it is the ability of an individual to survive and sire offsprings. Our phenotypic traits influence our ability to sire offsprings and therefore our genes influence our fitness. If the whole phenotypic variance is explained by the environmental variance only, then, even the the trait is under selection, there will be no change in allele frequency due to selection. Note: an allele is a gene variant. If eye color is a gene, brown eyes and blue eyes are alleles (to make it easy). This change in allele frequency is called a response $R$ to selection $S$. This link between selection, the response and the narrow sense heritability $h^2$ is given by:
$$R=S\cdot h^2 $$
So to answer your question. Yes, part of the variance in height, belly size, cricket playing ability, etc… is genetically coded. As the fitness depends on phenotypic traits, Yes, the fitness is genetically coded (otherwise there would have no response to selection). Therefore we're not all equal to playing crickets!

DNA testing is a growing trend in athletics since 2016 to design training regimens by analyzing a range of 40 genes that encode for different physical traits (scroll down for a list of those genes here).
The genes predict mitochondrial and muscle mutations which are good for speed and endurance.
We don't know which physical activities Indians are good at because some countries spend 4.5 million for every Olympic gold medal and India doesn't. They are perhaps better than Japan and worse than Jamaica.
Samoans are physically strong, and have 19% denser bones than caucasians. And they have been surviving maritime life in cold and food-deprived conditions for many centuries. India is the most food-abundant region on the planet, together with East Asia. Nepalese are good marathon runners.
There are two types of skeletal muscle fibers. Fast fibers, which use sugars for fuel and do not require oxygen, kick in for tasks that require maximum force and quick action, such as sprinting. Slow fibers, which employ oxygen-using (or aerobic) pathways, power activities that require endurance, such as long-distance running. A protein called alpha-actinin-3 is made mostly by fast fibers and is implicated in their capacity for rapid force generation. (science mag)
It has been speculated that variations in this gene evolved to accommodate the energy expenditure requirements of people in various parts of the world.(wiki)
https://www.thehindu.com/sport/cricket/indian-cricketers-undergoing-dnagenetic-fitness-test/article20321195.ece
https://www.sciencemag.org/news/2018/04/south-asians-are-descended-mix-farmers-herders-and-hunter-gatherers-ancient-dna-reveals
https://vdare.com/articles/indians-aren-t-that-intelligent-on-average
https://www.researchgate.net/figure/Anthropometric-data-for-European-and-South-Asian-men_fig15_49677710

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Do invasive species cause long-term damage to ecosystems they invade?
Growing up in the U.S., I was warned at various times of the dire consequences of a variety of introduced pests (usually insects).
Japanese beetles, gypsy moths, and most recently the brown marmorated stink bug are all introduced pests that, at various times, were described as serious threats to our ecology.
These threats aren't confined to arthropods, either.  The giant African land snail is causing a stir in Florida (indeed, Florida seems to suffer from an excessive variety of introduced species.
"Lack of native predators" is frequently cited as the primary reason many invasive species are considered such a risk to the ecology.
I understand that these introduced species can place tremendous pressure on native species that fill similar ecological niches, and may even push these species out of the region due to competition for food and habitat.  However, do the overall ecologies that these species are introduced to adjust over long periods of time?
The numbers of Japanese beetles and gypsy moths don't seem anywhere as high as when I was a child.  Has the ecosystem adjusted, or has the overpopulation self-corrected as the species ran low on food through over-consumption?  Or are the populations still just as problematic now as they were 30 years ago, and I just am not seeing the bigger picture?
What is the long-term impact that we've seen from invasive, introduced species?  Is there a significant difference on the long-term impact between introduced flora, arthropods, or mammals?

You may also be interested in the classic example of rabbits in Australia.

Good question, and I'm excited to read some good answers. I'd guess just as an idea that introduced species have fundamental effects on ecosystems when the native species that they detrimentally affect are community structuring species, eg. Emerald Ash Borer in an Ash woodland.

Oh, and Homo sapiens are a pretty seriously destructive / transformative invasive species, I suppose.

This is extremely broad and a little vague. It may help to break it up, or at least specificy the exact issues you are interested in. What do you mean by "damage"? That they drive out any other species? That they reduce productivity? That they reduce species richness? That they reduce the aesthetic value of the landscape?

It might also help to define what you meant by "ecosystem". If we consider the intestinal tract of a human as a microbial ecosystem, it's rather straightforward to show that invasive species cause long-term damage, by killing the host.

@EpiGrad I assumed it was pretty obvious from the context, and the commonly accepted use of the phrase "invasive species", that this question isn't asking "can diseases kill people".

@Beofett I used an extreme example, but it's never the less useful to make sure your question is bounded by scope and time, because it changes the answer.

@EpiGrad Given the notable lack of answers after 3 months, I'm not sure that it would be beneficial to draw lines that would exclude valid potential answers because they defined key concepts slightly differently than any (wholly arbitrary) boundaries I might add (e.g. I don't want to define "long-term" as 30 years, and thereby miss answers involving research on 25 year impact). If there were an over-abundance of answers, I might be inclined to agree that further refinement of scope could help, but I think this question is pretty clear in its intent as-is, as highlighted by the examples I cite.

It is maybe worthwhile adding, that if you take an other wildly spread definition of "invasive species" the question becomes circular (at least if we drop the "long-term"): Wikipedia e.g which takes it's definition from the GB non-native species secreteriat defines invasive species as: "a plant or animal that is not native to a specific location (an introduced species); and has a tendency to spread, which is believed to cause damage to the environment, human economy and/or human health"

The answer really depends on how you think of invasive.  One extreme answer is to say that all things are relative, and that the concepts of local and invasive are all relative.  This matters to a certain extent because ecologists draw a fuzzy line between invasive and naturalized.  You could start with some basic species that we all think of as either good, local, or neutral.  Take the earthworm.  Most people think of it as a common native species, but the earthworm is actually an invasive species that has radically changed much of North America that came over with the Europeans.  Similarly, brown trout are also invasive, coming to the US in the 1800's.
As far as why invasive species succeed, it's still an open question.  What you reference is the enemy release hypothesis, but there are others such as disturbance, diversity of the new community, and just the traits.  Here's a good review of biological invasions and a second one.
To answer your question about adapting, I wouldn't trust your memory. It's important to keep in mind that most likely your memory is flawed, and you are only observing a very limited number samples with an incomplete sampling methodology.  For instance gypsy moths undergo wild population fluctuations, and have for over 100 years.  How well do ecosystems bounce back from invasions depends on lots of factors.  Often time the ecosystem can survive, but the some species won't.  An easy example would be Norther Hardwood forests.  Chestnuts (extirpated by an invasive fungus)are mostly gone from the wild, but the forest persists, as well as many of the species that rely on them.  So in part the answer to your question depends on scale.  The forest survived, but an individual species was nearly destroyed.
Ecological economists have tried to put a value on the destruction that invasive species have caused too.


