What does "This variant falls on 11 transcripts in 3 genes" mean in the output from GnomAD? The gnomAD browser provides information on variants of genes (in this link, for the SAMD11 gene.)   The report on a particular variant, like this one,  includes the information in the header that says (for example): "This variant falls on 5 transcripts in 2 genes."

What does this mean? In particular, how can a variant occur on more than one gene? Isn't such a variant a variant of a particular gene -- SAMD11 in this case?

In this particular case, there is another unannotated gene at the same locus, running in the opposite direction as SAMD11.

http://grch37.ensembl.org/Homo_sapiens/Gene/Summary?db=core;g=ENSG00000268179;r=1:865499-865579;t=ENST00000598827


DAM enzyme distances move along the genome I am fusing a protein with a Dam enzyme (http://en.wikipedia.org/wiki/Dam_(methylase)).  The idea is that when the protein binds to the DNA, the Dam enzyme will start methylating nearby GATC sites, thus helping identify the protein binding region (using DpnI later on, and microarray technology).  However, I have no idea, in theory, how many (bps) will the enzyme traverse across the genome from its starting location.  I.e., how far (in terms of bp) from its starting location will the enzyme methylate the GATC sites.

There are methods for finding protein binding regions along the genome that use such technology, such example here: http://www.nature.com/nbt/journal/v18/n4/abs/nbt0400_424.html

Dam methyltransferase methylates large DNA molecules in a processive manner, with an effective range of up to 7 kb on either side of an initial methylation reaction.

My answer is taken from this paper:

  Urig, S. et al. (2002) The Escherichia coli Dam DNA Methyltransferase Modifies DNA in a Highly Processive Reaction J Mol Biol 319 1085-1096

The authors report on a kinetic analysis of E. coli dam methylase. For anyone using this system as described by the OP, this paper is essential reading. Their conclusion is that the methylation process is highly processive, which is to say that a single dam-DNA interaction leads to multiple methylations before the enzyme dissociates from the DNA.

I'll restrict myself to describing just two of their experiments:

Figure 5
In this experiment they analysed the time course of methylation of an end-labelled 879-mer with 4 GATC sites, using DpnI digestion to detect methylation. In this experiment all DNA was found to be either fully methylated or unmethylated - no evidence for the presence of partially methylated DNA molecules was detected.

Figure 6
In this experiment they analysed the methylation of λ DNA (48.5 kb) and were able to detect partially methylated molecules. A kinetic analysis of the data results in the following conclusions (MTase; methyltransferase):

  From these simulations, we [determine] a processivity of nav=3000. This means that after binding to the λ-DNA and starting the one-dimensional diffusion process, one MTase on average meets 3000 dam sites before it dissociates from the DNA. Since the enzyme performs a random walk, it will hit many sites more often than only once and the effective range of processivity corresponds to the square root of nav. Therefore, the dam MTase is able to methylate approximately 55 GATC sites on λ-DNA in a processive reaction in vitro. In this simulation, 4.6 associations of an MTase molecule to the same molecule of λ-DNA are required to obtain fully methylated DNA.

In a random DNA sequence GATC should occur on average every 44 = 256 residues. This suggests an approximate range of (55/2)*256 = 7 kb on each side of an initial methylation reaction.


Why has malaria only now started to develop resistance against artemisinin? Why has malaria only now started to develop resistance against artemisinin, considering the compound has been in use for about two millennia in its herbal form in China?

The WHO has reported:

  In recent years, parasite resistance to artemisinins has been detected in four countries of the Greater Mekong subregion: Cambodia, Myanmar, Thailand and Viet Nam.

However, the compound artemisinin has been used in its herbal form since at least around 400AD, when it was documented in the well known medical text 肘后方.

What are some reasons that malaria has only begun developing resistance now?

I would imagine that modern artemisinin would be more effective in completely eliminating malaria, as compared to use in its traditional herbal form. This means semi-resistant strains would more likely be killed before they are able to spread or develop resistance any further.

(archived WHO report)

Selection pressure (1, 2). One way or the other, there were few enough people taking the drug that it didn't really "matter" to P. falciparum (the deadliest of the malaria-causing parasites) on a population level until recently.

According to the 2014 paper
Spread of Artemisinin Resistance in Plasmodium falciparum Malaria (3), the driver of Artemisinin resistance is a single point mutation (ie a change of a single DNA base pair) in a single gene. The thing to keep in mind is that these single nucleotide mutations happen all the time. You yourself most likely have 3 or 4 of them relative to your parent's genomes. Thus, this particular Artemisinin resistance mutation probably has occurred in the past.

However, as with most drug resistance mutations there is likely some fitness cost paid by the individual in which this mutation occurs. In environments without the drug, wild-type (ie non-mutant) parasites will outcompete the mutants, and the mutation will quickly disappear from the parasite population. It is only when the drug becomes commonplace that the mutant parasites gain the upper hand and the mutation spreads.


Why does ampicillin in solution turn yellow? I have a universal tube with 10 mg mL-1 ampicillin. When I got it, it was supposed to be sterile. It was opened for approximately 20 minutes for an experiment and has since been standing around sealed for a good month now.

