How do small animals make loud sounds? Walking past the park today, I heard a cicada so loud I thought at first it must be some sort of large power tool. How is it that that very small animals like cicadas (crickets, etc.) can make such loud sounds? It seems intuitive that larger animals should be able to make louder sounds, but perhaps:

a) I just fundamentally misunderstand the physics involved

b) A theoretical larger animal should be able to make louder sounds, but cicadas are just extremely efficient, making up for their small size

c) ?

The Cicada

A careful study of the noise-making apparatus of the cicada can be found in a 1994 paper by Young and Bennet-Clark.$^1$ The authors generated sounds at about 0-16 kHz at peaks on the order of 100 dB using cicadas in various stages of deconstruction.  The cicada uses a resonant organ-system called the tymbal which buckles and unbuckles rapidly to produce sound. The buckling-in is caused by muscle contraction and is louder than the buckling-out (relaxation) phase. Air sacs (a feature of many other small noisemakers) serve to amplify the sound.  The tymbal itself, for the species in this paper, has a resonant frequency of about 4kHz (Young, page 1017). The song of the cicada as modified/amplified by air sacs and other structures, is often around 10kHz.$^{2}$

Pure Tone vs. Diffuse Tone?

The vocalizations of large vertebrates are a complex superposition of waves that in the frequency spectrum are somewhat spread out. To the extent that a frog or a bird emits a pure tone, the energy will be confined to a narrow frequency range and this may be a strategy for achieving greater amplitude. Given comparable audio sensitivity, however, the intensity of pure tones will depend on amplitude (intensity), regardless of frequency.$^{3,4}$

Other Small Loud Animals

While the songs of cicadas are intense, especially in concert, on an individual level there is competition from other species. According to a Gizmodo article quoting assorted scientists, the snapping shrimp produces a transient snap that is around 200 decibels, a level that one site describes as "deafening." For perspective, dolphins can emit short chirps of 220 dB but these are outside the range of human hearing. The lion emits a roar of 115 dB which is sustained and audible 5 miles away, according to the article. Elephants also are capable of 117 dB cries, as are howler monkeys.

Both the shrimp and the cicada use non-vocal vibration to create their sounds. The shrimp uses a "spring-loaded claw" (the spring is muscle). The localized force of one part of the claw hitting the other generates a bubble (this is known as inertial cavitation). When the bubble collapses it generates a shock wave (noise) that stuns fish (prey).$^5$ The noise of frogs is produced as air passes from the lungs through the larynx, amplified by distended air sacs which resonate. Birds can produce up to 135dB (the Mollucan Cockatoo). They generally force air past (membranes and) a specialized organ called the syrinx located at the bottom of the trachea (see the Wikipedia note on bird vocalization).

Micronecta scholtzi, a 2mm-long aquatic insect, is for its size the loudest known animal. It creates a sound of 99.2 dB intensity which (despite being largely lost in transition from water to air) is audible to humans ashore. According to the Wikipedia note it creates this sound by "stridulating a ridge on its penis across corrugations on its abdomen." The area involved is about 50$\mu m$ across. Details of the mechanism are poorly understood. The article's comparison of the sperm whale's 236 (underwater) dB song gives perspective, as a sperm whale can weigh 14 metric tons.

A Common Aspect of Sound Intensity: Cavity Resonance

Descriptive studies of sound-creation by small animals (with the possible exception of the snapping shrimp) do not fully explain why a one-gram bug can make a bigger noise than a lion. Purely vocal methods of larger vertebrates produce sustained noise on the order of 100 dB but the non-vocal instruments of smaller creatures are capable of short bursts of amazing intensity.

It is difficult to generalize but because air sacs are part of many sound-making schemes, cavity resonance probably plays an important role. Like spring-mass systems or RLC circuits, cavities have resonant frequencies at which amplitude of a signal may be increased (the policeman's whistle is a familiar example). Another paper by Bennet-Clark and Young gives a sketch of a theory along these lines. At resonant frequencies the impedance of the instrument falls sharply and instead of being dissipated (generally as heat) the energy emerges as sound.$^6$

$^1$ Bennet-Clark and Young, The Role of the Tymbal in Cicada Sound Production, J. of Experimental Biol. (1995) 198, 1001-1019.

$^{2}$ The frequency of cicadas is variable, mostly on the order of 10kHz but occasionally very low (< 1kHz), mostly due to body size. See this article.

$^3$ Sound--essentially a compression wave--diminishes with distance. So when the Wiki article on noise levels compares noise levels it includes the distance from the object. For example, 100 db (comparable to the cicada) is the level of noise associated with a jack-hammer at 1 meter away.

$^4$ Audible range for humans is roughly 15 Hz-16000 Hz. As mentioned below, the dolphin can emit very intense high-pitched sounds that we don't hear at all, so the analogy to EM waves (higher frequency = higher energy) doesn't help predict perception. See Pfaff and Stecker, Loudness and Frequency Content of Noise in the Animal House, Lab. Animals (1976) 10, 111-117.

$^5$ M. Versluis, B. Schmitz, A von der Heydt & D. Lohse (2000). "How snapping shrimp snap: through cavitating bubbles". Science 289 (5487): 2114–2117.

$^6$ Bennet-Clark and Young, Short Communication, The Scaling of Song Frequency in Cicadas, J. Exp. Biol. 191, 291-294 (1994).


Theoretically, is domestication of (virtually) any animal possible? Looking at ones that manage well alongside us human animals, such as dogs and cats, we see that this is possible for evolved, distant animals to have heritable, preferable traits around people. However, when especially looking at lions and the like, it doesn't seem to work out as well.

Some people have tigers as pets, but in general it is believed that they are more "wild" and not as tame and domesticated as other animals (such as dogs and cats).

Is it possible to selectively breed and enable any animal to be more like dogs and cats? Even sharks? Tigers? Alligators?

If domestication worked so well with dogs and cats, such as them living (for the most part) peacefully and well with people, wouldn't the process be beneficial for other animals so we could all live better side-by-side?

In short, can you theoretically get any animal to have heritable traits?

As the previous answers clarify, all organisms have heritable traits that may be manipulated through selective breeding. It is the pragmatics that can be prohibitively challenging. From an (zoo)archaeological point of view, few animals have actually been domesticated, and only recently in our species' history. The dog is an unusual case, perhaps domesticated 14,000 years ago; most domesticated animals only show skeletal changes within the last 10,000 years. Cats, compared to livestock's total dependence on humans, are 'barely' domesticated--they got used to humans while camping out in Egyptian storehouses where all the mice were, perhaps around 4,000 years ago, but even today a fluffy house cat will revert to a feral state if abandoned.

Many animals are behaviourally unsuitable for domestication. If an animal is dangerously aggressive, for example, they cannot be penned and isolated--so the many controlled generations it takes to reduce their baseline aggression cannot occur. Humans also tend to co-opt pre-existing social structures in a species, such as becoming the 'alpha' in a dog pack or the head 'ram' of a sheep herd. Species without a hierarchy or herd mentality are difficult to control and keep track of, and so do not lend themselves to human care.

You mentioned tigers in your question. Tigers have little to offer people (other than pelts), they're massive/aggressive, and they're jungle loners. You can't raise a herd of tigers; they'll kill each other and the survivor will kill you. That they're carnivores is also challenging, since a carnivore is much more expensive to feed than a bunch of grass-munching sheep. Altogether, there was never a situation in prehistory that would have turned tigers into giant house cats. House cats eat unwanted mice; tigers eat your cattle (and children). The occasional tiger 'pet' won't change that.

Domestication, outside of recent experiments (like the Russian foxes mentioned above), has always been a protracted, indirect process. People started interfering with animals that were already useful in some way(s). Dogs offer warmth, hunting aid, defence, transport, and (in a pinch) food. Alligators, tigers, and sharks are not useful enough to make the danger and cost of raising them worthwhile. Even if you did eventually produce a 'human-friendly' shark, there would still be a 'wild' population ready to eat you--and your complacent pet sharks, too!

For a very readable explanation, try the chapter on domestication in Jared Diamond's (1997) Guns, Germs, and Steel.


Is synthesizing DNA in-house feasible? I've been reading up about DNA writing, and it seems there are machines available around the five-figure US dollar mark for DNA synthesis, and I'm considering picking one up for my lab.
We normally order our DNA/oligos from IDT and similar companies, and for cutting down cycle time from a few days with next-day shipping to a few hours with in-house printing, as well as potentially saving on cost with enough scale (how much is enough scale?), this seems really promising for our lab.
Is this a reasonable thing to do?

So far as I'm aware, the big distinction right now is whether you want dsDNA or oligos.
If you often want lots of oligos, then getting your own synthesizer likely makes sense. Run the numbers and see what the time for return on investment will be and you'll see if it works for you financially.
If you want gene-scale dsDNA, you're currently generally better off getting a specialist company involved (or a foundry, if you've got one that you can access). Not only do they have economies of scale, but they have a lot of experience figuring out how to handle difficult sequences and assemblies.  If you take it all in house you might appear to save money but actually end up losing significant money and time when you count in the time and frustration that your lab ends up spending to go from oligos to genes.
If you've got particular expertise or highly specialized needs, it's a whole different story, but that doesn't sound like the case based on your question.
Note that there are a number of desktop synthesis companies that are working to make this answer obsolete right now, and it may well change quickly in the future.


What part of the brain controls depth perception? Specifically the part of the brain that does depth perception based on binocular vision. I have searched all over the web and have turned up nothing. Is it the same part of the brain that processes all images from the retina?

According to the article: Scientists uncover second depth-perception method in the brain:

  the neurons in the middle temporal area of the brain are combining visual information and physical movement to extract depth information

This Scientific American article states that there is a process involved:

  Visual-image processing from the eye to the brain happens in stages. Rudimentary features such as the orientation of edges, direction of motion, color, and so on are extracted early on in areas called V1 and V2 before reaching the next stages in the visual-processing hierarchy for a progressively more refined analysis. This stage-by-stage description is a caricature; many pathways go “back” from stage to stage—allowing the brain to play a kind of 20-questions game to arrive at a solution after successive iterations.

This process is discussed further in this article with what is known as the Laminart model.