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What is one Botulinum toxin medical unit?
How many Botulinum toxin molecules or grams are contained in one medical unit of Botox?

1 unit is approximately 10 pg
Source

One unit of MYOBLOC (botulinum toxin type b) corresponds to the calculated median lethal intraperitoneal dose (LD50) in mice. The method for performing the assay is specific to Solstice Neurosciences' manufacture of MYOBLOC (botulinum toxin type b) . Due to differences in specific details such as the vehicle, dilution scheme and laboratory protocols for various mouse LD50 assays, units of biological activity of MYOBLOC (botulinum toxin type b) cannot be compared to or converted into units of any other botulinum toxin or any toxin assessed with any other specific assay method. Therefore, differences in species sensitivities to different botulinum neurotoxin serotypes preclude extrapolation of animal dose-activity relationships to human dose estimates. The specific activity of MYOBLOC (botulinum toxin type b) ranges between 70 to 130 Units/ng.

UPDATE
10 pg of toxin (150 kDa) is 4 x 109 molecules

A Botox unit is essentially a measure of a defined amount of biological activity and corresponds to a fixed number of botulinum toxin molecules.
The biological potency of these preparations is expressed in mouse units. One mouse unit is defined as the intraperitoneally injected quantity of each pharmaceutical product required to kill 50 per cent (LD50) of an experimental group of female Swiss-Webster mice, each of 20 g body weight.
A 100 unit of Botox (Onabotulinum toxin A) contains approximately 5ng (nanograms) of toxin. And hence 1 unit of Onabotulinum toxin A contains approximately 0.05ng of active toxin.


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Bacterial cell lysis - what solution to use?
I am trying to determine how quickly detergents act on bacterial cells (cell lysis). I would like to compare some detergents at difference concentrations for bacteriolytic activity. I don’t care about all metabolites inside the cells (proteins, DNA, etc…). Many publications suggest that often more complicated solutions are used. My first thought was to use a simple prepared detergent in PBS or saline for lysing the cells. Do I need a complex solution to lyse the cells?
Could someone please give me a suggestion? Thanks in advance.

I wonder how you plan to measure lysis? You will find that many lysis methods for E. coli incorporate a treatment with lysozyme and EDTA. This is so that lipopolysaccharide (outer membrane) and peptidoglycan layers of the cell envelope can be breached before detergent (usually SDS or Triton X-100) is added to dissolve the inner or cytoplasmic membrane. I suspect that if you added detergent to intact cells it wouldn't be particularly effective, and any cells that were affected would remain as denatured cells which would, for example, still contribute to optical density.
Since they are usually able to withstand bile salts in the small intestine, Gram-negative bacteria can be quite resistant to detergents. For example many Enterobacteriaciae can grow in 5% SDS - see:

Rajagopal, S et al. (2003) Eight Gram-negative bacteria are 10 000 times more sensitive to cationic detergents than to anionic detergents. Canad. J. Mic. 49:775-779


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Why do humans alone have the capability to have religious/spiritual experiences?
What is it in our brain that makes having such experiences possible? I assume other species don't have these. Sure there are instances in the natural world where you can see individuals of the species gather around the dead one. Sometime even the alpha male in the group allows the kin/relatives of the dead individual to approach it (for whatever reason).
The kind of thing I don't see in the wild-life kingdom is an individual becoming "enlightened" or the likes.
Sure our cerebrum is highly developed and all. But "what" is it in our brain that makes it capable for humans to have such experiences?
I've read articles saying we have identified such regions in the brain. Just want to know what these structures are. Did such research establish that such structures also exist in other species too?

This recent paper looks like a good starting point.

But I'm not sure what an enlightened gorilla (for example) would look like.

I never realized that religious/spiritual experiences already existed and were certainly proven in a scientifical framework?!

what if the world is much more magic and full of spirits for animals than for men? For example, deer and horses see monsters everywhere. Animals have the capacity to fear imaginary beings that peer from unknown hiding places. It is said that human religion derives from the animal instinct that there is some very big powerful animal that could be watching you, tracking your every move. That instinct in humans if intellectualized into the surveillance of god, and his power over your life. The human rational cognition of the afterlife perhaps has similar animal cognitive roots

Its not clear that this is true.
Working with animals has been a little disconcerting over the past 50-60 years.  In the distant past, I think most evolutionary anthropologists and their like bought into the idea that humans were completely uniquely intelligent and spiritual.  But the more we try to define human sensibilities apart from other animals, the more we find its difficult to see animals as being completely incapable of human feelings and even thoughts.
I refer you to this question which describes the shift in intelligence theories over the years: Why have humans evolved conciousness?
The above reference is just to say that every definition of intelligence that is fairly broad has been overturned by animals (thumbs, socialization, tool use, self awareness, communication and language).
If you want to say 'I know we're special, but I just can't say how' you are in lots of good company... it's become pretty hard to lay down a definition that includes all human beings and excludes animals.
Lately it seems as if the definition of spiritual experience is similarly hard to define. What is your definition?  The capacity to receive and reciprocate affection or love is almost never brought up - that seems to be half of the internet.  Yet, that's a common component to many ideas of spirituality.   It was found a while ago that primates have some form of self-awareness to identify themselves as distinct from other individuals.  True this was only demonstrating that they know themselves in a mirror, but other experiments show it probably is deeper than just that.
I think the most confounding evidence is the work with animals who have been trained from infanthood to communicate to humans through sign language or symbols.  The most astounding example I know if is Koko the gorilla. She had the vocabulary of a 5 year old and the capacity to joke around, reason, and adopted pets as children including a cat called All Ball.  When All Ball who was killed by a car she mourned and remembered her adopted cat for years.  This page outlines all that, though there is a book that describes Koko's life.

The human staff sought to discover what Koko thought about death.  So they asked, “Where do gorillas go when they die?”  Koko answered, “Comfortable / hole / goodbye.”
  They asked, “When do gorillas die?”  Koko answered, “Trouble / old.”
  They asked, “How do gorillas feel when they die:  happy, sad, afraid?”  Koko answered, “Sleep.”

So this has been taken as evidence that gorillas have a concept of their own mortality or possibly even life after death.
So what is left?  Not clear to me.  Any thoughts?
Some regions of the brain and control of electrical activity in the brain have been associated with spiritual experiences or acts like prayer and meditation.  The temporal lobe is exciting because magnetic stimulation of that region can create the sensation that there is a presence in the room with you. there appear to be many regions which are active in different instances though, which is something you might expect.
There is no evidence yet that animals do not experience similar effects in their brains, though primates have very much the same structures as we do.   Its too bad Koko has died - she might have told us.


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Has medical progress stopped human evolution?
We can cure many diseases nowadays, and thus the natural selection is very limited.
Plus, mankind spent the whole beginning of its existence in almost the same hostile environment, and that's where he evolved the most, whereas our environment is changing very quickly. So, can we say that mankind froze, if not stopped, its own evolution ?

As long as some individuals reproduce more often than others then there will be evolution.

Not at all.