Within the last couple weeks, it has gradually turned yellow. Right now the colour is faint, with a green-ish tint.

Why would it turn yellow? I know NADH is yellow, so that was my first guess. But I couldn't exaplain why ampicillin would cause NADH to accumulate, so I discarded that.

Side info: Ampicillin acts on bacterial cell walls, maybe that might help.

Why is NADH the first thing to come to mind? Time for some physical chemistry.

Beta-lactams has a shorter ring structure which give it a different absorbance (around 322 nm apparently (source needed)) which gives it a blueish hue. Typically Penicillin and Ampicillin start off as an off-white. As hinted by @Mad Scientist, the beta-lactam rings are unstable and will undergo acid-catalyzed hydrolysis which breaks the 4-membered ring.

The Penicillin core also near a ketone which can attack the ketone in the lactam (I'm pretty sure this qualifies as enol chemistry but it has been awhile). The cyclization will form a 5-membered oxazole ring. Based on my experience, unsaturated 5-membered rings will absorb at a higher wavelength tending to result in a yellowish color (570-590 nM) so I am going to suggest that is the source of your color.

Ampicillin degradation


Why do animals have more heavy nitrogen and carbon than plants? There are two stable Isotopes of nitrogen N14 and N15. The ratio of
  15N/14N tends to increase with trophic level, such that herbivores
  have higher nitrogen isotope values than plants, and carnivores have
  higher nitrogen isotope values than herbivores. Depending on the
  tissue being examined, there tends to be an increase of 3-4‰ at each
  trophic level.

  The tissues and hair of vegans therefore contain significantly lower
  percentage of 15N than the bodies of people who eat mostly meat.
  Isotopic analysis of hair is an important source of information for
  archaeologists, providing clues about the ancient diets.

https://en.wikipedia.org/wiki/Isotopic_signature#Nitrogen_isotopes

But how does N14 'disappear' from plant to animal?

Organisms accumulate certain isotopes because their metabolic enzymes have a slight preference for molecules containing that isotope. A well-known example is ribulose-1,5-bisphosphate carboxylase (Rubisco) which is responsible for CO$_2$ fixation in photosynthetic plants: this enzyme is somewhat more efficient with $^{12}$CO$_2$ than with $^{13}$CO$_2$, causing plants to accumulate $^{12}$C.

In animals, there is an enrichment for $^{15}$N because the deaminases and transaminases that transfer nitrogen from amino acids to urea (for excretion) tend to favor $^{14}$N. So in this case, $^{14}$N tends to be removed from the body faster than $^{15}$N when breaking down dietary protein. The differences are very small though: the relative enrichment of about 0.4% per trophic level corresponds to 0.367% $^{15}$N in a herbivore, compared to 0.366% $^{15}$N in a plant.

Source: this article.


Spider identification please Can someone tell me which spider this is please? I've found a few of them in my home in North-London, are they poisonous?

It think this spider is a Tegenaria domestica also known as the barn funnel weaver in North America and the domestic house spider in Europe. See here or here (picture taken from the first link):

They are not poisonous and usually avoid confrontations, but can bite.


How does DNA damage cause ageing in yeast? As I understand it, in yeast ageing there is daughter cell and mother cell. The daughter cell is has newly "fresh" DNA and mother cell dies after some counts of replication.

What happens to the accumulated DNA damage in the yeast mother cell?

One of theory of human ageing is accumulation of damage in nuclear DNA. The daughter yeast cell is clone of mother, and has same DNA. What happens with this damage?

Edit to simplify: Why is the DNA damage not transferred at all to the daughter cell? The repair mechanism in humans is evidently not perfect, because DNA damage is one of major ageing theories. So if we die from this, how do yeast get around the detrimental affects of DNA damage that cause ageing in humans?

In eukaryotic cells there is no difference between a mother and a daughter cell - the later is an exact copy of the mother cell. This is true for yeasts as well for example for human cells. The only thing that happens over time is that the telomeres at the end of the chromosomes get shorter (unless the cell has an active telomerase which most cells doesn't) and it reaches the Hayflick limit where every further division will lead to a shortage of coding chromosmal regions and thus cause problems. If cells do not acquire any other chromosomal damage and have enough ressources, this would be the limit for their lifetime.

Of course there are DNA damages occuring over time. Most of them are either repaired by the highly efficient DNA damage repair system of eukaryotic cells, which consists of different checkpoints during the cell cycle. These checkpoints are located at transition between the different  phases of the cell cycle. If a DNA damage is identified, the cell cycle is stopped to enable a DNA damage repair by special proteins and to prevent that damaged cells undergo mitosis (here the G2-M checkpoint is important). This works schematically like in this figure (from the Wikipedia article on DNA repair):

If the DNA damage cannot be resolved, cells will either go into senescence (basically go into a permanent dormant state) or undergo apoptosis. If there are damages which are (for whatever reasons) are either not spotted or occur during the repair of DNA double strand breaks by non-homologous end joining, these are then replicated and inherited by further generations. Unless these errors occur during the replication process mother and daughter cells are genetically identical.