Why does the gc content deviate from 50% in prokaryotes I have read quite some articles but I can't figure out the main reason for gc content deviation in prokaryotes. In eukaryotes I can understand it, because the genome isn't composed at random, like TATA boxes and CpG island, because they are important for functioning in the production of proteins.

However in prokaryotes there is such a variety, GC% is ranging from 20% up to 70%. Most of the time it depends on the environment, high temperature needs a stable genome (= high gc content).

I also read the answer to this question How does GC-content evolve? however it's still not clear to me. I hope someone can explain the deviation a little bit more.

Question

Prokaryotes have an AT drift, but what mechanism causes some of these bacteria to higher their GC% instead of lowering it.

Interesting question. I think that bacterial GC content diversity boils down to a mix of mutational biases, such as using different polymerase and replication/repair gene isoforms, and environmental pressures, such as temperature and salinity, that have placed different selection pressures on the various microbes.

I would read over the linked papers for more detailed info, but at least in broad strokes, I think that the two mechanisms listed above account for most of the observed variance.

NB: This isn't my main field, so you might get a more detailed answer if an actual microbiologist weighs in. :-)


Why do we get runny noses in the cold? The most annoying thing for me about being cold is a runny nose. Is there an advantage to having a runny nose when cold? What does having a runny nose achieve?

There are two reasons for this:

Nasal mucus helps warm inhaled air before it reaches the lungs. In cold weather, the mucus tends to dry out, so the membranes increase their production.
At the same time, exhaled air is warmer than the surrounding air, so it contains more moisture than the outside air can hold. This moisture condenses around the tip of the nose.

Explanation found here.

So there's no particular advantage to getting a runny nose; it's just a normal reaction occurring in extreme conditions.


How to Calculate how many times an enzyme would cut a plasmid I'm a little confused as to how to figure out the formula needed to figure this out.

I have a plasmid that is 7.3Kb and am told that it is cut with an enzyme of 4bp. For some reason I thought that the formula needed to figure this out is:

(1/4)^4 x 7300

But it gives me such a low number that I don't think it's right so I'm just a little confused.

There are $4^4$ 4-cutters, which means that given a 4 cutter, you expect it to cut once every 256 bases on average. $7300/256 = 28.5$, so you expect 28 or 29 cut sites in the plasmid. This is identical to what you calculated.


Why does the insulin taken from pig when injected into humans causes allergy but not the insulin taken from bacteria? At earlier times, insulin was injected to human patients that were taken from pigs and horses. But that caused allergy it seems.

But why is the insulin produced by the recombinant bacteria not causing such types of allergy?

Proteins and peptides vary across species, even if we give them the same name. Some are very homologous among even distantly related organisms, others differ even within a genus. Of course there are also variations across individuals of the same species.

Insulin from pigs and horses is pig or horse insulin. It differs slightly from human insulin because the genes that encode insulin in pigs and horses are slightly different than the genes that encode insulin in humans.

We inserted the genes responsible for producing insulin in humans into bacteria, so the insulin produced by recombinant bacteria is actually human insulin. That's why it doesn't produce an immune response.

There is also the issue of isolation and purification, and it is easier to produce very pure insulin free of other contaminants from recombinant sources than from animal sources.

That's the idea, anyways. Many humans tolerate porcine insulin just fine, and it isn't necessarily clear that human insulin is actually better (for example, this study).


Possible for bacteria to burst container? This is kind of a thought experiment, but are there any conditions under which bacteria could multiply enough to burst the container they're in?

Thoughts so far: Bacteria often need oxygen to multiply, but I believe not always? They need a food source, but perhaps despite that mass already being present they might still have a larger overall volume afterwards?

For the sake of this question, I'd like to be fairly loose with the word "container", i.e. not necessarily something solid glass or even solid for that matter, but at least closed. Perhaps I could have bacteria in a bubble and they could burst that?

Thanks for indulging!

Yes. Bacteria (and fungi) can digest sugar to produce CO2 gas. The latter occupies more space, and can burst contains such as closely sealed bottles (e.g.: for a bacteria / yeast co-culture: http://kombuchahome.com/how-to-prevent-your-kombucha-bottles-from-exploding/ )


Why are genes expressed as proteins rather than other types of bio-molecules? I guess, we could infer that the structure of an amino acid has the same functional units as RNA is used to synthesise it. Therefore, from a logical point of view it would make sense that genes are expressed as proteins.
However, why is this the case; why are genes expressed as proteins rather than any other type of bio molecules? Also, from what are other bio molecules expressed if not for genes?

Wow - like a biophilosophy question! The answer lies in in building up the largest diversity with minimal subunits. Efficiency if you will. In this case we are talking about amino acids. We only need 20 of them to approach unfathomable numbers of diversity.

The protein acts as a messenger, as an enzyme, a carrier and it's own building unit. If you wanted that kind of range out of any other known biomolecules, you would need a gene to code for each of them, and itself a gene a completely different mechanism to build them which we can't even fathom. It's so much simpler to code for a protein, which can act as an enzyme to build other biomolecules.

However if you are asking about why the central dogma of molecular biology is the way it is...well then, it seems to be axiomatic.


is it necessary that every theca of an angiospermic anther must contain two microsporangia i basically don't know the procedure or sequence of steps involved in the formation of anthers but i have read it somewhere it is formed from the dedifferentiation of shoot apical meristem of the axillary bud through mitotic divisions

so is it necessary that every theca of an anther of an angiosperm must contain two microsporangia, if yes then why are they two in number., can i get an account on the development of microsporangial lobes [here i am not asking about the process of development of pollen grains in them].

i am asking how the microsporangial lobes itself are formed

a diagrammatic answer would be highly appreciated

Is the necessary that stamens have two microsporangia per theca? No. Many species in Cryptocarya group of Lauraceae have microsporangia that have fused such that they have only two microsporangia instead of the typical four (Rohwer et al. 2014). I interpret their description as saying that the microsporangia within a theca but it's not clearly stated as such.

Within the Magnoliidae, one pollen sac of a theca is lost is some taxa (Endress et al. 2008). Evolutionarily, the Hamamelidaceae have reduced the number of pollen sacs from two to one (Endress 1989). I could not find examples of plants with more than two microsporangia per theca.

Why do most plants have two pollen sacs per theca?  It's probably a result of the evolutionary history of plants in general because it is so common. Even those that have only a single pollen sac seems to start out developmentally with two.  It's probably due to the underlying genetics.

The genetics of floral development is complex but being slowly teased apart. The overall development of floral patterns is set by a group of developmental or regulatory$^1$ genes called MADS genes.  Collectively, the MADS genes (along with other regulatory genes) control the overall organization of the flower structure. For example, MADS genes determine the arrangement of floral whorls from sepals (outermost whorl) to petals to stamens to carpals (innermost whorl). Changes in use or timing of the MADS genes can contribute to different types of floral morphology, such as the loss of sepals or big, showy sepals but no petals.

Some of these same MADS genes contribute to the formation of the stamen structure. The review by Goldberg et al. (1993) gives a thorough but now dated review of the developmental genes that control anther development. The figure below (their figure 3) gives a nice overview of the stages that lead to development of the theca with two microsporangia and ultimately to the final stage of fertilization. Even more specific, Bowman et al. (1991) show that AGAMOUS is one regulatory gene that is active during the development of the theca and microsporangia.

I can't speak in detail about how regulatory genes work in flowers (I know a bit more about regulatory genes in animal development, especially from an evolutionary developmental perspective). In animals, regulatory genes often work by concentration gradients, both by the concentration of the regulatory gene itself, by the concentration of other regulatory genes, and by the concentration of the regulated genes. This process helps to determine the anterior-posterior axis in animals with bilateral symmetry, as well as the left and right sides.

I suspect that floral regulatory genes work in a similar fashion.  Changes in regulatory expression can lead to bilaterally symmetric flowers (think of mint flowers, monkey flowers, etc. See Hileman and Cubas (2009 for a good review.). I suspect it is some type of symmetric expression of regulatory genes that leads to the formation of two microsporangia per theca.  Mutations that cause changes in the expression patterns of other regulatory genes can cause the initial expression but subsequent loss of one of the microsporangia, as noted for the Lauraceae and the Hamamelidaceae.

Footnote

Broadly but simply, regulatory genes are genes such as transcription factors that regulate or control the expression of other genes.

Literature Cited

Bowman, J.L., et al. 1991. Expression of the Arabidopsis floral homeotic gene AGAMOUS is restricted to specific cell types late in flower development. The Plant Cell 3: 749-758.

Endress, P.K. 1989. Aspects of evolutionary differentiation of the Hamamelidaceae and the Lower Hamamelididae. Plant Systematics and Evolution 162: 193-211.

Endress, P.K. and L.D. Hufford. 2008. The diversity of stamen structures and dehiscence patterns among Magnoliidae. Botanical Journal fo the Linnean Society 100: 45-85.

Goldberg, R.B., et al. 1993. Anther development: Basic principles and practical applications. The Plant Cell 5: 1217-1229.

Hileman, L.C. and P. Cubas. 2009. An expanded evolutionary role for flower symmetry genes. Journal of Biology 8: 90.

Rohwer, J.G., et al. 2014. A phylogenetic analysis of the Cryptocarya group (Lauraceae), and relationships of Dahlgrenodendron, Sinopora, Triadodaphne, and Yasunia. Phytotaxa 158: 111-132.


How could one calculate the gene flow between two populations? Imagine there are two populations X and Y, and for each population you have the genotypes of each individual in that population (e.g. Aa, AA, aa, etc.), but for multiple loci (e.g. AABb).

How could one calculate the gene flow between population X and population Y?

An answer would ideally recommend either or:

An R/Python/C++ library, or any other software tool
the breakdown of the maths, for which I would be much obliged, but not entirely necessary in the answer

Background reading

Indirect measures of gene flow and migration: FST≠$\frac{1}{4Nm+1}$

Related questions

Variance in Fst in the infinite island model (by Remi.b)

Theoretical Background

From Slatkin 1991, at equilibrium

$$F_{ST} = \frac{1}{1+4Nm\left( \frac {d}{d-1} \right) ^2}$$

, where $N$ is the per island population size, $m$ is the migration rate and $d$ is the number of islands ($d$ stands for "deme"). As $d \rightarrow \infty$, $\left( \frac {d}{d-1} \right) ^2 \rightarrow 1$ and Slatkin equation becomes the standard Wright's equation $F_{ST} = \frac{1}{1+4Nm}$.