Mutations accumulate independent of medical progress. In fact harmful mutations which would otherwise cause an individual to die can now be "cured" thus if anything increasing the gene pool.
Typically medical progress extends our lives when we are much older, thus we have already passed mutations on to our children before a bottleneck in evolution could occur
We are getting taller, less hairy and women are getting more attractive which is another form of evolution
As new diseases develop the selective pressures on humans are ever changing. HIV which was never as widespread is now pushing certain immunogenetic traits to be favourable, the same is true for malaria (HLA 5701) and many others

In conclusion, whilst there are fewer and fewer strong selective pressures forcing extreme evolution, our bodies are designed to evolve slowly unlike viruses like HIV. Our mutation rates are around 1 in 10^9, allowing us to always slowly evolve as there will always be traits which are slightly more advantageous.

Women are getting more attractive?! Could you please elaborate?

Women that are going to have children pass their traits on. Some people believe that the women who are more likely to get married and have multiple children are those that are most attractive. Other theories suggest that the most attractive women do not have children. Either way a certain trait, whatever it is, is the one more prevalent in women bearing children and thus this is the one that is passed on.

It doesn't sound like there is a testable hypothesis in any of this. Do you have a cite or two?

here's a post if not the primary reference.  This sounds reasonable to me, though i'm sure its not completely proven.  http://www.abc.net.au/news/2009-07-29/evolution-makes-women-more-attractive/1371676

Evolution is not entirely progressive - look up the 'red queen' on wikpedia.  Competition changes traits by selection, but there is constant competition from the outside that reinforces change only for change's sake - it doesn't necessarily make the traits stronger. If you get the most masculine man and the most feminine woman, will the children have both extreme traits when and where you want them?  Many exceptional trait combinations are not reproduced in offspring - they are as much coincidence as they are the product of selection. Look at pictures of Schwarzenegger Sons - not that big.

All this is not a simple question well tastes in what is attractive also changes.  I'd say our appearance does and has changed over time, and this is because of sexual selection to a great extent.  its a viable hypothesis, and there's evidence, but there are also definitely other forces in play here.

As an example that we do change with evolution and a further Arnold reference, you can see that Neanderthals definitely were physically quite different from us.  "Modern man a 'wimp'" :  http://www.independent.co.uk/news/science/modern-man-a-wimp-says-anthropologist-1802501.html

Keep in mind that most people live in environments where antibiotics are of limited availability and hygiene is not as rigorous as in the "western" world. Combine this with high population densities and you get, if anything, more natural selection due to the spread/proliferation of pathogens and the subsequent mortality of the patient.
Also, don't confuse natural selection for evolution. Natural selection is one of only five causes of (micro-) evolution. Mutations will continue to occur. Sexual selection continues unabated, and migration is more important now than ever. The only evolutionary factor I'd argue is being diminished is genetic drift since there are so many people today.

authors: άθλια βδέλυγμα


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Diffusion across cell membranes
I got this question and don't really understand the difference between the answers.
Diffusion is (in cell membrane):
a) passive by nature, no metabolic energy is needed
b) driven process by pressure or voltage

Diffusion is always a passive process that doesn't require energy.  Therefore it would seem that A is correct, B doesn't really make a whole lot of sense.  In the case of the cell membrane diffusion will often be in the form of 'facilitated diffusion' through carrier proteins, however the transport is still not active.

Diffusion relies on the fact particles move randomly in whatever they're in. If they are concentrated (I.e. there are lots of them in one place) they will fill out the whole place. With respect to cell membranes, anything that can diffuse freely will be the same concentration inside and outside the cell. It doesn't require metabolic energy as the cell doesn't need to do a thing. Thus the answer is A.
Facilitated diffusion is where the cell puts protein channels on its membrane to allow diffusion of things that can't pass through the cell membrane normally or do so really slowly. This can be driven by a voltage or by pressure, which "facilitate" or help the diffusion. Glucose for example moves like this into the cell. It uses the fact that there's a high concentration of sodium outside the cell that "wants" to move in because of the cell inside being negative and low concentration inside. So glucose hops onto a sodium ion whilst it is moving in.

AndroidPenguin's answer has really muddied the water, but I can't fit my response into a comment.
When a glucose molecule moves from the blood into, for example, a muscle cell, it is indeed diffusing down a concentration gradient, and the GLUT transporter protein acts to facilitate this process by providing a route for the polar glucose molecule to get across the membrane. This is facilitated diffusion. The movement of the glucose molecules requires no input of metabolic energy. That part of AP's answer is ok, and really that's all that the OP was about.
In direct contrast to this, enterocytes can transport glucose from the gut lumen into their cytosol even though the gradient of glucose concentration is in the other direction. They do this by linking the inwards movement of the glucose molecule to the outwards movement of Na+ ions, down the electrochemical gradient for these ions. This Na+ gradient is, in turn, generated by a pump which uses ATP to move Na+ out and K+ in. So in this example the energy derived from ATP hydrolysis is 'stored' in a gradient of Na+ concentration, and this gradient is tapped as a source of energy to power movement of glucose. This is NOT an example of facilitated diffusion. The ATP-powered movement of ions is an example of primary active transport, and the action of the Na+/glucose transporter is an example of secondary active transport. Note also that the glucose and the Na+ move in opposite directions (antiport) so there is no question of a direct interaction between the ion and the glucose.


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What vegetation would thrive in the Martian atmosphere?
Most plants require carbon dioxide for their photosynthesis, which Mars has in overabundance.
Would atmosphere composition (let's ignore temperatures for the purpose of this question) of Mars allow vegetation to grow?

Check out the answer here http://biology.stackexchange.com/questions/1242/what-is-the-lowest-pressure-at-which-plants-can-survive

This is not my field by a long shot, so take what I say with a grain of salt. However, this question is very hard to answer because whether or not a plant will grow depends on a great variety of factors. Even if we ignore the temperature as you say, there are other considerations. These include, but are not limited to:

Soil composition, I doubt that Martian soil can support earth vegetation even if its atmosphere could. Plants need various nutrients, and specific pH ranges among other things.
Atmospheric pressure, I am not at all sure that the Martian atmosphere (though it is, indeed rich in CO2) would be enough to drive an earth plant's photosynthesis. Bear in mind that the atmospheric pressure on Mars averages 600 pascals (0.087 psi), about 0.6% of Earth's mean sea level pressure (source). This makes it highly unlikely that unmodified earth plants would be able to thrive there.
Water water water...
Pollinating species. Many many plants depend on other species (e.g. bees or hummingbirds) for their propagation. These would be hard to find on Mars.
Sunlight I don't know if Mars receives enough sunlight at its distance from the sun to drive an unmodified plant's photosynthesis.