So eukaryotic cells acquire DNA damage over time (one of the reasons why late pregnancies pose a greater risk than early), but we are different from yeast in one point: Yeast has an active telomerase, which is not active in most of our cells (mainly except in stem cells). If the cells collect too much chromosmal damages than they will die.

The references listed below go deeper into the topic and are interesting to read.

References:

Negative regulation of yeast telomerase activity through an
interaction with an upstream region of the DNA primer
Cell cycle control in the kidney.
The evolution of diverse biological responses to DNA damage:
insights from yeast and p53
DNA damage and decisions: CtIP coordinates DNA repair and cell cycle
checkpoints
Cellular Responses to DNA Damage: One Signal, Multiple Choices


What is the scientific and common name of this bug? Captured this under my stereo microscope. Much more beautiful than appearing on my camera sensor.
Can someone help me identify it and explore more?
Also is it having a compound eye ?
Location: New Delhi.

Definitely appears to be Pentatomidae (as others have pointed out) due to shield-like, broad bodies. With over 4500 species and larval stages demonstrating significant variability even within species, ID can be difficult without knowing specific fauna, size, habitat, etc.
The OP doesn't list a size, but because OP is viewing under a scope, I assumed this is a fairly tiny species.
I came across this similar-looking unknown species (simply labeled "PK03") of the genus Eysarcoris

 Credit: CBG Photography Group, Centre for Biodiversity Genomics
The Eysarcoris genus is present in India (e.g., see indiabiodiversity.org with example of "two-spotted sesame bug")
A similar species well known throughout Europe is Stagonomus venustissimus (previously classified as Eysarcoris):

 Credit: Jose Manuel Sesma (2016); appears to be originally posted here
I cannot say if either of these species is correct (doubtful), but I think they are closer than the other provided answer.
I'll update if I find anything specific.


Domains in cell membrane How is movement of proteins and lipids between different domains of cell membrane prevented?

Why is the noncytosolic layer not able to do lateral movements between domains but cytosolic layer is able to do so?

There are various mechanisms through which membrane proteins can remain localized in the membrane. See the below figure from MBOTC (book):

(A) They can aggregate together so that their relative positions are constant.
(B) They can be anchored to the Extracellular Matrix
(C) They can be anchored to the cytoskeleton
(D) They can be anchored via cell-cell interactions (adherens junctions, hemidesmosomes etc)
(E) Not mentioned in the figure; mentioned in the comments. Lipid rafts are membrane regions which are composed of rigid lipids like cholesterol and sphingolipids. Lipid rafts are thicker than regular membrane and do not diffuse into the latter. Some proteins are specifically anchored to/incorporated into the lipid rafts (T-Cell receptor, IgE receptor) and their relative position with adjacent proteins (co-receptors) remains constant.

  Why is the noncytosolic layer not able to do lateral movements between
  domains but cytosolic layer is able to do so?

Where did you read this. Both layers can do lateral movements; if proteins are specifically "anchored" to one side of the membrane then the concept of domain applies to that side only.


When you take a very cold or hot bath how is that influencing your breath? It looks like when you take a cold shower or bath your veins get smaller and when you take hot shower your veins get wider. But is that right and do you need to breath more in both cases because you got less oxygen? If so how does it work in both cases?

There is an adaptation to being submerged in cold water in mammals called the Mammalian diving reflex.  Have you ever noticed when you jump into cold water, or enter a really cold shower you take a big breath?  While not exactly correlated with the dive reflex, it shows that there is a neurological reflex of entering cold water.  Here is a brief overview of what can happen when you submerge yourself in cold water:

Lower heart rate - aka Bradycardia, slowing down the rate of blood pumped will decrease the oxygen requirement of red blood cells, which in turn allow organs like the brain to use oxygen.
Smaller veins - aka Vasoconstriction, the blood flow in your fingers and toes is reduced, allowing more blood to be used in the more important organs.  Eventually the vasoconstriction will apply to hands and feet.
Blood shift - this adaptation allows the submerged animal to dive without having their thorax to collapse due to increased pressure.  Not necessarily attributing to breathing patterns though, so I left the boring stuff out and paraphrased.

In hot water, the opposite happens with respect to #'s 1 and 2.  Increased heart rate, like when you go running, tends to increase breathing frequency.  Vasodilation allows blood to flow more easily and is primarily for heat exchange.  Have the warmer blood in your fingers exchange heat to the environment will cool it for the return to systemic circulation.  Surface area is a large factor with heat exchange.  Hope this provided some insight.


Why is traditional rank based taxomomy considered by some as logically inconsistent with phylogenetic knowledge? Following is from wikpedia:

  Under the traditional nomenclature codes, such as the International
  Code of Zoological Nomenclature and the International Code of
  Nomenclature for algae, fungi, and plants, taxa that are not
  explicitly associated with a rank cannot be formally named, because
  the application of a name to a taxon is based on both a type and a
  rank. The requirement for a rank is a major difference between
  traditional and phylogenetic nomenclature. It has several
  consequences: it limits the number of nested levels at which names can
  be applied; it causes the endings of names to change if a group has
  its rank changed, even if it has precisely the same members (i.e. the
  same circumscription); and it is logically inconsistent with all taxa
  being monophyletic.