From the above, it is easy to show that

$$m = -\frac{(d-1)^2(F_{ST}-1)}{4 d^2 F_{ST} N}$$

For 2 islands, it becomes

$$m = -\frac{9}{16} \frac{(F_{ST}-1)}{F_{ST} N}$$

In consequence, in a 2 island model the expected $F_{ST}$ is almost twice as low $\left(\frac{9}{16} = 0.5625\right)$ than in the infinite island model.

The above equation is an approximation that assumes...

low mutation rate (would not apply to microsatellite data)
relatively low migration rate (there is a $m^2$ term that is dropped)
symmetric migration rate (backward and forward migration rates are equal)
equal population size per island
equilibrium!

Further Reading

I recommend reading this paper (Slatkin 1991), it is IMO one of the best on the study of $F_{ST}$. I would also recommend Nei 1973, Slatkin 1985 and Whitlock and McCauley 1998.

The specific software to use depends on the kind of data you have. In any case, if you average $F_{ST}$ over a number of loci, make sure to use Weir and Cockerham 1984 method.

Bioinformatics

The first step for you is to calculate your $F_{ST}$. Assuming you have a number of SNPs, you will want to use Weir-Cockerham estimate of $F_{ST}$. There are a number of solutions to compute such estimates. One solution to calculate this is vcftools. The following (Bash) will do the job

./vcftools --vcf MyFile.vcf --weir-fst-pop individual_list_1.txt
--weir-fst-pop individual_list_2.txt --fst-window-size 800 --fst-window-step 100

, where MyFile.vcf are your data in vcf format (you might eventually want to use PGDspider to reformat your data). individual_list_1.txt and individual_list_2.txt are files containing the list of individual names (seperated by \n) belonging to the first and second population, respectively. The options --fst-window-size and --fst-window-step allows you to compute the estimate over a sliding window. I chose arbitrary numbers above. EggLib is another good alternative.


Possible Genotypes of 4 Alleles of Adh There are four alleles of Adh which are Adh-1, Adh-2, Adh-3 and Adh-4.  Their respective frequencies are 0.11, 0.84, 0.01 and 0.04.  What are the Hardy-Weinberg frequencies of the possible 10 genotypes?

My Attempt:  First I thought that there were more than 10 genotypes (4*3*2*1) = 24.  I've never done HWE with 4 genotypes so im not sure how to use $p+q=1$ or $p^2+2pq+q^2=1$.

Those Hardy-Weinberg equations are the general case, used for only two alleles.  This question is basically answered here, for three alleles; you've got a situation of four alleles.  That means you need to have:

$(p+q+r+s)^2=1$

Where $p$, $q$, $r$, and $s$ are the frequencies of your respective alleles.  This expands out to the rather unwieldy:

$p^2+2pq+2pr+2ps+q^2+2qr+2qs+r^2+2rs+s^2=1$

Now it becomes a plug 'n chug assignment; simply assign the frequencies and calculate.

   Assuming $p$ is Adh-1, $q$ is Adh-2, etc., $p^2=0.0121$, $2pq=0.1848$, and so on.


Why do dozens of preys run away from a clearly outnumbered predator? (e.g. zebras and lion) We are all familiar with scenes where dozens (if not hundreds) of zebras, sheep, or other preys are chased by one lion, one wolf or other predator. Examples are all over youtube, but here is one of lion versus zebras. In that video you can count at least 30 zebras. Even more, zebras (particularly adult ones) are bigger than lions. There is also evidence of prey defending itself against predators, but this seems to be not the norm.

So my question is, why do high numbers of preys always run away from a clearly outnumbered predator?

Surely evolution would have already taught these animals that numbers can make a difference, so that coordinated defense strategies would be part of their natural repertoire, or of their social learning. Why nature seem to be so oddly incapable of making use of relative numbers as defense strategies?

Why run?

To some extent, selfishness. Remember that natural selection acts within species.

Combat is dangerous. Very dangerous. Even if you are not immediately killed and successfully fend off a predator, wounds can weaken you, damage your senses, and/or kill over time with infection.

If you are a zebra, or a sheep, and you are in a group of other conspecifics, the safest action for you may be to not be the individual that is attacked. Sometimes, you might achieve this by simply advertising being a tough target. Other times, your best bet is to run away. This concept is sometimes humorously discussed in the context of humans and bears: you don't have to be faster than the bear, you have to be faster than the slowest person with you. This is called selfish herd behavior.

Fleeing predation is likely to be the default behavior

If you imagine an allele that changes an animal's behavior to combat an attacking predator (when other conspecifics predominantly run from predators), it is difficult for this allele to grow in the population. Individuals with the allele will get in fights, and although they may reduce predation of the herd as a whole, they will individually be selected against.

Similarly, imagine an allele that changes an animal's behavior to run from an attacking predator (when other conspecifics predominantly attack predators). Individuals with this allele will avoid fights, stay healthier, and breed better than their conspecifics that are getting beaten up, and eventually the herd will be mostly escapers.

Exceptions to the default

However, as pointed out in a comment by gardenhead, not all prey try to escape.

To avoid the 'default' escape behavior, there must be some other motivation: fighting back has to be special some how. In the context of group selection, fighting back may be selected for if it means improved survival of related conspecifics. This behavior is often seen in defense of offspring, but can expand to larger related groups. However, even defense of offspring can be risky, and it is not uncommon in nature for mothers to abandon offspring they cannot defend. It may be safer and more productive in the long run to survive and produce new offspring next year.

Another alternative would be some sort of social/sexual selection, where strong individuals who defend the group (likely males) have increased likelihood to mate.

References

Fischhoff, I. R., Dushoff, J., Sundaresan, S. R., Cordingley, J. E., & Rubenstein, D. I. (2009). Reproductive status influences group size and persistence of bonds in male plains zebra (Equus burchelli). Behavioral Ecology and Sociobiology, 63(7), 1035-1043.

Hamilton, W. D. (1971). Geometry for the selfish herd. Journal of theoretical Biology, 31(2), 295-311.

King, A. J., Wilson, A. M., Wilshin, S. D., Lowe, J., Haddadi, H., Hailes, S., & Morton, A. J. (2012). Selfish-herd behaviour of sheep under threat. Current Biology, 22(14), R561-R562.

Sjare, B., & Stirling, I. (1996). The breeding behavior of Atlantic walruses, Odobenus rosmarus rosmarus, in the Canadian High Arctic. Canadian Journal of Zoology, 74(5), 897-911.

Smith, W. P. (1987). Maternal defense in Columbian white-tailed deer: when is it worth it?. The American Naturalist, 130(2), 310-316.

Wood, A. J., & Ackland, G. J. (2007). Evolving the selfish herd: emergence of distinct aggregating strategies in an individual-based model. Proceedings of the Royal Society of London B: Biological Sciences, 274(1618), 1637-1642.


How can I verify my true genetic relationship with my close relatives with simple physical traits? Question
I don't know if it is ethical to ask a question like that, but I would like to know every simple physical trait that I can observe on me, my parents and my siblings which are regulated by a single or really low number of genes.  I don't want any disease-related traits, just simple traits that could illustrate genetic relatedness.

Already done search
During my research I've found about:

Hair on the second phalanx which is controlled by a single gene and absence of hair being recessive. (Recessive means you need two copies of the allele to have the trait absence of hair!) So if both parents have the trait absence of hair (on second phalanx), every child must have it as well.
Merged ear lob is also a recessive trait.

These are some for which I am not sure of the underlying genetics.

Hair in V on the forehead
Presence of dimples
Able to make a U with tongue
Able to detect Phenylthiocarbamide (PTC)

Don't hesitate to answer with references

EDIT: This site is saying that both hair in second phalanx and merged ear lobs are not as simple as they seemed...

Question: What trait can I use to illustrate genetics?

Here are the answers for your four questions:

Widow's peak (hair in V): dominant: Dominant and recessive characteristics, blinn.edu; Dominant Inheritance, Genetics Generation
Dimples: irregular; tendancy toward dominant *: Mendelian Genetics, uni.edu; What Is the Genotype for Dimples?, seattlepi.com; Understanding Genetics, genetics.thetech.org
Curling tongue: complex; tendancy toward dominance: Myths of Human Genetics, udel.edu; Debunking the biggest genetic myth of the human tongue, Cathrine Woods
Phenylthiocarbamide detection: dominant: Phenylthiocarbamide tasting, Encyclopedia Britannica; Genetic study of phenylthiocarbamide (PTC) taste perception, Egyptian Journal of Medical Human Genetics, Volume 13, Issue 2; PTC The Genetics of Bitter Taste, genetics.utah.edu

Hope it helps!

*See comments


At which point does a cell switch its function? In a multi cellular organisms there are many cells of different functions. How / when does a cell change its function compared to its parent?
Is it done by influence of other cells after its has been created?

As MattDMo suggested there are so much possibilities. I would recommend to take a look at this information:

Cellular differentiation wiki
The Cell: A Molecular Approach. 2nd edition (NCBI)

I will summarize some points, however note that this will not include every aspect.
Every cell contains the same genome (same DNA), so what can make these cells to differ so much form each other (e.g. neurons vs muscle cells). As noted in the Wikipedia article:

  Since each cell, regardless of cell type, possesses the same genome,
  determination of cell type must occur at the level of gene expression

I added this figure just to give a representation of the hierarchy.
However probably you already knew this because you were asking about the mechanism of how these cells can become different from their parent cells.
I will provide two important examples (again notice that this is just a simple summary):

first let's talk about Cytoplasmic determinants

  Cytoplasmic determinants are special molecules which play a very
  important role during oocyte maturation, in the female's ovary (wiki)

the cytoplasmic determinants are molecules such as mRNA or proteins which are e.g. unequally distributed in the egg cell, which means that if this cell devides one half will get other proteins(e.g. transcription factors(TF)) and mRNA than the other half. Different TFs --> different gene expression --> different proteins --> different cells.
Secondly we have induction which is really important in cell differentiation:

  frequently we find that cells become different from one another as a
  result of inductive signals coming either from other cells or from
  their external environment (source)

These two (induction and Cytoplasmic determinants) are important to determine the fates of cells(we also have gastrulation, HOX genes, etc). But how does the induction and the cytoplasmic determinants cause a change in gene expression? The same is true for this, there are a lot of different ways how this can happen (see gene silencing):

Genomic Imprinting
Paramutation
Transposon silencing (or Histone Modifications)
Transgene silencing
Position effect
RNA-directed DNA methylation

I can write pages of Cellular differentiation because this question is really broad. So I will advice you to read the following articles:

Differential gene expression and development
The process of differentiation
Cellular differentiation


Why is brown fat brown? I read in Tortora and Derrickson Anatomy and Physiology that :

  Another type, called brown adipose tissue obtains its darker color
  from a very rich blood supply , along with numerous pigmented
  mitochondria that participate in aerobic cellular respiration.