Now, that said, it should theoretically be possible to start with some extremophile archaea or bacteria that would over the course of many many many years (at least hundreds, thousands more probably) terraform Mars to make it suitable for human habitation. Specially engineered plants could play a role then but I find it very hard to believe that any existing, unmodified, multicellular plant life of earth origin could survive on Mars.

i know mars soil will not be up to the task as we know it is highly acidic, i'm just wondering about the atmospheric composition alone

@lurscher I'm just pointing out that the atmosphere alone is meaningless. In any case, even if everything else were OK, there is probably not enough atmosphere on Mars to provide sufficient CO2 to unmodified plants.

I'll stick to considering the atmospheric composition, as referred to in the original question: Although there may be some rare exceptions that I can't recall, under normal circumstances all green plants use aerobic respiration with O2 as final electron acceptor for energy production. This means that they require oxygen, which is essentially absent from the Martian atmosphere (0.13%). Even though our hypothetical Martian crop could produce oxygen as a byproduct of photosynthesis, that oxygen would be lost into the atmosphere, and would not be available for respiration.
I believe that under waterlogged conditions some plants can switch temporarily to some sort of anaerobic metabolism as a stress response, but I don't know if this is just to survive or whether the plants can grow in this way - I suspect it is the former.

+1 I said it wasn't my field :). Would the oxygen present in Mars's atmosphere be enough if combined with that produced by the plants themselves?

It took (anaerobic) cyanobacteria one billion years to raise the atmospheric oxygen concentration on earth up to a level that supported aerobes.

I work on photosynthesis in algae, blue-green algae and anoxygenic photosynthetic bacteria.  All would more or less be able to live on Mars in a blow up tent equipped with a simple blow compressor (like some tennis courts in cold climates).  This could be used to raise the air pressure up enough (say 100 millibars) for water to exist in liquid form over a reasonable range of temperatures (Mars atmosphere is about 10 mB, Earth about 1000 mB).  The tent material could be made of UV opague material.  Besides many algae are quite resistant to UV anyway. The light intensity on Mars is no problem.  Most earth plants saturate photosynthesis at about 30% of full sunlight anyway.   Keeping the inside warm enough would not be a huge problem because the Mars atmosphere is essentially a near vacuum and so is a very poor conductor of heat. I do not think it would be all that hard. Low O2 is no problem for many algae. You could grow many higher plants quite easily if the O2 level was resonable.


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How does yeast dissolve in sugar?
There's this fascinating "kitchen experiment". Take a "brick" of baker's yeast (not dry yeast), and a couple teaspoons of sugar, put them together in a cup and stir together. There's no doubt both are solids: yeast is a firm block, you must use quite a bit of force initially to crush it and even then it should remain a rather thick paste. The sugar is crystals, nothing tricky about that. And then, within a minute or so of stirring, your cup contains only liquid - not entirely fluid like water, but not much thicker than cream. Solid+Solid -> Liquid.
What process leads to that? What happens with the baking yeast when it comes in contact with sugar, that it turns from solid to liquid, and releasing enough water to dissolve the sugar?

If if you find that impressive, try baking something that calls for a mashed banana. It's typically listed as a liquid ingredient for a reason.

There are a few solids that when mixed dissolve into a liquid. It's a pretty neat thing.

The whole process is called osmosis. In it there is the flow of liquid along a concentration gradient. Water then flows from the side which contains the low concentration of dissolved molecules (this can be salts or sugar for example) to the side with the higher concentration until it reached equilibrium. This principle is shown in the image below (all images from the Wikipeadia article on osmosis):

The blue dots are the dissolved material, the concentration is high on the right side and lower on the left. Through the dotted line in the middle (which is a semi-permeable membrane) only the solvent can pass to reach a concentration equilibrium. There is a pretty cool osmotic pressure simulator available on Molecular Logic which can also help understanding the principle.
And this is exactly what happens to the yeast cells. The sugar crystalls get dissolved (at least partly) by some of the humidity from the yeast block (this will not work with dried yeast) and form a highly concentrated sugar solution (also called hypertonic). The sugar concentration inside the cells is relatively low (called hypotonic). This leads to the effort to balance the concentration inside the cell and outside of it which then leads to a massive efflux of water from the cells. This goes so far, that the cell membranes break and the interior of the cells is released (nucleus, DNA, proteins and so on) and the sugar is completely dissolved in the released water. The reason why this mixture is so "gooey" afterwards is the DNA, which forms long, thick strains.

This method can be used in the lab to break up cells relatively gently without applying too much force.
When baking you should make sure, that your yeast is not coming directly into contact with undissolved sugar (or salt which works the same way), as this will kill a part of your yeast cells. However, for baking you usually dissolve the yeast in water or milk, so there is a huge excess of water which dissolves the sugar (or salt) and protects the cells. Addionally your yeast is much better distributed in the dough and gives better results.


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What is the most recent non-primate ancestors of humans?
If we go down the evolutionary tree of humans, (Homo sapiens, Homo erectus, ...), what will be the first non-primate ancestors?

Note that humans did not evolve from the tree shrews, both they and we share a common ancestor. See here for more.

I see that you edited the question to include "ancestor". @terdon makes a very good point. We do not think of ancestors in the fossil record in the same way that a person has ancestors (parents, grandparents, etc.). The most recent common ancestor of primates and tree shrews is neither a primate nor a tree shrew. There is no name for that taxon.

According to the Tree of Life, tree shrews (Scandentia) are the sister group to Primates. So Scandentia are the most closely related extant mammals that are not Primates. Here's an image:


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is it possible to completely reconstruct a family tree by DNA comparison alone?
Having DNA samples of all or almost all members of a population of, say, a few hundred or thousand individuals, is it possible to draw the entire family tree of those individuals? (Let's not assume monogamy or any other facilitation).
This may be a sum of two different questions:

does comparison of two DNA samples give any information other than topographical distance between individuals? In other words, is it possible to tell two sisters from a mother and a daughter by DNA alone?
(more a mathematical question than a biological one, maybe) having the relative topographical distance of all members of a group, can their full graph be drawn?

Not confident enough to post an answer but I very much doubt it. There is a large element of randomness involved, I am not simply a mixture of my parent's DNA. Processes like chromosomal crossover ensure that a significant part of my genome is original so to speak. Therefore I doubt you can reconstruct a genealogy from this information.

@terdon: recombination is easily modellable. I'm pretty much sure it is possible even with relatively sparse genotypic data, not to talk about whole genomes.

@har-wradim how can it be modeled? It is a largely stochastic process so I don't see how you could infer my parent's genomes from mine.

@terdon: it's not completely stochastic on the one hand and many stochastic processes are modelled on the other. You are still nearly 50% identical to each one of your parents and this identity covers long stretches of DNA.

@terdon: The task is not to infer your parents' genomes - the task is to find them in a set of genomes known beforehand.

@terdon: but, could you tell someone's parents from someone's two children?

@har-wradim re not completely stochastic: no it's not, that's why I said largely. As for choosing the right genome from a set, absolutely, that's a completely different proposition. However, in the OP we have to choose between siblings or mother/daughter so we don't have a set to choose from, we need to decide which hypothesis fits the data. That's what I don't think is possible but this is way out of my field so I don't pretend to know.