  Especially in recent decades (due to advances in phylogenetics),
  taxonomists have named many "nested" taxa (i.e. taxa which are
  contained inside other taxa). No system of nomenclature attempts to
  name every clade; this would be particularly difficult in traditional
  nomenclature since every named taxon must be given a lower rank than
  any named taxon in which it is nested, so the number of names that can
  be assigned in a nested set of taxa can be no greater than the number
  of generally recognized ranks. Gauthier et al. (1988)[6] suggested
  that, if Reptilia is assigned its traditional rank of class, then a
  phylogenetic classification has to assign the rank of genus to
  Aves.[7] In such a classification, all ~12,000 known species of extant
  and extinct birds would then have to be incorporated into this genus.

What is the precise meaning of "it is logically inconsistent with all taxa being monophyletic"?

You can find discussions of problems with rank-based taxonomy in light of phylogenetics in Ereshefsky 1994, de Queiroz 1996 and Ereshefsky 2002. To summarize, the main problems they identify are:

It's hard to define what exactly an "order", "family" or "genus" is; in particular, taxa at the same rank aren't always comparable. For example, order Hymenoptera, which evolved 250 million years ago and consists of over 150,000 species, with order Carnivora, which evolved 42 million years ago and consists of "over 280 species".
Not enough ranks: NCBI recognizes 29 higher taxa for Homo sapiens. That would require dozens of sub-and-super ranks to render into Linnaean taxonomy.
Names based on ranks: current nomenclature allows certain ranks to be identified by their ending, for example names ending in "-ini" refer to tribes (e.g. Hominini, Canini). If one of these tribes turns out to be non-monophyletic, it may have to be moved to a higher or lower rank to keep its monophyly -- which would have to be renamed, increasing confusion.
Redundant taxa: take division Ginkgophyta. It contains a single class, the delightfully named Ginkgoopsida, which contains a single order, Ginkgoales. In the Linnaean hierarchy, each of these taxa contains the next one along, but in terms of monophyly, they are exactly identical to each other, as they share exactly the same most recent ancestor.


Are there beneficial genetic mutations identified by consumer DNA genotyping? I'm looking at services like 23andme, and see that they identify a wide variety of genetic-based risks, like predisposition to diseases, hair loss, cancer, etc.

Are there a more "positive" DNA analysis outcomes out there? Like increased strength, cheerfulness(resistance to depression), etc?

First of all, I think it is, to a large extent, the way you perceive it. Instead of cancer-causing allele and hair-loss allele, you can think of them as cancer-protection and great-hair alleles. If you don't have disease alleles, that means that in some sense you have "life-extending" genes! Sounds much better, doesn't it?

Second of all, most funding for research is directed at disease so it is not surprising that most of the scientific knowledge is regarding this type of genetic variation.


Can we create custom gene/protein? Does it possible to create any custom gene or protein we want with current technology?
I have a protein sequence or a gene sequence about 4000 bp write down on my computer, is there anyway to "print" it to real gene molecule or protein molecule (for example use chemistry and enzyme and automatic machine..) ? What is the challenge ?

Yes, there are well established methods for synthesizing DNA with any sequence you want. Several commercial companies will accept DNA sequence (a text file) and generate the DNA for you. Genscript for example is well known.

Synthesizing the protein can be bit more tricky, depending on what it looks like and what you want it for --- proteins are way more heterogenous than DNA. There are commercially available cell-free protein synthesis systems that might be useful if you are merely interested in a peptide. Most people express the protein of interest in cultured cells though. In either case there is some biochemistry work to purify the produced protein. Genscript provides protein synthesis services as well. (No, I'm not paid by them, just don't have the energy to google other companies :)

In most cases, this works fine, and with a bit of tweaking you can produce quite large amounts. But for some proteins that depend on posttranslational modification for their function, expression can be difficult: see Can any enzyme be produced?


Online Molecular and Cellular Biology Video Lectures? I am looking for video lectures to go through to guide my reading in intro molecular and cellular biology. I've had intro bio and I study evolutionary theory, but my molecule- and cell-level knowledge is weak.

I'm finding it impossible to know where to look in a big book like Alberts, or to read Lodish without a guide, so I really need lectures to help me out. I've tried the MIT OCW assignments and a few other similar sites, but I can't seem to find a course that includes lectures. Does anyone know of any? Ideally they'd follow Watson et al. for molecular and Lodish for cellular, but I can find other textbooks too.

MIT OpenCourseWare provides very interesting material, and not only on biology.

You may be interested in seeing the video lectures from some of the Introductory biology courses, such as this one, this one or this other one.

There is, however, much more, check out the index of the available material for biology.


Confusion regarding niches in evolution theory This is the definition of a niche from Crash Course:

  An area of the environment that requires a special set of skills or traits to extract food and reproduce.

Obviously, this version of the definition has been dummed so that it appeals to mass audiences, but after some research, I believe that the general concept remains the same.

Here is what I've learnt about species living in a niche:

The more the competition, the slower the evolutionary process.
Lack of competition provides an ideal environment rapid evolution.