From Wikipedia :

  ...brown adipocytes contain numerous smaller droplets and a much
  higher number of (iron-containing) mitochondria, which make it brown.

The conclusion seems to be that there should be some iron containing pigment in the mitochondria of  BAT which (along with a rich blood supply) gives brown colour to the BAT.

What is the brown pigment present in the mitochondria of BAT ? Is it the uncoupler protein - thermogenin ?

Brown fat is so-called because it contains a large number of mitochondria, certainly greater than its white fat counterpart. The reason for the excess in mitochondria is to participate in thermogenesis (incidentally, brown fat is also called thermogenic adipose tissue). Nearly all mammals have brown fat (excluding pigs), especially those that hibernate. Brown fat require larger numbers of mitochondria in order for the fat to be used in beta oxidation (which is carried out directly by mitochondria), and subsequently produces heat via the electron transport chain. This also requires greater access to oxygen from the blood, and as a result, greater capillary density also darkens the appearance of the gross tissue. Mitochondria themselves are dark because of the iron content; vitamins B2, B6 and B12; as well as the pigmented flavins (FADx).


Does Yerba Mate contain Beta carbolines like harman and norharman? I know that this is true of (roasted) coffee but haven't been able to find any reliable information about mate in its smoked or steamed state.  Thank you.

After a bit of research I can say that Yerba mate does not contain beta-carbolines. Now, I don't know if this makes you happy or sad but the tea has many antioxidant properties which makes it good for health. You can find a list of the components in Yerba mate in paper 1 and this article.


What does the point in the middle between two numbers mean? [...] cells were removed to a cover glass and treated with plasma for 2 min, then returned to TS broth and centrifuged for 10 min. Cells were harvested and washed twice with PBS, then mixed with tryptic soy agar. The agar block was fixed with 2·5% glutaraldehyde in 0·1 mol l−1 PBS. Samples were postfixed in 1% (w/v) OsO4 in 0·1 mol l−1 PBS for 2 h at room temperature, washed once with the same buffer, dehydrated in a graded ethanol series and embedded in low‐viscosity medium. Thin sections of the specimens were double‐stained with uranyl acetate and lead citrate...

What does mean this bolded point? Is it a decimal separator, or has other scientific meaning?

If this is decimal point, why is vertically middle aligned?

Source: a recent Korea researchers team article

Short answer

It's a decimal point.

Longer answer

A point in the 'middle' of the neighboring characters is called an interpunct, and was the standard in UK typography for marking a decimal at one point in time (possibly elsewhere as well). You're most likely to encounter it in older issues in UK and UK-inspired journals, and no doubt some have lagged behind the trends for reasons of tradition/stubbornness or whatever else and still use it.

Note that you will also encounter countries that use the comma as a decimal separator; Wikipedia has a list that includes most of mainland Europe and South America, for example.


Are fish averse to extreme heat? Terrestrial animals face two common sources of heat extreme enough to pose a danger to them: Sunlight and fire.

It therefore stands to reason that they would evolve systems for sensing heat and behavior making them averse to extreme levels of heat, and most terrestrial animals have indeed done so.

Fish, on the other hand, live in an environment where neither of the above heat sources have a profound impact, and the one source of high temperatures underwater (geothermal activity, such as underwater volcanoes) does not exist within the habitat of many species of fish.

In summary, there does not appear to be any pressure for fish to evolve or retain an aversion to heat like terrestrial animals have.

Are fish averse to extreme heat?

Temperature affect pretty much all metabolic pathways. There are incentive in fishes as well to control their internal temperature.

Control of Body temperature can be categorize along two axes, one concerning the source of heat and the other the magnitude of temperature variation. Please have a look at this post to understand the terms endo-, exo-, poikilo-, homeo- terms.

Below is a figure to give a general overview of the diversity of species in terms of temperature regulation.

As you can see fishes are found in different parts of the figure.

So, yes there is incentive in fishes to control their internal temperature and to avoid extreme heat as well as extreme cold.


NCBI EUtils. Get Homolog infromation using Gene ID How to retrieve homologs information in xml or json format from NCBI using gene ID?

I tried one URL:

http://eutils.ncbi.nlm.nih.gov/entrez/eutils/efetch.fcgi?db=homologene&geneid=9&WebEnv=???&query_key=???

I dont know what to add in question mark regions

From Entrez Programming Utilities Help [Internet]:

  Input: Any Entrez text query (&term); Entrez database (&db);
  &usehistory=y; Existing web environment (&WebEnv) from a prior
  E-utility call

To avoid the error messages, web1, and key1 can be used as terms (these are usually being used to associate with other searches), however this returns no data, probably because the ID you supplied was simply "9", and it remains unclear exactly what you're searching for in the context of other queries.

For example:

esearch.fcgi?db=<database>&term=<query>&usehistory=y

# esearch produces WebEnv value ($web1) and QueryKey value ($key1)

esummary.fcgi?db=<database>&query_key=$key1&WebEnv=$web1

So whilst view-source:eutils.ncbi.nlm.nih.gov/entrez/eutils/efetch.fcgi?db=homologene&geneid=9&WebEnv=web1&query_key=key1 is a valid query, it's not pointing to anything.


Do miRNA and antisense RNA do essentially the same thing? Don't they both just disrupt RNA so it can't make a protein? If so, then what is the difference between the 2?

Antisense simply means that a sequence is the complement of another. miRNAs are naturally occurring antisense RNAs yes. The "difference" is that antisense RNA is often used for sequences developed in the lab and used for processes such as RNAi.

miRNAs, on the other hand, are encoded by the genome and are used by the cell for regulating gene expression. They do this through the RISC complex, just like artificial antisense RNAs such as siRNAs.

Basically, antisense is the general term, and can be applied to any sequence whose complement exists in the genome. miRNAs are a particular class of antisense RNAs.


Differentiating Antaresia (Children's Complex) Pythons using something other than color pattern I have a standard wild-type Children's python (Antaresia childreni) that I'm planning on breeding in the next few years and was just sold a male "Children's python" that I think might actually be a spotted python (Antaresia maculosa). Unfortunately, he's of some kind of reduced pattern morph (granite, I think) that has completely blown out his natural patterning, so my main method of identification is useless.

I know that along with the Stimson's python (Antaresia stimsoni) all of these snakes have been identified as "Children's pythons" at some point in the not-too-distant past, but someone saw fit to distinguish between them and I can't seem to find any basis for doing so that isn't based on range and pattern, both of which are meaningless for a captive-bred snake of a morph that makes its natural pattern indiscernible.

Is there some reliable way to tell the difference between these snakes other than coloration and range? Perhaps some difference in number or placement of certain scales or details about the eyes?

I've included a picture in case anyone can comment and tell me what this little guy actually is on the basis of the modified pattern - but I'd still like a better way if anyone can provide a real answer.

I finally got frustrated enough to dig up A Revision of the Liasis childreni species-group (Serpentes: Boidae) L.A. Smith, 1985 - the original paper that split up this species complex, and when even Smith made primary determinations off of pattern and color alone, I took matters into my own hands and dug into the his raw data.

I have compiled the mean scale counts for each species into a table, and truncated any rows that showed no useful degrees of deviation for any species, resulting in the following:

             A. Childreni  A. Maculosa  A. Stimsoni  A. Stimsoni Orientalis  A. Perthensis
Ventrals     272.8        263.5         279.5        263.8                   232
Subcaudals   47.3         42.1          46.2         42.8                    38.7
Midbody      41.3         38.3          43.4         40.3                    32.7
Loreals      7.9          4.7           12.2         7.9                     7.3
Postoculars  3.6          3.1           4.2          3.8                     3.4
Pits         4.5          4             5.6          4.8                     3.1

I am including this table in its entirety to assist future identification efforts within the complex, as the original paper did a poor job of presenting this data.

The most useful difference for my purposes - distinguishing between A. maculosa and A. childreni - appears to be loreal scale count. The loreal scales sit between the eye and nostril of the snake, and do not include scales which belong to the orbital and nasal structures (The region marked "l" in the diagram below).

Following up on this, I examined a number of close-up photos of known examples of both species, and very quickly identified a distinctive difference in not just the count but also the pattern of loreal scales. Once you're looking in the right place, the difference is obvious.

A. Childreni showing its distinctive granularly-clustered loreal scales:

A. Maculosa showing its smaller number of tightly structured loreal scales:


Does someone know of a website that keeps track of a species population? I am planning on doing some math on population growth, but I need a reliable source of data on population growth of some species over time. Does anyone know of a resource (website/publications/public repository) that has such information?

How about human?

You will find the data of human population growth on the webpage "Our World in Data". Scroll to the second graph, click on the tab "data" and download the .csv file.

Just google for any specific species of interest

Otherwise you can just google things of interest. Look for large emblematic mammals or commercially important species.

If you google "bald eagle population growth", you will easily find these data.
If you google "moose growth population breeding pairs", you will find these data.
If you google "killer whale population growth", you will find these data.
If you google "tuna population growth", you will find these data.

COMADRE

COMADRE is a database of animal matrix population models. It can be of interest to you.


Is there a biological environment that we can we assume glutamate exists as glutamic acid? In the body we almost always assume that glutamate exists as glutamate rather than glutamic acid. It is so commonly glutamate yet glutamic acid and glutamate share the abbreviations of Glu and E. From the wikipedia page:

  The side chain carboxylic acid functional group has a pKa of 4.1 and therefore exists almost entirely in its negatively charged deprotonated carboxylate form at pH values greater than 4.1; therefore, it is negatively charged at physiological pH ranging from 7.35 to 7.45.