No, it is not possible to determine ancestry with just two DNA samples, but it is possible with three: http://www.nature.com/nature/journal/v487/n7407/full/nature11251.html.
Essentially, each sequence region in the progeny can be traced to either the mother or the father, but you really need both sequences to have any confidence.  That would get you one node on your tree.  You would need additional samples from higher generations to rebuild an entire ancestry.
However, it might be possible with hundreds of samples from laterally related individuals.  In fact, I think this is the fundamental hypothesis of the 1000 genome project, http://en.wikipedia.org/wiki/1000_Genomes_Project, and it pretty much worked.  Isolated populations can be discriminated by broad DNA sequence analysis.
To reconstruct your tree for a single ancestry, you would just want to use more closely related individuals (many, many of them), and then generate a phylogenetic tree, which should roughly correspond to the family tree you are investigating.


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Evolving a smaller brain
In Kurt Vonnegut's novel Galapagos, a certain mammal species, due to drastic and peculiar environmental changes, evolves (among other features) a smaller and smaller brain.
Has this ever happened? Are we aware of any species whose ancestors had remarkably bigger brains?

Could these be an example of island dwarfism affecting a human-like species?

Brain size vs intelligence
Of course brain size and intelligence are two very different things. Sure these two characteristics are correlated (assuming we manage to define intelligence in any intelligible way). The sperm whale has a brain that is 8 times larger than the human brain for example and the Brown thrasher (small bird) can learn thousands of songs while other birds can memorize the location of thousands of seeds. So really size is not the only thing that matters.
You might want to read about brain-to-body mass ratio and the encephalzation quotient.
Evolution toward smaller brain size
I am pretty sure such examples should exist but it might be hard to come up with good citation on the subject because

It is hard to tell other than through fossil record how big was the brain of a certain ancestor
It is quite a specific question

Someone might well come up with good answers. Of course, most examples of evolution toward smaller size (such as through insular isolation as pointed out by @user137) will result is reduction in brain size however, I am not sure these example would satisfy your needs/curiosity.
Evidence of metabolic cost of brains
In the meantime, I would like to point to a few among many evidences that brain comes at a fitness cost (that might be compensated by benefits of learning and other "brain abilities"). Those evidence mainly comes from experimental evolution in labs but some comes from comparative genomics as well. In short:
Brain consumes a lot of energy (Magistretti 2013). There are evidences in Drosophila (Mery and Kawecki 2003), birds (in this review I think: Nowcki et al. 2001) and guppy (Kotrshal et al. 2013) that evolution of learning abilities comes at an important metabolic cost. Johnston (1982), and more recently Snell-Rood et al. (2009) made reviews on the cost and benefits of learning abilities that you might want to have a look at.

Thank you, I'll read the resources you linked. Just one thing: the key word in my question is drastic: I'm not looking for a little reduction in brain size, but to a great one, so much that it almost certainly must involve a reduction in intelligence.

@giorgian I expanded the first part a little bit just to give an indirect justification of the importance of this part ;)

The acanthonus armatus is famous for its small brain. As a deep-sea fish it is required by its environment to consume very little energy, and so it is at least plausible that this is an adaptation to its environment. It's hard to compare it to the fossil record because brain size is usually estimated by the size of the cranial cavity, but a. armatus has a fairly ordinary cranial cavity .It is very nearly empty, with the small brain filling only a small fraction (dwarfed by the semicircular canals). The authors of the paper linked above weighed a number of brains, the largest of which was 48.7 mg in a 180 g fish.


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What is the correct medical procedure(s) for taking a resting heart rate?
Note: I thought the Biology stack exchange would suit this question better than the Fitness stack exchange. Please let me know in the comments if this is not suitable here.
I am interested in tracking my resting heart rate as it decreases with aerobic training.
At the moment I take it immediately after I have woken up before I get up out of bed.

What is the correct medical procedure(s) for taking a resting heart rate?
I'm aware a standardized procedure is important but what about:

Body position: Should I be sitting or lying down?
Heart rate: Should I take the lowest value or an average HR?
What duration should I take it for?
How relaxed should I be?

In an academic situation how would one reliably take resting a heart rate?
Please include answers that can be referenced to scientific or medical literature.

1) According to this article you should be taking it in the most preferred position you want. It would change according to the position you are in so make yourself comfortable sitting or lying down (reference).
2) You take the number of beats of your heart in a minute. If you take the number of beats for 2 minutes, then average your count by 2.
3) One minute (reference).
4) Completely relaxed, most articles recommend taking it in the morning while waking up so you are doing the right thing (reference).
I don't understand what you mean by an academic situation so I could try and answer it if you clarified it.


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Sexual selection in cats or other animals
I was wondering if you could answer some of my questions regarding sexual selection in cats (or any other animals). I would like to apologize beforehand for my incorrect term use.

When it comes to mate choice, is mutual choice for both males and females the norm? If not, is it mostly a tomcat or a female cat who does the choosing?
Do female cats always have freedom to choose, or is it more like a rape or consensual sex?
How do cats choose their prospective partners in the wild, what are the mechanics of this process? Does a prospective partner come with the territory or are there any courtship rituals? I am interested in mate availability for female cats and sexual selection from a female cat perspective.

Thank you very much in advance.
P.S. Any other animals will do if they do not live in groups, prides or harems. I am interested in individual choices.

Are you also interested in lions ? (Technically, they are also cats.) I can help you with that , if you are interested.

Yes, thank you, that would be nice to know. Maybe they have the same behavior patterns.

Wilson and Reeder (Mammal Species of the World) count 40 species of Felidae. Most of them are small cats (subfamily Felinae). Lions are in the subfamily Pantherinae, which contains only 6 species, one of them the jaguar, Panthera onca, which is solitary, like the tiger, Panthera tigris. By what I know of small cats, Puma concolor included, and the tiger and the jaguar, it seems that lion social behavior is not typical of felines. (Would add that as a comment, but can't comment with reputation < 50).
EDIT:
Looking for "Felidae sexual selection" or 'Felidae "sexual selection"' in google I have found some links. Look for "sexual selection" or "Felidae" in the text. Though I'm afraid most of them are not exactly what you're looking for, maybe they can open new windows of thought. Hope that helps!
http://www.journals.elsevierhealth.com/periodicals/aaeth/article/0304-3762%2883%2990116-5/
http://www.catsg.org/cheetah/05_library/5_3_publications/E/Eaton_-_The_Evolution_of_Sociality_in_the_Felidae.pdf
http://onlinelibrary.wiley.com/doi/10.1111/j.1095-8312.2010.01520.x/pdf
http://www.jstor.org/discover/10.2307/3544917?uid=26584&uid=3737664&uid=5909624&uid=2&uid=26582&uid=3&uid=67&uid=62&sid=21103320511793
http://en.wikipedia.org/wiki/Machairodontinae
http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0048352?utm_source=feedburner&utm_medium=feed&utm_campaign=Feed%3A+plosone%2FPLoSONE+%28PLOS+ONE+Alerts%3A+New+Articles%29
http://books.google.com.br/books?id=FhvmHW972mAC&pg=PA752&lpg=PA752&dq=Felidae+%22sexual+selection%22&source=bl&ots=Ns8iRUQxXW&sig=r5ZEgp-nH9mll5cYgB5GzNaThZs&hl=en&sa=X&ei=FBPQUq63LPDLsQS0m4DAAw&ved=0CDYQ6AEwADgK#v=onepage&q=Felidae%20%22sexual%20selection%22&f=false
http://www.mapoflife.org/topics/topic_203_Baculum-%28penile-bone%29-in-mammals/
http://www.sciencedirect.com/science/article/pii/S0169534703003999

Thank you very much for your comment. If you could provide any links about female cats' sexual selection, I would be very grateful.

it would be great if you can make this more digestible.