But these points seem non-intuitive to me, because:

Why would a increased competition slow down the evolutionary process? Shouldn't it speed it up, as different species will try to evolve the fastest in order to beat adversaries?
Why does a lack of competition promote rapid evolution? Won't it slow down the evolution, as there is no reason to evolve?

I know that there is a logical reasoning behind this, and I would very much like to understand it.

My source is Crash Course, specifically this  video. I've found it to be extremely reliable over the past, and highly doubt that they are supplying incorrect information. If anything, it is probably my inability to understand the concept.

I think part of the confusion is that these terms are very loosely defined.  Also this discusses evolution in terms of taxanomic radiation, e.g. macroevolution at large spatial and temporal scales.

Problem 1 is that you haven't been clear about what kind of competition, inter or intraspecific competition?  These will have opposing effects generally which can counter balance each other [1]
[2].  When a species is free from interspecific competition, but under high intraspecific competition, that will promote an adaptive radiation, which concurrent morphological changes.  The most famous example of this would be Darwin's finches as studied by the Grants [3].  With a lack of interspecific competition, the finches exhibited rapid morphological divergence.  Following the logic of this, you'll see that lack of competition will lead the kind of rapid taxanomic radiation the video is discussing, especially over a longer time scale.

However increased interspecific competition will have two effects. It will reduce the number of available niches for an existing species to expand into [4], this generally will drive specialization of a species, which tends to limit genetic diversity which will lead to less "raw material" for evolution to work with. This specialization though is also technically evolution.  However with fewer niches, the new species tend to arise via replacement of existing species in an existing niche, as opposed to an adaptive radiation.

So you can see how actually both conclusions are right depending on the type of evolution and competition being considered.

More interspecific competition -> More specialization (one type of evolution), less adaptive radiation (another type of evolution)

More intraspecific competition -> More adapative radiation, less specialization.

I hope that helps answer your question.


Are chilies technically peppers? Nando's chain of restaurants (UK) refers to chili peppers as just "chilies". My friend and I had a discussion with regard to whether chilies can be called "peppers" or if they do not belong to the pepper family at all. In fact, my friend added that there are 2 types of this specimen - "chilies" and "chili peppers."
To what extent is this all true, and what exactly are chilies?

Chili is a common reference to chili peppers in an abundance of countries, but they fall within the same designation as other so-called "peppers" such as bell pepper, cayenne, jalapeno, etc. because they are all of the same genus Capsicum. They differ, however, from traditional real peppers (black pepper for example) of the Piperaceae family. Capsicum actually belongs to the nightshade family (Solanaceae), but so do potatoes.

The word pepper originates from a south Indian term for the long pepper plant which was used as spice at the time and is a member of the Piperaceae family. I think that people have generalized chili as a pepper in this case due to the heat component, but this section of the answer is also off topic for this site.


How much genomic variation one usually find within a given bacterial species? If I find the exact starting position (say 1152471) of the coding sequence of a given gene in the genome of a bacterium, is the genome of the bacterium in general stable enough so that I can expect to find the same position in a different member of the same species?

Genetic variation within bacterial species can be much higher than one might expect.

First, this can be a difficult question to answer quantitatively because even just testing whether two strains are part of the same bacterial species is difficult: the "gold standard" method is actually experimental and involves whole-genome DNA-DNA hybridization (with a cutoff of 70% relatedness). Modern sequencing approaches have shown this usually corresponds to around 95% average nucleotide identity (ANI) (see here).

However, an ANI of 95% does not actually mean that the genomes are 95% identical: it means that of the shared sequences, one expects 95% of the nucleotides to be the same. The percent of the sequences that are actually shared in the first place can be much, much lower. For example, this paper compared 61 sequenced strains of E. coli. Out of the ~15K genes observed in at least one genome sequence, only 6% of genes were observed in all strains. Variably-present genes made up around 80% of a typical E. coli genome. This is a high level of variability, but not outrageous: an analysis of only nine P. putida genomes, for example, showed a core of at most 33% (ref).

So, if a gene is indeed indeed present in two strains of the same bacterial species, then it is likely to be highly conserved. But there is also little guarantee of finding the exact same set of genes in two strains of the same species. This means you cannot naively take chromosomal coordinates from one strain and apply it to another: you need to actually figure out which sequences correspond to one another in your genomes.


Variance in Fst in the infinite island model The most famous result in the study of structured populations come from Sewall Wright. He showed that in an island model, where each subpopulation is of size $N$ and the migration rate is $m$, then the pairwise $F_{ST}$ is

$$F_{ST} = \frac{1}{4Nm+1}$$

This equation gives the expected $F_{ST}$. Because populations are finite in size ($N$), genetic drift yield this value to vary.

What is the variance in $F_{ST}$ in the infinite island model?

References

evolution in mendelian population is the original paper who derived this result from Sewall Wright.

Indirect measures of gene flow and migration: FST≠$\frac{1}{4Nm+1}$ is an influential paper in the field.

GENE FLOW IN NATURAL POPULATIONS is a famous review as well.