Glutamic acid:

Glutamate:

Given that the pKa of glutamate is 4.1, is their any biological situation (a cell type, organel etc.) that glutamic acid is preferred?

Additionally, does this have any large biochemical implications, or is that outweighed by the (relatively speaking) "extreme" acidic environment?

At typical physiological pHs glutamate does exist as glutamate.

Broadly the acidity in the digestive track is enough to reduce glutamate to glutamic acid. The stomach for example has a healthy pH of between 1.5 to 3.5.

Canadianer points out in the comments that the active site during catalysis are protonated. There are obviously a lot of examples of this and sensitive evaluation by looking at the isocontours and surface potential of the protein structure are needed to draw conclusions if this might be important.


Could a single cell be brought to life? If a scientist is observing a single cell under a microscope, and then realizes that the cell has died, is it possible to bring that dead cell back to life?

For my inquiry, let's assume that the death of the cell has occurred without disease or external circumstances.

Has such process ever taken place in a lab before? Thx.

There are species where cells and even whole organisms can go into a state called cryptobiosis where their metabolism is suspended but can be revived later. This usually happens when the conditions become too bad for survival (dry/cold etc.) and is reversed once the conditions improve again (rehydration warming up). One prominent and fascinating example are tardigrades.

Also, it is possible to freeze cells in liquid nitrogen where all metabolic processes are extremely slow. With modern freezing/thawing processes cell survival rates >90% are possible. However, before you ask this will not work on whole tissues let alone people!

Cryptobiosis only works for specialized species and only under certain conditions. Normally, once a cell starts to die, it either does so because it is too damaged to keep living, a process called necrosis or because apoptosis (programmed cell death) was triggered upon which its DNA is fragmented and the proteins are degraded by proteases. Neither process is reversible once started.

Note: I find your restriction "the death of the cell has occurred without disease or external circumstances" a bit puzzling and too vague. Unless something happens to them cells don't just die. Therefore I explicitly ignored this restriction until you formulate it more specifically so that it makes sense.


Finding proteins in DNA sequence I have to do a task for a university task and I need to understand some things
before figuring out how to do it.

The task is the following:

  Find matches of known proteins (DNA-PolyI,II,III) to the specific E.Coli DNA, sequence.

I downloaded in FASTA format the protein sequence of DNA-Poly3 DNA-Poly1 of E.coli (strain K-12) and the entire DNA sequence
of the E.Coli.

I've studied a bit on-line and using the BioRuby gem and the Ruby programming language I wrote a program that translates DNA to protein sequence.
Then I tried to match the known DNA-Poly3 sequence but it did not match. After searching a bit on-line again, I learned about ORF and
and the 6 possible reading ways of each frame. The longer, in terms of codons, ORF conformation is chosen but there's no way of telling for sure that the protein was made using
this frame.

Then I've read about TATA boxes, but I can't use those since they can be found only in Eukaryotic and Archaea.

So how should I proceed in order to solve this problem: How can I prove that the DNA-Poly3 gets produced by a specific area (gene) in the DNA sequence?

Thanks for your time,

ps. Insights and hints are very much welcomed as this is just the tip of the iceberg for me and I'm very willing to study bioinformatics :-)

EDIT: This is an update for info requested in relevant answer

The files I have used are the following:

➜  Bioinfo  ruby dogma.rb
----------------
DNA Length: 4639675
gi|48994873|gb|U00096.2| Escherichia coli str. K-12 substr. MG1655, complete genome
----------------
DNA Poly-1 sample: 928
gi|16131704|ref|NP_418300.1| fused DNA polymerase I 5'->3' polymerase/3'->5' exonuclease/5'->3' exonuclease [Escherichia coli str. K-12 substr. MG1655]

You can download them here: E.Coli DNA and E.Coli DNA-Poly1.

NOTE: My sample protein is DNA Polymerase I (and not 3).

IMPORTANT EDIT : In your particular case, if you are working with bacterial genes, splicing is not an issue since bacteria do not have introns. I am leaving the information here since it may be useful to someone else. However, I recommend you focus on the UTRs since they are probably what is causing you problems.

There are three things that could be causing you problems. I will briefly touch on each one. I will talk about all genes, bear in mind that bacteria have no introns so any discussion of splicing and/or introns and exons is not directly relevant to your problem.

1. UTRs

Untranslated Regions (UTRs) are sequences at the beginning and end of a gene that are not translated into protein. UTRs are regions that are part of the original genomic sequence, they are also part of the mature mRNA (indeed, UTRs are sometimes modified by splicing events, they are exons not introns) but they do not get translated into protein. To illustrate, have a look at this simplified representation of an mRNA molecule:

Only the green exons will make it into the final protein. Introns are spliced out and UTRs are not translated.

Therefore, if you translate the entire gene, you will not get the correct protein.

2. Reading frames

Genes are read in words of three letters (the codons). The sequence ATGTGTACCTGA has six possible reading frames (three on each strand) which can be read and translated as follows:

5'3' Frame 1

    ATG TGT ACC TGA
     M   C   T  Stop

5'3' Frame 2

    a TGT GTA CCT ga
       C   V   P

5'3' Frame 3

    at GTG TAC CTG a
        V   Y   L

3'5' Frame 1

TCA GGT ACA CAT
 S   G   T   H

3'5' Frame 2

t CAG GTA CAC at
   Q   V   H

3'5' Frame 3

tc AGG TAC ACA t
    R   Y   T

DNA is double stranded. The sequence of one strand is complementary to that of the other, therefore if you have one strand you can infer the sequence of its complementary one. Genes can be found on either strand, the two are equivalent biologically. However, sequencing projects choose one of the two strands (randomly) and call it the plus (+) strand and then save all sequences with respect to that strand. This means that sometimes the genomic sequence that you download from a database might be the complement of the actual sequence you are looking for.

3. Names

I once heard someone say in a conference that

  Biologists would rather share a toothbrush than a gene name.

While that might be a little exaggerated, naming conventions vary between research communities and species and databases. So, are you sure that you have downloaded the correct gene? Where did you get it from? How did you identify it? Does the sequence also contain up/downstream regulatory regions, promoters, enhancers and the like? If you post the exact sequence you are attempting to use I can give you more specific help.

For example, the first 20 hits when searching for the E. coli DNA Polymerase 3 in ncbi's nucleotide database, are whole genome shotgun sequences. These do not correspond to the gene sequence you are looking for. They are huge pieces of the genome (or even the entire genome) that will contain your gene and many others. Look at the Tools section below for suggestions on extracting your gene from the whole genome.

4. Splicing (irrelevant to bacteria)

Another possible problem is splicing. Lets start with the basics, the process of producing a eukaryotic (bacteria have no introns) protein from a genomic sequence is summarized in the image below (modified slightly from here):

Transcription begins at the transcription start site (TSS) but not all the transcribed sequence is translated into protein. First, the introns are spliced out of the mRNA to produce the mature mRNA (other things like capping and poly-A addition also occur but are not relevant here). So,the mature mRNA contains the exons of the coding gene. This means that a linear translation of the gene's sequence will not correspond to the protein produced. You will need to take splicing into account.

Also, bear in mind that splicing will change the reading frame.

Now, if the sequence ATGT were spliced at, for example, AT/gt (most splice events cut/join at GT/AG sites) and joined with the sequence agATTATT, the resulting (spliced) sequence would be (the splicing process will remove the gt from the first sequence and the ag from the second):

ATATTATT

As you can see, the reading frame has now changed. Where before, in the first reading frame, we had the codon ATG, the canonical translation initiation codon, we now have ATA which codes for isoleucine (I). I hope that is clear,  the main point is that splicing can change the reading frame.

5. Tools

OK, that was the background. Now, what you will need to do is use existing programs that model splice sites and can correctly align a protein sequence to genomic DNA. My personal favorites are exonerate and genewise. On a Debian-based Linux distribution, you can install them with this command:

sudo apt-get install exonerate wise

Then, to align the protein to its gene do:

exonerate -m protein2genome -n 1 prot.fa dna.fa > out.txt

or

genewise -pep -pretty -gff -cdna prot.fa dna.fa > out.txt

In my experience exonerate is (much) faster but genewise is a little more accurate. I usually use exonerate if I am dealing with a whole genome and genewise if I only have a few kilobases of sequence. Both are very good and both will be able to align a protein to its genome of origin.

I will not explain all these options because that is beyond the scope of this site. Have a look at their documentation (which is quite good and clear) and if you still have problems, you could ask a question on our sister site, Bioinformatics Stackexchange

Alternatively, you could link your web application to the ucsc genome browser BLAT service. Click here to see the results when aligning the human
DNA-directed RNA polymerase II subunit RPB1 protein.


How much variation in mutation rate in there in the human genome? In humans, the average mutation rate is estimated to be around $2.5 \cdot 10^{-8}$ (Nachman and Crowell, 2000). Of course this mutation varies from sequence to sequence.

Can you please give some ideas of how much variation in mutation rate there is in the human genome?

There are many ways to express such variation. One could give the lowest and highest mutation rate or shows a mutation rate map over either the whole genome or a randomly chosen sequence.

Cool question. Unfortunately, I don't have a complete answer; the best I can do is summarize some literature. I'd be happy to look more if you want to discuss though. Also, sorry the answer is a little scattered and I apologize if you were already aware of all this!

One thing I will suggest though is that this is hard to do for the human genome in isolation; hence why much of the literature draws on other animals as well.

In any case, the literature on this topic is quite expansive, so I am afraid this is merely the tip of the iceberg. Hopefully it's helpful though.

Firstly, I know of two genomic mutation rate maps that might interest you (as you suggest in your question). One in Genome-wide patterns and properties of de novo mutations in humans by Francioli et al, looking at de novo mutations in humans (obviously more concerned with germline mutations), and another in Mutational heterogeneity in cancer and the search for new cancer genes by Lawrence et al, which (unsurprisingly) is concerned with somatic mutation rates and the resulting oncogenics.