Thanks for providing all those links. I will check them out!


text:
Why does a tumour's genome change depending on the environment?
According to the book "Primer of The Molecular Biology of Cancer" by Vincent, Theodore and Ateven, the tumour cell is changed depending on its environment.

performed genome-wide analysis on three tumor samples: a patient's primary breast tumor; her metastatic brain tumor, which formed despite therapy; and a xenograft tumor in a mouse, originating from the patient's breast tumor. They find that the primary tumor differs from the metastatic and xenograft tumors mainly in the prevalence of genomic mutations

Why the tumour cell changing on different places?
why suddenly the breast tumour cells changes on the xenograft tumour and why the metastasis on the brain are now different from the place they came from?
How does this alteration obtained? in the DNA or microRNA or something else?

Tumor cells can have very unstable genomes, as much of the error repair machinery is damaged or missing. Since the cells are rapidly dividing and the DNA gets duplicated each time a cell splits, more and more mutations accumulate as the tumor grows and metastasizes. Just like in evolution as a whole, mutations that are either neutral or help the cell survive better in its environment are kept, whereas cells that develop deleterious mutations (perhaps killing the cell outright, making it more visible to the immune system, or just giving it a growth disadvantage as compared to neighboring cells) either die out or get outnumbered by other cells. This is why, over time, tumors can become resistant to therapies intended to kill them, as their cells accumulate mutations that help it evade the treatment and keep growing. There may be a disadvantage that the cells might grow more slowly than the original ones, but since the original ones were killed by the treatment, the resistant ones survive. So, this means that a tumor is rarely homogeneous, with all the cells having the exact same genome. Deep sequencing using next-generation methods is being used to gather information on all the different mutations throughout a tumor, which can help doctors learn which mutations are most common and prescribe patient-specific combination therapy which can kill all the various cell populations at once.
So why are metastatic and xenografted tumors different from the parent? Metastases can arise from single cells or very small clumps of cells, and xenografts are generally made with very small pieces of tumor, so both may start with a different set of mutations than is common in the original tumor. As they grow and divide, as described above, they will become different from their parents. The surrounding environment definitely affects this: the amount of oxygen present, degree of vascularization and blood supply, number and kind of immune cells present, etc. With all these and more factors, a metastasis or xenograft will evolve differently than its parents.


text:
What is the relationship between migraines and histamine?
A family member suffers from migraines so I have been reading a little around the subject.
There seem to be any number of "triggers", but I have seen mention several times of the role of histamine in migraine activation as an active area of research. The suggestion is that high histamine levels in the body can cause migraines.
Is there solid evidence that histamine can trigger migraines?  How does this mechanism operate?

Yes, this is true.
Histamine is thought to induce the enzyme Nitric Oxide (NO) Synthase.  NO is then available to act locally on the vasculature as a vasodilator.
NO binds to guanylyl cyclase in vascular smooth muscle cells, which leads to the production of cyclic GMP, which in turn forms phosphorylated protein kinase G. PKG phosphorylates Ca2+ channels, slowing the influx of calcium into the cell, which leads to smooth muscle relaxation, and vasodilation, which leads to migraine.
The only silver lining is that there is a check in place: with the binding of histamine to H3 receptors on c-fibers in the central nervous system, feedback inhibition prevents the further release of histamine from these sites.
References:

Akerman S, Williamson DJ, Kaube H, Goadsby PJ. (2002).  The role of histamine in dural vessel dilation.  Brain Res. 956(1):96-102.
Gupta, S., Nahas, S.J.,Peterlin, B.L. (2011) Chemical Mediators of Migraine:
Preclinical and Clinical Observations.  Headache: The Journal of Head and Face Pain, 51(6): 1029–1045.

This seems to suggest that some sort of antihistamine would be effective in treating this class of migraine. Is that right?

@Poshpaws I didn't run across that information in any of the articles.  Perhaps, but without knowing more about the affinities of the antihistamines for the different types of receptors, the drug might bind to the H3 receptor just as readily and stop that valuable feedback inhibition.

I've experienced migraines for 10 years, and now for the last 14 months that I've taken anti histamine medicine to see if there would be a benifit I've had good results. The frequency has dropped from approx 3 times a month to a migraine approx every 6-8 weeks. For me thats a sizeable drop. The other benifit is the severity is less intense.
 Now I'm trying to find why my body produces too much histamine, so I hopefully can eliminate the anti histamine med's.
 Recently I've greatly reduced foods with refined sugar, also processed foods, and added more whole foods, and I'm seeing excellent results.

james, welcome to Bio.SE. As a science-based site, and one that is NOT for medical advice (please see the first point of the FAQ ) your answer is not really what we're looking for here. Personal experience is certainly appreciated in some types of answers ("this is the protocol I use for PCR, and it works great"), but here it's not really appropriate. Ideally, for this type of question which already has a good answer, you'd add to the science being discussed, and perhaps at the end add a quick personal touch if it's warranted.


text:
Filamentous algae - what exactly am I looking at?
I have just taken some images with my light microscope at 400x of  (what I think is) some form of filamentous algae from a local pond.
Now, I think I am looking at a single cell (centre) with some sort of arrangement of chloroplasts. Is this correct? Can anyone give me some more information on these structures?
I also have included a higher-constrast image of the specimen.

beautiful micrographs!  the chloroplast(s) look filamentous.

thanks @shigeta. I currently don't have a camera attachment so I had to hold my SLR up against the eyepiece!

It looks indeed like a Spirogyra, or at least a member of the Zygnematales.
And yes, the green things are the chloroplasts (or one long chloroplast?), and they are arranged in spiral.
The "empty" space in the middle is likely the nucleus, and the darker circles within the chloroplast(s) could be the starch accumulated at the periphery of pyrenoids.

Spirogyra. Apologies for the terse answer, but I think it does qualify.

also the name of a pop-jazz band of the 80s.

...and a 70s UK prog rock band before that!

ha no that's the one - i'm only remembering it from my uncles record collection, not from personal experience.  it was so progressive it didnt' sound like rock to me!