From Lewontin and Krakauer 1973, the ratio

$$\frac{F_{ST}(d-1)}{\bar F_{ST}}$$

approximatively follows $\chi^2$ distribution of degree $k=d-1$. Here $d$ is the number of demes (number of islands), $F_{ST}$ is the random variable of the $\chi^2$ distribution and $\bar F_{ST}$ is the average $F_{ST}$ that is $\bar F_{ST} = \frac{\sum F_{ST}}{n}$, where $n$ is the number of $F_{ST}$ values.

The variance of a $\chi^2$ distribution is $2k$, therefore

$$var\left(\frac{F_{ST}(d-1)}{\bar F_{ST}}\right) = 2d-2$$

Taking $\frac{d-1}{\bar F_{ST}}$ out of the ratio, the variance of $F_{ST}$ becomes

$$var(F_{ST})=\left(\frac{d-1}{\bar F_{ST}}\right)^2(2d-2)$$

, which simplifies into

$$var(F_{ST}) = \frac{2(d-1)^3}{\bar F_{ST}^2}$$

The above expression is probably the most interesting result but one could go further and express the variance independently from the mean (by replacing $\bar F_{ST}$ by Slatkin 1991 expectation for $\bar F_{ST}$ in a finite island. It yields to

$$var(F_{ST}) = \frac{2(d-1)^3}{\left(\frac{1}{1+4Nm(\frac{d}{d-1})^2}\right)^2}$$

, which again "simplifies" into

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


What is the name of the groove down the middle of an anther? I thought it had a name along the lines of interlocular groove, but I haven't been able to find that term anywhere.

I think what you are looking for is the connective. Anthers are usually two-lobed and connected by a band of sterile tissue that also connects the anther with the filament - therefore the name, I guess (see Wikipedia article for stamen). It says

  Most commonly anthers are two-lobed and are attached to the filament either at the base or in the middle area of the anther. The sterile tissue between the lobes is called the connective.

Each anther lobe usually consists of two pollen sacs (see Wikipedia article for microsporangia). It says:

  Each anther lobe develops two pollen sacs. Thus, a two-lobed anther develops four pollen sacs situated at four corners of the anther.

And further (accentuation by me)

  The cells of endothecium possess fibrous thickenings. They remain thin-walled and constitute stomium (line of dehiscence) in the shallow groove in between the two microsporangia of the anther lobe.

This groove frequently is called by its orientation, i.e. longitudinal groove, even though I do not think this really is a well-defined technical term (but do a quick Google search for "longitudinal groove" anther and you will find several biology books using the term, e.g. this).


What are the function(s) of Alu elements in the cell? My 2008 biology book (1) states that some 10% of the human genome consists of relatively short (~300 nucleotides long) Alu elements which do not code for proteins but many of which are transcribed into RNA. Do these Alu elements have any function in the cell?

(1) Biology, 8th ed., Campbell & Reece, 2008

Alu elements are a type of transposable element. They possess the means for their own duplication and movement.  Alu is a SINE-like element that is transcribed by RNA Pol III, and so a single DNA copy can make multiple RNA copies, each capable of inserting into DNA, so it's no wonder they have a very high copy number.  Here is a picture of one means of insertion http://www.nature.com/nrg/journal/v3/n5/box/nrg798_BX1.html, although there are likely others.

They do not have "a function" per se, in that they are not selected for, they are just rarely selected against and there are so many of them.  They do not add functionality, but rather are one half of the "war" between transposable elements and viruses versus the genome's evolution to mitigate the damage they cause.  They are, of course, commonly used as sources of new DNA for sequence evolution, or can be used to create transpositions or other chromosome rearrangements, but mostly they just fail to cause too much damage and so tend to accumulate in the genome.


What is the difference between vegetable and fruit? Is there any exact definition of vegetable and fruit? How can new plant be classified?

A true fruit is a ripened ovary that usually starts ripening when it is fertilized. And vegetable is any vegetative part of the plant which is edible and contains stored food probably in the form of starch.
These definitions are not exact as there are a lot of fruits which are fruits but do not strictly follow the given definition. See Syconus, Composite fruits, Sorosis.etc

Classification is based on several different criteria, for example the mode of reproduction, arrangement and design of flowering parts and flowers and also on the basis of habitat and habit.


Can brain damage caused by physical injury affect the social behaviour of a person? Can a physical injury to the brain, resulting from an accident, and not the result of a diagnosed mental illness, affect a person's social behavior?

Socialization is a cognitive and executive brain based function that requires higher level thinking mechanisms usually dependent on the prefrontal coretex. A lot of social cues we obtain from our environment when we are young can shape our brains during its developmental growth (infancy-post puberty) and cause our brains to develop social habits and access specific social functions.

A great text book example of altered social behavior due to brain injury is Phineas Gage. He had a metal rod shot through the prefrontal cortex and it caused a severe change in his behavior. He no longer cared about social cues and people often referred to his behavior as becoming "rude" and "out of context." There are many subtle aspects of behavior that are regulated by brain functions and there are many books on the topic.

Source: Wikipedia page on Phineas Gage and
Pyschopharmacology, book by:  Meyer and Quenzer
DSM-5, text book on clinical psychology

Further Reading on Phineas Gage
- What were the symptoms of Phineas Gage after suffering his brain injury?