A great review, although not entirely human-specific, is Variation in the mutation rate across mammalian genomes by Hodgkinson and Eyre-Walker. They note that:

Small-scale effects: G & C mutate more than A & T, CG dinucleotides are highly correlated to higher mutation in non-coding DNA, and there appear to be hyper-mutable sites (conserved across species) that are susceptible to SNPs. These effects vary across the genome as well. Indeed, certain regions of mitochondrial DNA also have highly variable mutation rates. Oddly, GC-rich islands may be less mutable (for certain mutation types), and may affect nearby nucleotides, particularly methylated ones.
Transciption sites: somatic tissue has lower mutation rates of transcribed areas than non-transcribed ones. In germ tissue, there is an interesting effect for certain types of mutations increasing as one moves away from the transcription start site, but not others.
Other mutations: indel mutations tend to co-occur with point mutations
Mutation rates are spatially correlated at multiple scales.
Chromosomes: for humans, it seems the Y chromosome is the most mutable, followed by the X, and then the autosomes. There is also a difference in the mutation rate between autosomes, but it appears this is overshadowed by the intra-autosomal mutation rates.

Not explicitly noted by the paper, but intutive and sometimes implied, is the lower mutation rate in coding and regulatory regions (e.g. enhancers, promoters,...).

Another paper is Evolution of Local Mutation Rate and Its Determinants by Terekhanova et al. They note local mutation rates in primates (obviously including humans) are highly correlated across the genome. This correlation weakens as evolutionary distance grows (e.g. humans to mice). They also look at the influence of several genomic features on local mutation rates.

Not in humans, but Evidence of non-random mutation rates suggests an evolutionary risk management strategy by Martincorena et al look at mutation rates across E. Coli genomes, finding enormous variability, particularly lower rates in highly expressed genes.

Since we have not yet seen chromatin structure pop up much, I'd like to point out the cool paper The effects of chromatin organization on variation in mutation rates in the genome by Makova and Hardison. Therein, they find that mutations of different types are affected differently by open vs closed chromatin states; roughly, closed chromatin encourages base substitutions, whereas indels occur more often in areas with open chromatin.

Finally, some of the difficulties in assessing mutation variability are explained by Eyre-Walker and Eyre-Walker, in How Much of the Variation in the Mutation Rate Along the Human Genome Can Be Explained?

Some related work

For mutation rates in germ-line cells specifically, see:

Properties and rates of germline mutations in humans by Campbell and Eichler
Determinants of Mutation Rate Variation in the Human Germline by Segurel et al
Variation in genome-wide mutation rates within and between
human families by Conrad et al

which describe some patterns in mutation variability across the genome, but are often more concerned with inter-individual factors.

Also here are two early papers using comparative genomics to look at mutation rates:

Mutation rates in mammalian genomes by Kumar and Subramanian
Deterministic Mutation Rate Variation in the
Human Genome by Smith et al

which focus on inter-species comparison, but also discuss compositional differences (e.g. GC richness).


Does amount of sperm affect fitness of baby? If there's a 3 day ovulation period in which to have intercourse, would it be better (to create a more fit/healthy baby) to have sex once and ejaculate more sperm than have sex three times with reduced sperm count?

You would think that the more sperm ejaculated at once would result in much more competition to reach the egg, leading to a more fit spermatozoa, and presumably a more fit baby.

If the egg is fertilized during a lower level ejaculation, a less fit spermatozoa can fertilize the egg since there's less competition. Meaning a less fit baby?

Keep in mind I'm NOT asking about the chance of getting pregnant, I'm talking about the fitness/health of the baby. Obviously having sex once instead of three times decreases the chance of getting pregnant.

I can see where you're coming from, and keep in mind I am no expert in the area, but have you considered that there may be many, perhaps important factors at play than if the sperm had many competition or few? Take the parents genetic and epigenetic profile for instance, meaning not only what the mother and father could each pass on, but whether or not what they pass on will be active or not. And to use your own example, the fittest sperm, who outperformed the larger group; say it required more energy and thus produced more ROS, with which to damage to it's DNA, than the winner in the smaller group - which would be weaker and which stronger? Say the health of the sperm which fertilises the egg could not be influenced by you in any practical way, which method would you choose then?


What "algorithm" are carnivorous larvae using when foraging? What algorithms are carnivorous larvae (lady bugs like Adalia bipunctata, Coccinella septempunctata, common green lacewing (Chrysoperla carnea) or hoverfly (Syrphus)) using as they are foraging for aphids?
Is it just random walk or something more efficient?

I'm going to assume that when you say algorithms, you mean the forms of innate behavior an organism may have relating to their senses (e.g. when sunlight is detected by a worm through the photoreceptors in their skin, it will move towards the opposite direction of the source of light to stay in their preferred environment).
These mentioned species of insects are very different taxonomically, but their number of sensory organs are for most part similar including during larval stages.
Examples of innate behavioural responses seen in invertebrates include taxis and kinesis.
Taxis is a change in movement in response to an environmental stimulus – either towards (positive) or away (negative)
Kinesis is a change in the rate of activity in response to an environmental stimulus
So, when talking about rough algorithms, when a larva detects a particular stimulus (e.g. chemicals of prey via chemoreceptors),  The organism will either have a 1 or a -1 value for Taxis response (e.g. it runs towards or away from the prey), and a rate of activity relative to taxis which represents kinesis (e.g. it gradually moves faster towards the prey as the chemical stimulus becomes stronger (meters per hour for example).
So, you could say that the theoretical formula/algorithm for hunting prey relating to the chemoreceptors as an example would be:
Taxis ('1' or '-1' to symbolize moving towards or away from a prey) multiplied by the number of 'prey' chemicals received by the chemoreceptors equaling the strength of the larva's response which could be (as an example) translated to the velocity of larva
Of course all the other senses such as photoreceptors and the chordotonal organ (vibration sensor) must be considered and I couldn't find any actual algorithm for how these species hunt. This is just a way to percieve how insects both in and past their larval stages respond to stimuli through their innate behaviour.


Does every nerve ending send information to the brain separately? Does every nerve ending send information to the brain separately? Is there a nerve path (I don't know their scientific name) from every nerve ending to the brain; or are they sent to brain from the same paths in the dorsal root ganglion? If not, how can we determine the (almost) exact location of pain in our hand?

I am not very familiar with the biology except the lessons I had taken in the high school. So please try to use daily language explaining this.

There are two main structures in the human nervous system:

The central nervous system, which includes the brain and spinal cord
The peripheral nervous system, which is all of the nerves in the rest of the body (fingers, arms, feet, etc.)

The signals taken by the peripheral nerves mainly travel to the brain through the spinal cord, and the brain sends signals back to the peripheral nerves through the central nervous system.

There are a lot more complex mechanisms and various exceptions, but essentially: the nervous system is a vast network of signals, and the majority of these signals travel through the spinal cord to the brain and from the brain to the target nerves.

The signals travel via different nerve "branches" — think of it like a tree of nerves, with the common root being the brain.

For more information please see:

Overview of the nervous system for dummies

Wikipedia (with strong references and lots of detailed information)


What is known about the coding sequence of Factor H in the human genome? Factor H is a protein coded in 20 domains.

My question is whether these domains form some kind of repeat cluster in the human genome. Basically, I'm interested in the coding sequence from an assembly point of view: Is the coding region fully resolved? Apparently there is only one copy of the gene per haplotype, but are coding domains maybe similar to each other or repetitive in themselves?

As clearly stated in the WP article:

  The molecule is made up of 20 complement control protein (CCP) modules (also referred to as Short Consensus Repeats or sushi domains) connected to one another by short linkers (of between three and eight amino acid residues) and arranged in an extended head to tail fashion.

So in your terminology yes, it is a repeat cluster. Each of those 20 domains will be similar to the others, although not identical.


Evolution of insects, spiders and jellyfish Well we all learned at school the classic evolutionarily theory

From:          To:
fish           amphibian
amphibian      reptile
reptile        mammal
reptile        bird

But what always interested me:
What about invertebrates?
Do they also have some evolutionary table like vertebrates or was there evolution never that interesting to begin with?
I can roughly imagine that there are giant evolutionary gaps between an insect and a jellifish but is there any common ancestor of all of them?

So my question has essentially two parts:
1. What is the common ancester between vertebrates, arthropods and molluscs
2. Is there an evolutionary Tree for the last two like for the vertebrates

Welcome to Biology.SE

Answering your question fully will require to write a whole book. Evolutionary Biology is a big field and I would recommend that your take some time to get an introduction (slightly more advanced than what you received in school). I am suggesting you take advantage of this free online resource.

I am briefly making comments and answering your question(s) below. They may be hard (or easy, I don't know) to understand but for more info you should really get to the above free online resource.

Species A evolved from species B

Evolution did not make mammals out of reptiles, mammals are reptiles. Evolution did not make birds out of reptiles, birds are reptiles as well (I am using here the phylogenetic definition of reptiles (Reptilia), more info there). It is wrong to think of any two extant species as one having evolved from the other one. But it is correct to understand how closely related are two extant species. It is also correct to make predictions about how the most recent common ancestor (MRCA) look like and it is true the the MRCA might look more like one of its descendents than like another.

We talk about clade as a lineage including many species. In these terms both any lizard species and any given bird species belong to the same clade, the Reptilia, they are both reptiles. They are also both vertebrates (Vertebrata) and animals (Metazoa) and eukaryotes (Eukaryota).

If the statements of the kind "mammals evolved from reptiles" are very misleading the statement "amphibians evolved from reptiles" is simply wrong. The MRCA of reptiles and amphibians was not a reptile (neither an amphibian), it was a tetrapoda (vertebrate).

I can roughly imagine that there are giant evolutionary gaps between an insect and a jellyfish but is there any common ancestor of all of them?

Any two species on earth have a common ancestor. The universal common ancestor, that is the common ancestor that any living thing (bacteria, plants, lizard, human, fungi, jellyfish, Archea, etc...) is called LUCA (Last Universal Common Ancestor). So yes, jellyfish and insects have a common ancestor. LUCA is one of them. Their MRCA is the same guy as the MRCA between jellyfish and you, as insects and primates are more closely related than are insects and jellyfish. This MRCA is an animal (a metazoa) and therefore is also a eukaryote (Eukaryota).

Do they also have some evolutionary table like vertebrates or was there evolution never that interesting to begin with?

Evolution occurs in every single living population. So yes, evolution occurs in jellyfish as it occurs in insects. The clade of jellyfish contains several thousands of species (most of them belong to the clade Hydrozoa). There are almost a million species of insects.