Further research reveals that they are now classed as " acid folk" which, as far as I recall, didn't exist as a genre back then. That's probably what confused you.

pond slime to 70's rock - i love it.


text:
How does laughing gas (N₂O) work?
Laughing gas (N2O), well, makes people laugh.
How does just a gas make us do that, there has to be some hormones at work...
So, I wanted to know how this works?  What is the mechanism?

This information is all strictly for Entonox - a brand of analgesic gas comprising 50% Oxygen (O2) and 50% Nitrous Oxide (N2O), Laughing Gas.  This mixture is known as 'Gas and Air' and is in very common use.
The active ingredient in Entonox is of course the nitrous oxide, so the discussion of the mechanism below refers solely to the N2O as you asked for.
Nitrous oxide enters the blood by diffusion from the alveoli whilst it is being inhaled, but does not bind with haemoglobin.  It is fat soluble so quickly moves into cells, including synapse ends in the brain.  Because of the stability of the compound, N2O is not metabolised by the body so has its effect as that molecule, then is eliminated by diffusion out of the lungs once inhalation has ceased (taking roughly 2 minutes for on and offset).
According to the material that BOC pharmaceuticals provide, the exact mechanism of the analgesia is not fully understood.  It is known, however, to induce "inconsistent changes in the basal levels of thalamic nuclei".
N2O inhibits NMDA receptors in the brain whilst simultaneously encouraging the stimulation of the parasympathetic GABA receptors.  This eventually produces an anaesthetic effect.  It is also understood that N2O promotes the release of endogenous opioid neurotransmitters ('natural painkillers' e.g. endorphins) that specifically activate descending pain pathways.  This inhibits the transmission of pain.  In this way the analgesia provided by nitrous oxide is antinociceptive (literally pain reducing) rather than a generalised limbic depressor.
However, nitrous oxide also positively effects potassium ion channels too [ref] - reducing the chance of an action potential being generated in affected neurons.  Research into this area of the effects of N2O is ongoing.
Euphoria is a common side effect of N2O usage, hence the name laughing gas.  This is as part of wider emotional changes that can occur when nitrous oxide is being administered.  For example, some people instead of laughing become scared or in other cases extremely aggressive towards those nearby. The emotional excitement may result in depressive or manic behaviour even to the point of psychosis and hallucinations especially in those who have a preexisting vulnerability to mental illness. The precise mechanism for these disinhibiting is again not fully understood.
Whilst it seems a lot of the answers are missing, the course I'm taking this information from is available online at Discover Entonox - modules 8-10 have relevance to this question.  It's free to register and view the materials, they're all nicely narrated with diagrams etc.

great answer ... but il just wait to see if others post something more

This answer lacks references. References to many of the facts stated are available.

@WYSIWYG this is very true, I'll try and go through it when I have a bit of time


text:
From a computer science perspective, how is DNA compared for various purposes?
I am very interested in privacy preserving technolgies, such as Microsoft PINQ and would like to see if this is applicable to DNA comparison.

Given that I don't have a background in biology, I would appreciate it if someone could tell me how DNA is represented in a computer (in computer science terms), and how DNA is compared in a binary format (or logical equivalent).

The privacy preserving technology I'm using allows the patient to have granular control over what DNA data they share, and how it's used. The receiving agency (medical research, FBI, fertility clinics) will receive cryptographic proof of a DNA result, without exposing all DNA values.
I suspect that each of the following use-cases focus on a certain subset of data, and if the same information was presented to all of them, it would be a breach of privacy:

Combined DNA Index System, or CODIS
State DNA index system (SDIS)
National DNA Index System (NDIS)
FBI's 13-Loci
Other government's DNA matching requirements for inclusion/exclusion
Disease susceptibility via single nucleotide polymorphism (SNP), and related heredity
Paternity tests
Evolutionary patterns

Furthermore, based on my independent research, I understand that there are many ways to determine the DNA of a given sample.  What I don't understand is if every test has the same output? (e.g. are all chromosomes are returned, vs only 23? (or less))
The value-add I am trying to provide the patient privacy, while fulfilling all legal, moral, and ethical disclosures of data requested of them.  The recipient will have assurance the data is authentic, despite the inherent double blinding of the field data.
The cryptography allows for

Redacting (or black out) certain values
Anonymously compare a numerical value, (greater than, less than, equal to) without disclosing that value.
Prove, or verifiably disprove, that a value is not in a certain list of arbitrary values.
The agency to know which DNA testing firm generated the results
The DNA testing firm to not know who the patient is, especially in cases of partial disclosure of DNA data.

Your response will help me contribute what I believe to be the moral, ethical, and socially responsible way to handling PII and DNA data.  (yes it will be open source)

DNA sequences are typically stored in FASTA format. There are indeed many methods to sequence DNA, on which depends the data that is returned (ie the output) and the analysis required. You're not going to sequence all 46 chromosomes in a single experiment. Analysis of CODIS markers, for example, only requires amplification of specific short tandem repeats (STRs) and does not even require sequencing.

DNA sequences are usually compared using BLAST (https://en.wikipedia.org/wiki/BLAST), which breaks sequences into short words which can be searched efficiently. However, that does require having entire sequences around somewhere, which might be a privacy violation.

From a computer science perspective, there's nothing at all special about DNA. It's stored as a simple ASCII text file consisting of repetitions of 4-15 different letters.
DNA, the molecule, is a long chain of nearly identical smaller molecules (nucleotides) joined together. The nucleotides differ only in which of four possible bases (A,C,T/U or G) they have attached. Therefore, when representing a DNA sequence, we only need to represent the bases.
There are also the so-called "ambiguity codes" which represent different possibilities:
IUPAC Code   Meaning
  A            A
  C            C
  G            G
  T/U          T
  M            A or C
  R            A or G
  W            A or T
  S            C or G
  Y            C or T
  K            G or T
  V            A or C or G
  H            A or C or T
  D            A or G or T
  B            C or G or T
  N            G or A or T or C

The vast majority of sequences, however, won't use the ambiguity codes and will only have A,C,T,G and the occasional N.
The most common DNA sequence format is FASTA, which consists of one or more sequences each of which has a header (lines beginning with a >) and 60-character long sequences. This, for example, is an excerpt of human chromosome 17:
>chr17
AAGCTTCTCACCCTGTTCCTGCATAGATAATTGCATGACAATTGCCTTGT
CCCTGCTGAATGTGCTCTGGGGTCTCTGGGGTCTCACCCACGACCAACTC
CCTGGGCCTGGCACCAGGGAGCTTAACAAACATCTGTCCAGCGAATACCT
GCATCCCTAGAAGTGAAGCCACCGCCCAAAGACACGCCCATGTCCAGCTT
AACCTGCATCCCTAGAAGTGAAGGCACCGCCCAAAGACACGCCCATGTCC
AGCTTATTCTGCCCAGTTCCTCTCCAGAAAGGCTGCATGGTTGACACACA
GTGcctgcgacaaagctgaatgctatcatttaaaaactccttgctggttt
gagaggcagaaaatgatatctcatagttgctttactttgcatattttAAA
ATTGTGACTTTCATGGCATAAATAATACTGGTTTATTACAGAAGCACTAG
AAAATGCATGTGGACAAAAGTTGGGATTAGGAGagagaaatgaagacata

So, in conclusion, there's nothing special about DNA. If you're writing software that compares DNA sequences, you are writing software that compares ASCII text. You can hash it, salt it and anything else you might want to do.
The only thing you should be aware of is that minor variations are very rarely meaningful. The level of identity you will need will depend on the precise biological question being asked but as a general rule, a single nucleotide difference is as likely to be a sequencing error as a real difference. You will need to collaborate with biologists in order to set up the right threshold for whatever your project is looking at.