Partial pressure of gases in alveoli Atmosphere has partial pressure of oxygen as 160mmHg but it's 105mmHg in alveoli, and the partial pressure of carbon dioxide in atmosphere is 0.3mmHg but it's 40mmHg in alveoli.
How is the difference maintained, and can I know the mechanism behind it?

There are two main reasons for the pO2 in the alveolar air being lower than the atmospheric pO2. First, the diffusion of CO2 from the blood lowers the alveolar pO2. But the most important is the second one: there is a lot of water inside the lungs, and all this water lowers the alveolar pO2 as well.

This is the equation:

PaO2 = FiO2(Patm - PH2O) - PaCO2[FiO2 + (1-FiO2) / R]

Source: https://en.wikipedia.org/wiki/Alveolar_gas_equation


Why I have to pee more often in low temperature? I realised that I have to pee more often in winter or simply the temperature is low. Is there any scientific explanation, or just simply psychology?

This phenomenon has been demonstrated in studies [1][2] which show a significant increase in urine output in the cold. The latter study shows the biggest increase is when a person is initially exposed to the cold rather than when they continue to be exposed or rewarmed up. In the study, the average urine out was 157 mL/hour when a person was initially exposed to the cold, 103 mL/hour when they were being maintained at that cold temperature and 70 mL/hour when they were being rewarmed.

The mechanism however is unclear. This study showed that the mean arterial pressure increases. It is well known that the cold causes our blood vessels to constrict (in order to keep the blood and therefore heat inside our core body). The thought was therefore that our kidneys try to lower our blood pressure by taking more fluid out and emptying it into the bladder. This is called cold-induced diuresis.

Other thoughts include that we lose the water we ingest by sweating (perspiring), pooping (defaecation) and peeing (micturition/urination). In the winter, we don't typically sweat as much, which ISN'T counterbalanced with a lower water intake, so we need to pee more.

Another possibility is that aquaporins (the pores that water comes out from our kidneys) are inhibited by the cold. This means more fluid would be filtered out. However there isn't really much research in this area that I am able to find.


Venom Denaturing with Heat My friend got stung by a stingray yesterday and the lifeguard quickly stuck her foot into hot water (she said the water burned slightly on contact) and remarkably, she was walking without pain in a hour. I have heard that rattlesnake's bites can be helped by applying heat to denature the proteins. I am assuming this is what happened here, please correct if wrong. Because I am often in areas where immediate help in cases of animal bites/stings is not available, this is important to me as a first response as I get the person to help.

What kinds of venom are susceptible to denaturing by heat? How do I know which the previous categories a given venom falls into?
Is there a rough temperature I should aim for to denature the venom?
How likely is it that I would end up doing more harm by applying heat out of ignorance than doing nothing till I get to help (could be a day or more depending on the location)?

Regarding snake venoms, they tested 28 snake venoms at 100'C: 19/28 of the venoms were still very dangerous after 5 minutes at 100'C.

"Heating all venoms led to the denaturation and loss of some proteins; however, most of the venoms retained a significant number of proteins. Seventeen venoms contained more than seven proteins after heating, whereas five venoms contained only one to three proteins. All but nine of the heated venoms had substantial hemorrhagic activity, and Agkistrodon piscivorus piscivorus venom had very high activity, almost four times that of the second most hemorrhagic venom from Crotalus viridis lutosus."

There is a good chance that land animals have higher heat tolerance spiders and snakes can experience a lot higher heat than marine organisms.

study of marine venoms and hot water says:
Sting ray venom is especially fast to denaturize in heat, and most fish spine venoms are. HWI hot wat immersion is recommended for fish spine stings by some organizations. They did tests to find that box jellyfish, sting rays and other sea creatures stings react significantly to HWI.

They tested that 122/138 marine envenomations were improved by HWI from a variety of surveys.

there are 50,000 marine stings a year from 2000 species and
about 5 million snake bites, 2mn envonomings and 20-125,000 deaths by snakes every year from 400 species out of 3000 species of snakes which are dangerous to humans.

Dangerous snake and spider bites are generally treated in hospital, and the only wise thing to do is not to not make your blood go around your body very fast by being active after a bite, stay calm and alert.


Choosing PCR conditions How does one choose PCR conditions? Does it depend on the taxon, on the DNA concentration, on the primers or anything else?

You need to first build an initial protocol and then optimize it.

The most important to determine the conditions is the polymerase used. Some polymerases work at higher or lower temperatures and will work faster or slower. Find the default protocol from the polymerase seller and this will give you a good idea where to start.

The second most important is the primers used. Depending on the GC % in the primers and their length, the times or temperature of each step will change, or if you prefer will need to be Optimized.
The length of the DNA fragments will also determine the length of the cycles. Most polymerase sellers will includes steps to optimize the reaction depending on the quantity of DNA used, primer length and other parameters.

For more information:

Designing primers:

Taq DNA polymerase protocol example:

Optimizing PCR

PCR thermal profile, Deoxynucleoside Triphosphates and Primers are interesting paragraphs


Interpreting ChIP-qPCR or ChIP-seq I have a really basic question. Studying ChIP coupled with q-PCR or sequencing, I see different levels of a certain protein among a genomic region. I cannot really understand how can we have different protein levels. I thought that the binding of a protein in a region is bivalent-it occurs or not. But, as I can understand, we can have different concentration/quantity of protein bound to a region? And if this is the case, how in ChIP-qPCR we get finally DNA fragments, so how can we measure this binding from the quantity of fragments?