Here are just a few fun facts that come to my mind when I think about jellyfish:

Some species have tentacles, some don't.
Some species have alternance of generation (a given individual is either a sticking thing on the ground while its descendent is swimming).
Size of jellyfish vary wildly

And a few fun facts about insects:

Some have evolved 3 pairs of wings to fly (we think it evolved from gills but it might have evolved from the exoskeleton as well).
Some live in water, some not, some live in water in the larvea stage and not in their adult stage.
They have all sorts of diet
When flight evolved at first, they had 3 pairs of wings. All extant species (who are descendents of this species that evolved flight) have now lost at least one pair of wings, the one closest to the head.
Some species have lost flight.
Some species have lost a second pair of wings (diptera)
Some have evolved crazy mimetism and defense mechanism from the developmental pathway of the third pair of wings.
Eusociality (which is arguably one of the most mind boggling things in evolutionary biology) has evolved several times in insects.
Some species have sex that is determined the ploidy (number of sets of chromosomes) level (it is the case in many eusocial species).

1. What is the common ancestor between vertebrates, arthropods and molluscs?

You can explore the tree of life by yourself on tolweb.org. Arthropods and molluscs are more closely related than any of them are to vertebrates. The MRCA of vertebrates, arthropods and molluscs was a Bilateria (animal, eukaryote). You can see this bifurcation here on tolweb.org. I'd recommend to explore a bit this tree of life, it is pretty fun to do.

2. Is there an evolutionary tree for the last two like for the vertebrates?

Yes, see above.

BTW, I noticed that you talk about spiders in your title but not in your post. You'll find the spiders here on tolweb.org.


Will ants arriving with travel luggage form a new colony? I have found a few dozens of ants in my luggage after arriving back from holiday. Am I at the risk that they will form a colony in my home? Are those ants able to form colonies that are normally gathering food? Will any other kinds of ants be present in the luggage? What will happen to these ants after they start exploring my flat (which is distant from their original colony)?

An ant colony is started by a queen ant (reference). Worker ants are sterile, and cannot start a new colony (reference). The ants in your luggage are worker ants (unless you have a colony in there :) ). The original queen ant never leaves her colony, but during a nuptial flight, new queen ants will land in (hopefully) good nesting sites.  (reference) These ants can be told by their wings, which are non-existent in worker ants.

The worker ants have an average life span of 45-60 days (reference), so the ants in your luggage won't be around for very long.

Also see:

  If a worker ant gets separated from its colony, it's doomed. No other colony will take it in, and it can't start its own colony--only queens can do that. It might be able to live for a while, but generally not that long--a lost worker is generally more concerned with hunting for its colony than with feeding itself, and its energy reserves are fairly small (depending on the ant species--some have workers that are adapted to taking long foraging trips). A few ant species, however, have "supercolonies," where neighboring colonies are established by queens directly related to one another. When queens are close relatives, their workers tend to have similar chemical profiles, meaning they can move from colony to colony without triggering the usual colony defenses against intruders. (Intruders are recognized by their chemical profile--their odor--and not by appearance, ID card, etc.) In such cases, workers routinely transfer between colonies, so a worker may end up working for its grandmother or, forgive me, its aunt. (From this page)


What advantage does an enzyme serve over catalysis by the addition of heat energy? I understand that an enzyme lowers the activation energy, allowing the reaction to run faster, however I am not sure, how it may be favorable during the addition of heat energy. Wouldn't that lower the activity of the enzyme since the enzyme is sensitive to heat?

Enzymes have two benefits over raising the temperature:

First, reducing the activation energy by reusable enzymes is far more energy-efficient, apart from the fact that the required temperature would vary for different reactions.

Second, enzymes are able to be controlled by allosteric mechanisms, which facilitates metabolic control by feedback loops, feedforward motivs and receptor-mediated processes. In the example of glycolysis this enables the cell to fine-control its supply with energy equivalents (see figure from Wikimedia Commons below). This mechanism may be the most important function of enzymes.

Reference

William C. Plaxton: Principles of Metabolic Control. In Kenneth B. Storey (ed.): Functional Metabolism: Regulation and Adaptation, John Wiley & Sons, Inc. 2004


How was Crisper Cas9 function discovered? What paper outlines the discovery of how the CRIPER DNA, CrRNA, and Cas9 interact?

The two "classic" papers cited in terms of Crispr/Cas9 discovery include the Doudna/Charpentier initial discovery, and the Feng Zhang application to gene editing.  There is an ongoing, famous patent dispute as to whom really discovered the Crispr/Cas9 gene editing technology.

As a quick timeline that better answers your question, a good publication is Cell Paper and there is actually a great podcast, but I will summarize:

Yoshizumi Ishino et al. in 1987 Discovers Crispr mechanism - the authors simply noticed the odd regular repeats of DNA in bacteria and noted: “no sequence homologous to these has been found elsewhere in procaryotes, and the biological significance of these sequences is not known.”
Francisco Mojica in 1993-2005 - Furthers research into CRISPR, at this time the terms has been coined by Jansen, however it is Mojica who really notices the Crispr pattern in several bacterium and suggests that it is involved with an immune response.
Alexander Bolotin in 2005 - Looking into the bacteria Streptococcus thermophilus, Bolotin discovers that the genetic material in between the spacers is viral DNA, providing definitive evidence of the Crispr hypothesis.
Marakova in 2006 - First proposal that the protein Cas9 can be used in a bacterial adaptive immune response, although Bolotin is also credited around this time from noticing the use of Cas9.
Koonin in 2006 - The first one to piece the Crispr storage of viral DNA and the Cas9 reports of an immune response together as a related system that might be able to use the Crispr DNA with Cas9 in an immune system.
Marraffini in 2007 - Studying the Crispr-Cas9 system further, he provides the first definitive microbiological evidence that Cas9 is a programmable restriction enzyme, and that it targets DNA not RNA. At the same time Philippe Horvath, Danisco France also provided the best evidence yet of the adaptive immunity system.
Doudna and Carpentier in 2010 - Through sequencing, definitively put the Crispr and Cas9 system together as complete unit that is able to cut DNA, they also described tracRNA as the RNA piece that join with Cas9 to program DNA cutting.
Feng Zhang in 2013 - While Doudna previously suggested that the Cas9 system could be used to target mammalian DNA, Zhang was the first one to actually that it was possible and therefore open to the door as the Crispr/Casa9 system as a tool that easily edit genomes.

While I definitley missed several key steps, and did not fully explain the actual mechanism of Crispr/Cas9, I think this provides a decent timeline.  For more information about the actual mechanism see: Harvard, Wired, Science News.


Which extinction event killed the highest proportion of organisms? The P-T extinction (a.k.a. the Great Dying) tends to be considered the worst - for example, Wikipedia states:

  It is the Earth's most severe known extinction event, with up to 96% of all marine species and 70% of terrestrial vertebrate species becoming extinct. It is the only known mass extinction of insects. Some 57% of all families and 83% of all genera became extinct. Because so much biodiversity was lost, the recovery of life on Earth took significantly longer than after any other extinction event, possibly up to 10 million years.

Presumably the "96% of all marine species" (which references two books, neither of which I have) is in terms of multicellular marine species or some similar subcategory that's easier to observe in the fossil record (I could be wrong).

My question is this: Would the Great Oxygenation Event not have killed a higher proportion of organisms (taking into account all organisms)?

I know that we don't have any records that can tell us how many died in the GOE and hence this question is necessarily speculative, but surely nearly all organisms pre-GOE would have been obligate anaerobes (and therefore found oxygen to be toxic)?

What I'm unsure about is how single-celled organisms fared in more recent (Phanerozoic) extinctions, as most discussion seems to be in terms of opisthokonts (i.e. animals + fungi) and archaeplastidans (i.e. plants + algae).

This is a great question. I decided to research it and here is what I found. For some reason the GOE is not on lists of the "big 5" mass extinctions. The question is why?

I think it's due to the pace of the event. The event is described as happening 2.45–2.32 billion years ago.

This is a timescale in billions of years. So it isn't really a proper mass extinction. Little is known about the time scale of the evolution of cyanobacterial lineages.


What is the difference between optokinetic and vestibular nystagmus? Optokinetic nystagmus is for stabilising the pictures we see when we are observing moving objects for example if we are rotating on an office chair. If we wear a mask while rotating however, the optokinetic nystagmus will not occur since we don't see. But I read that vestibular nystagmus will occur even if we are wearing a mask.
What is vestibular nystagmus exatly and how does it differ from optokinetic nystagmus?

The vestibular reflexes are the main cause for stabilizing eye movements. The labyrinth canals in the inner ear detect changes in head direction, movement and acceleration. This is important for balancing body and visual field. These are fast involuntary reflexes thanks to almost direct connections between the sensory hair cells in the ear and the eye muscle innervating neurons.

The optokinetic reflexes are complementing the vestibular reflexes for slow movements or visual field motions independent of head movement (source and further reading). It needs the visual input.

In my studies we actually did this experiment ourselves, measuring the eye muscle activity while rotating with opened or closed eyes. The results were basically the same in both conditions. With opened eyes you try to fixate something in the moving image for longer and have therefore larger jumps in the eye movements, but with closed eyes the saccades are still there.

Edit: The two senses can also be in conflict with each other. For example reading a book in a car (your vestibular system detects motion, while your visual field is steady) or watching a movie in the cinema (your visual system detects motion while your vestibular system doesn't). This causes motion sickness.


Can bacteria metabolize fatty acids for fuel? I'm not a microbiologist, but rather a physiologist  curious about microbial metabolism. Much like humans bacteria can utilize glucose, but when it comes to long chain, medium chain, or short chain fatty acids, what are the pathways that microbes use to break these compounds down for fuel?

It seems plausible that bacteria can take up short chain fatty acids, but with longer chain species are there impediments to uptake? Are the oxidative enzymes similar between bacteria and humans?

I found this review about bacterial lipid metabolism. There it says:

  Exogenous long chain fatty acids are utilized by E. coli in two ways. Firstly, they can
  be incorporated into the membrane phospholipids by the acyltransferase system (PlsB
  and PlsC; Section 4). Secondly, they can be used as the sole carbon source for growth,
  and are in fact an important source of energy for E. coli in their normal habitat, the
  intestine [16]. The CoA thioester of the fatty acid is the substrate for both of these
  pathways. Fatty acids greater than 10 carbons in length require the fadL gene product
  to be taken up from the growth medium in sufficient quantities to support growth.