Thanks this is a great primer! Do you know why some letters are lowercase? Also do you know where I can find sample data for any of the above listed purposes (paternity, disease testing, other examples...)?

@LamonteCristo lower case can mean various things depending on the source of the sequence. It is often used to indicate i) low quality data, cases where sequencing errors are likely or ii) masked sequences, repetitive elements and the like. You probably don't need to worry about it. As for sample data, no, sorry. I've never worked with that sort of thing. Sample sequences in general are trivial to fins (have a look at the NCBI nucleotide database.


text:
What industry regulations protect the privacy of DNA results in the US? (UK, or EU wanted as well)
I am writing computer software that allows users to learn more about their own DNA and (optionally) allow some of that data to be used for research purposes.
I'm very concerned about a future/theoretical situation in which an insurance company uses that DNA data to disqualify someone on the basis of pre-existing conditions.
Question

What privacy regulations exist that would assure users that there is no insurance risk in a collecting information about one's own DNA? (Primarily interested in the USA, but UK and EU would be valuable)
Outside of legal regulations, what should users look for when shopping among providers? (for quality, scope of services provided, etc)

There might be different regulations in different parts of the world. Maybe you want to specify a country/area.

I'm voting to close this question as off-topic because it is not about biology.

That might be a question for Law.SE. I am voting to close for the same reason than canadianer

While the subject is biology based, ethics and laws are not... so I am voting for closure as well.


text:
Did the Zika virus mutate?
The Zika virus was already present and known to the world (mostly in Southeast Asia) before the current outbreak.
Why has the virus caused such an extreme outbreak?
Has it mutated from its ancestral form such as that found in Southeast Asia?

There is one main answer to this question: The Zika virus spreads so fast because it never emerged in this part of the world. Hence there is no natural immunity available in the population and a lot of infections occur. Once this "first wave" of infections is over, the level within the population will fall drastically. Some more information on this topic can be found here.
It is of course possible that the Zika virus has acquired a new mutation which adapts it better to humans and allows spreading much easier, but this is not yet known, since the situation in South America is still changing very fast with a lot of cases occurring and analysis going on. It still can be enough that the virus never emerged in Southern America and that there is no natural immunity available.
According to the paper in reference 1 (which is only a brief communication) the sequences of the envelope proteins of the virus are similar to the strains circulating in Asia and do not carry novel mutations:

The Surinam strains are the ones published in the paper mentioned above and are from South America. I haven't (yet) found any other analysis, but this will only be a matter of time. At the moment we cannot make a final statement on this although there is some speculation around.
Edit 23/02/2016: There is still no final conclusion available, but there is an interesting paper available on the Biorxiv-Preprintserver, which analyses the mutation rate in the genomes of the publically available strains. It can be found in reference 2.
Based on the available genomes, the author calculates the mutation rate of the Zika virus to about 10 Mutations/year. The virus is a RNA virus which have generally higher mutation rates than DNA viruses.
In the analysis he finds a number of non-synonymous mutations (mutations which lead to a basepair exchange), as seen in table 2:

Especially named is the M2634V mutation, but since this is in one of the envelope proteins, the author finds it relatively unlikely (although not completely), that this causes a much higher mutation rate.
In the Diskussion of the paper he writes:

The sudden spread of Zika to South and Central America does not appear
  to have been due any particular change in the mosquito vector or
  anything to make the Zika virus itself more virulent. But rather from
  the fact that infected people are now able to fly rapidly from country
  to country, thereby spreading the disease extremely easily. This means
  there is little to stop the epidemic continuing to spread to further
  areas of population which have little, if any, herd immunity against
  the virus.

Edit (23.10.2016): There is now an interesting website which builds a realtime phylogenetic tree from the data published (it can be found here). The data also shows where in the virus the mutations occur:

References:

Zika virus genome from the Americas
ZIKA - How Fast Does This Virus Mutate ?

A mutation isn't necessary to explain the outbreak in the Americas, given the low immunity of the population, but there is tentative evidence that this strain of the Asian lineage of the virus may have developed some novel characteristics, which appear likely to have first emerged in the South Pacific.
The virus in Brazil is very similar to the form that drove a 2013 outbreak in French Polynesia:

Phylogenetic studies showed that the closest strain to the one that emerged in Brazil was isolated from samples from case-patients in French Polynesia and spread among the Pacific Islands

Two of the novel features of the Brazil outbreak were also seen in French Polynesia in 2013:

WHO note that, like in Brazil, it was concurrent with a rise in the auto-immune condition Guillain-Barré syndrome, which can cause paralysis:

During the first outbreak of Zika from 2013 - 2014 in French Polynesia, which also coincided with an ongoing outbreak of dengue, national health authorities reported an unusual increase in Guillain-Barré syndrome

While they didn't notice it at the time, a retrospective analysis in French Polynesia prompted by the Brazil outbreak noted that their outbreak had also been concurrent with an increase in cases of microcephaly. I can't find a primary source but here's a quote from  Dr. Lyle Petersen, director of CDC's  vector borne diseases division, taken from an official CDC briefing transcript:

...in French Polynesia where an outbreak occurred which involved more than 30,000 persons retrospectively after the Brazilian data became available - they went back and looked and saw an increase in microcephaly cases in their area

It has been theorised that it may have mutated significantly, for example by Flaminia Catteruccia, associate professor of immunology and infectious diseases at Harvard T.H. Chan School of Public Health, who concludes:

What is worrying is that we don’t know what may have changed, and why. There need to be genetic studies to understand the origin of this virus.

It's been a profound backdrop to the American anti-vaccine movement I've witnessed, when you see what happens in a population with no intrinsic immunity. WHO advertently just declared Zika an emergency.

There is no need to speculate, the complete genome sequence of an isolate from the Americas has been published and can be compared to earlier isolates. These data show that the genome is very close to the sequence of the virus isolated from French Polynesia.

"Very close to the sequence" still allows potential for mutation causing the spread, so this is still speculative and therefore misleadingly assertive - a single nucleotide point mutation could explain it

For those viewing this in the LQP queue - just because an answer may be incorrect or lacking details does not necessarily make it low quality or a target for deletion. It is an attempt to answer the question. If you don't like it, simply down-vote.