So yes, bacteria can grow on fatty acids alone and they can utilize long fatty acids as an energy source. However the uptake of the long fatty acids requires the protein produced by the fadL gene.


Which organisms have introns? From Wikipedia:

  For example, introns are extremely common within the nuclear genome of higher vertebrates (e.g. humans and mice), where protein-coding genes almost always contain multiple introns, while introns are rare within the nuclear genes of some eukaryotic microorganisms,[8] for example baker's/brewer's yeast (Saccharomyces cerevisiae). In contrast, the mitochondrial genomes of vertebrates are entirely devoid of introns, while those of eukaryotic microorganisms may contain many introns. Introns are well known in bacterial and archaeal genes, but occur more rarely than in most eukaryotic genomes.

In my biochemistry course we learned that bacteria have no introns and eukaryots nearly always have them. What's correct?

Do viruses have introns as the Wikipedia article claims?

As a general rule, a blanket statement in Biology should always be considered false.

It so happens that bacteria do have 'introns' (or at least the intron genomic sequence has been determined) in the sense of the cis-acting autocatalytic Group I and II introns. These are sequences of RNA that adopt such a conformation to catalyze their own excision from an mRNA transcript, and thus may be considered ribozymes, enzyme made of ribonucleic acid.

Although not generally considered 'introns' segments of RNA are removed during the course of tRNA in both prokaryotes and eukaryotes.

Now introns that are removed by the action of the spliceosome are strictly found in eukaryotes, as bacteria lack the spliceosome.

There seem to be a considerable number of papers regarding the question of intron (particularly spliceosomal) phylogeny that should be relatively easy to find if you are so interested.

One example paper in which viral introns (Group I) are reported:
http://nar.oxfordjournals.org/content/22/13/2532.abstract


DNA & mRNA During Transcription Just a simple, quick question: how are the mRNA and the template strand of the DNA structured during transcription? I've seen models and videos of them when they're both flat/straight (is that just for simplicity?) and others where they're spiralling around each other. Could someone just briefly shed some light on my situation please?

Transcription occurs in a special structure known as transcription bubble. Inside the bubble are present the mRNA, template DNA being transcribed and the RNA Polymerase. Upstream of bubble is the DNA already transcribed and downstream is the DNA to be transcribed. There is not enough space in cell to have completely unfolded DNA for transcription, so transcribed DNA has to be re-annealed as soon as it is transcribed, giving a bubble-like appearance to the RNA polymerase-bound DNA. Hence it is called a transcription bubble. See this image for illustration:

Source

The mRNA formed quickly leaves the bubble and hangs behind like a thread coming from RNA polymerase.

Source


What causes the bright flash of light when poking my eye? Recently, I poked myself in between my eye and eye socket, right below my eyebrow, and sometimes I would get this flash of light. Others have tried this too, and they also had a flash of light. I am wondering why is this the case. Does it have to do with the nerves in the eye?

Short answer
Pressure phosphenes are believed to be induced by stretch-induced activation of retinal ganglion cells.

Background
Flashes of light (phosphenes) due to pressure on the eye ball are referred to as pressure phosphenes. Based on an electrophysiological study (Grüsser et al., 1989), eyeball indentation presumably tangentially stretches the retina locally, which variably depolarizes horizontal cells. This in turn depolarizes ON-bipolar ganglion cells, while hyperpolarizing OFF-bipolars. Some ON-center neurons also seem to respond to the removal of the deformation. Bipolar cells connect to the retinal ganglion cells. These ganglion cells carry visual information from the retina via their axons in the optic nerve to the brain. Hence, to answer your question: yes, pressure phosphenes are related to activity in the optic nerve.

Reference
- Grüsser et al., Vis Res (1989); 29(2): 181–94


Why prefer $MgSO_4$ over $MgCl_2$ in recipies Many molecular biology recipes use MgSO4 (and not MgCl2). Is there indeed a preference? If so, why?

My guess is its the solubility properties of the anions.

Chloride ions can precipitate with some metals that might appear in a complicated buffer or medium. And yes they could even compete with enzyme binding.  Sulfate will remain in solution with just about anything.

There are exceptions, but if you're making a buffer you're probably going to do better if you use the general solubility rules.


Why People have skin color between fair and dark? According to Mendel's laws traits do not show any blending. So according to his laws people only with fair or dark skin should exist. Do the alleles in this case blend? And why?

Mendel's laws were very basic to aid in the comprehension of genetics.  You think of Mendel's genes as an +- pair where + is dominant and - is recessive, making our +- gene produce offspring with the + trait but still being a carrier of the - trait.

However, when it comes skin colour, eye colour, hair colour, height, tendency to muscle growth, and a thousand other things, the gene is more like a series of ++-++-+++-, + is more recessive than -, but some of + will still show up over -.

In short, the colour of a person's skin is not a simple +- gene of dark and fair; everyone carries a certain amount of pigment genes and certain number of non-pigment genes.  The amount that one carries of each of the genes will determine his skin colour and his/her ability to pass on the dark/light characteristic.


how did we breed after the fusion ? and why can't we bread with chimps? after the chromosome fusion happened to one of our ancestors, how did he breed ? if he was allowed to breed because the chromosomal differences were still not very big back then, why can donkey and horse breed then ? ain't we supposed to be able to breed with chimps as well ?

There are plenty of people today with balanced Robertsonian translocations, they breed mostly fine, though Down's is more common than in the rest of the population, because meiosis is more likely to be messed up. If due to drift, people with those translocations became more common, eventually they could breed with each other, and make offspring with 22 pairs of chromosomes.  In theory, this drift could take over the whole human population.


Can viruses stabilize and increase the shelf life of wine and other foods? When you make wine, you use the yeast Saccharomyces cerevisiae to ferment sugary juices. After you're done, you want to avoid them doing anything by using some chemicals etc. There are also other living things (especially bacteria) that can ruin your wine or food during storage. For example, there are bacteria that would turn your wine into vinegar.

Have viruses been identified that infect and kill the bacteria that spoil wine or other foods?

There is at least one bacteriophage ("phage") that targets bacteria that spoil wine:

  The Gluconobacter phage GC1 is a novel member of the Tectiviridae family isolated from a juice sample collected during dry white wine making. The bacteriophage infects Gluconobacter cerinus, an acetic acid bacterium which represents a spoilage microorganism during wine making, mainly because it is able to produce ethyl alcohol and transform it into acetic acid.

This particular linked paper does not say anything about usage of bacteriophages as a food preservative or for food safety, but there is interest in using bacteriophages for this general application, as an alternative to the use of antibiotics in food production.

Phages are everywhere. Craig Venter went out on his yacht and scooped up a bunch for one of his papers. Phage therapy may end up augmenting or replacing antibiotics, which would be good for us humans as many disease-causing bacteria have developed or are developing resistance to them.


What causes inhalation during breathing? I have read here that the two major inhalation muscles are the (1) diaphragm and the (2) external intercostals.

Additionally, inhalation can also be caused by (1) expansion of the abdominal cavity, or (2) movement of the pelvic floor.

I thought that inhalation was caused by muscles that essentially cause the intra-thoracic pressure to drop, thus causing air to flow into the lungs to fill the absence, like a straw. This is what I thought caused us to inhale.

MY QUESTION

If my understanding is correct, then do the muscles cause this drop in pressure? Which spaces within the trunk experience this drop in pressure? If not, how exactly do these muscles facilitate inhalation?

Other than the branching, gas filled spaces within the lungs themselves, there are no other spaces within the trunk and above the diaphragm that contain gas - for a normal healthy lung. All the other space is filled with either tissue or fluid that serve to extend any pressure applied by the muscles you mentioned to the pleural sac that surrounds the lungs - like a hydraulic device. It's only the gas space that expands in volume and this is what causes air to move into that space through the upper airway. Exhalation is caused by elastic recoil - the springing back of this compartment.


Indian tropical fruit trees and fruit bearing Most Indian tropical fruit trees produce fruits in April-May. The best possible explanation for this is

  optimum water availability for fruit production.
  the heat allows quicker ripening of fruit.
  animals have no other source of food in summer.
  the impending monsoon provides optimum conditions for propagation

This was asked in a competitive examination, and being a mathematician with interest in plants, this caught my attention. Please note that this was asked in aptitude section, and I feel it more aptly belongs this SE, correct me if I am wrong.

My thoughts:

April-May is summer in (tropical) India (where I live, Kerala) hence optimum water availability looks out of option.
Considering fruit production being a part of process of propagation, though this is a favourable factor, I doubt if it is a determining factor
Animals help disperse the fruits, and less availability of food may be a favouring factor attracting animals to fruits, it is not a determining factor.
which for me looks like the factor influencing increased fruit production more than the other two.

Sorry for the layman language, I would be grateful if someone can correct me if my reasoning is wrong and explain it more precisely (preferably in layman language, though I can understand some botanical terms)

Trees fruit before the monsoon season to maximize seed germination and seedling recruitment. previous studies have shown that in many species, fruiting occurs just before the wet season such that seeds germinate and establish during the wet season when conditions are most favourable.

Smythe N. 1970 Relationships between fruiting seasons and seed dispersal methods in a Neotropical forest. Am. Nat. 104, 25–35. (doi:10.1086/282638)

So the answer is 4.


Is there a maximum testosterone limit, or is it more accurate to say use? I am constantly amazed at how we cannot differentiate between male and female.

The International Olympic committee sets the target testosterone at 5 nmol per deciliter with active androgen receptors.

What are active androgen receptors? Do they count sex hormone binding globulin (SHBG) bound Testosterone, especially in the brain? If I was serious about asking someone who would I ask ?

Whatever is the exact definition of the threshold that the Olympic committee sets, it's going to be relatively arbitrary and unfair to some people.

When it comes down to it, biology is generally messy and blurry, and that includes matters of sex and gender.  Thus, even if most people cluster in a fairly straightforward manner into male and female, there are all sorts of things like androgen insensitivity syndrome that can end up causing a person's normal body state to be judged as too extreme for their gender.

In the end, there is no simple line that can be drawn simply because the biology of gender permits many different ways for naturally occurring variations to form a continuum across any given metric that one might wish to establish.