Protein binding to DNA is not bivalent. ChIP is enriching for DNA to which your protein of interest is bound, but that protein may bind certain sites throughout the genome more strongly and frequently than others. Stochiometric effects play a role, as do the strength of the binding motifs.

Some proteins bind very specifically to a given sequence, but most allow for some degeneracy in their binding sites. A strong site will be bound more frequently (and thus more highly enriched during ChIP) than a weaker site. Not just the presence, but the frequency of binding is what ChIP really measures.


Can Naegleria fowleri enter through wounds into the bloodstream? All the sources I've read said that Naegleria fowleri enters the brain through the nose. But lets say that someone had cuts on their arm or leg and they are swimming in water that is conducive to Naegleria fowleri growth. Could it enter the cut into the bloodstream and then into the brain or cause some other type of damage if it enters the bloodstream?

No, Naegleria fowleri is a free-living excavate form of protist that lives in warm fresh water. Fowleri finds its way into the brain by eating through the olfactory neurons in the nose where it multiplies itself greatly by feeding on nerve tissue.

Once it penetrates the nervous tissue, fowleri's feeding  results in significant necrosis of and hemorrhaging in the olfactory bulbs. The protist then climbs along nerve fibers through the floor of the cranium via the cribriform plate and into the brain.

Since the protist travels by feeding on nervous tissue, fowleri could not enter the brain via bloodstream.

Just some more facts about Naegleria:

Death usually occurs within 14 days of exposure due to destruction the autonomic nerve cells of the medulla oblongata.
Luckily for everyone this disease is rare. There were only 300 cases as of 2008


What happens to lactic acid I eat? Let's say I drink some Kefir Milk, what happens to the lactic acid in the Kefir Milk that has entered my digestive system?

First, there are two different isomers of the lactic acid, the L(+)- and the D(-)-form. Both differ in the position of the OH-group in the molecule:

Both turn polarized light in different ways, the D(-) to the left and the L(+) to the right. The physiological form of lactic acid for the human body is the L(+) form, which is taken up in the gut and then metabolized by the L-Lactatdehydrogenase to form pyruvate and NADH.

For the D(-)-Lactate is has been thought the the D-Lactatedehydrogenase is only present in some lower animals and bacteria and that this lactate isoform is mostly excreted. This seems not to be true and there is some D-Lactatedehydrogenase in humans (and other mammals) as well.

See these publication for more information:

D-lactate in human and ruminant metabolism.


Why isn't life expectancy normally distributed? Lots of phenomenon in nature can be plotted onto some sort of normal distribution, and that makes intuitive sense to me (such as human height). Why then, does global human life expectancy drop off so suddenly after ~85 years old? Is there some factor which suddenly increases mortality significantly? How come so few people (statistically speaking) age above 85 years old?

Inspried by this question

The histogram you show isn't a distribution of age-at-death for individuals, it's a distribution of life expectancies for different countries.  The post you link takes data from a table on the Wikipedia page List of countries by life expectancy.  Interpreting the histogram you posted, we see average life expectancy seems to hit a wall around 85.  This does not mean that individual human life span is not normally distributed.
Excluding deaths at infancy, the peak of the death rate curve appears to be at about 88 years for women in the United States in 2014, as seen in a blog post by the The Max Planck Institute for Demographic Research:

Lifespans are increasing and becoming more similar: While life expectancy of US women rose by almost 19 years between 1933 and 2014 (from 62.8 to 81.3 years), the variance in the distribution of deaths over age shrank by ten years. Data: Human Mortality Database © MPIDR


How are individual neuron firing rates characterized? I'm reading this paper that the Human Brain Project published in Cell and I'm confused how they recorded the firing rates shown in the firing below:

In the publication, they mention that they use the Petilla convention. However, upon reviewing that publication, I was unable to determine the procedure of characterising neuronal firing rates. How are they able to isolate a neuron's firing behaviour away from the network it is usually contained in? Where do they measure the outputted firing rate?

I am aware that usually to characterize a neuron in a network, Spike Sorting or single-neuron recording can be used, however this doesn't seem like a valid way to characterize the physiological properties of an individual neuron.

If you consult the experimental procedures section of the paper, you can find that they used methods previously established in three papers. However, upon reviewing these papers, it appears that the neurons were stimulated while still inside the tissue, but after the tissue had been sliced. However, this seems so absurd that I must be misreading it.

How were the electrophysiological properties of these neurons characterised?

However, upon reviewing these papers, it appears that the neurons were
  stimulated while still inside the tissue, but after the tissue had
  been sliced. However, this seems so absurd that I must be misreading
  it.

You're not misreading it. I can't access the paper you refer to, but this is a standard way to measure the electrophysiological properties of individual neurons, and has been for more than 25 years. (I'm really curious what you find "so absurd" about this).

I'll take an educated guess (since I can't read the methods online) that these recordings are from rats (or possibly mice), using whole cell patch clamp technique in thin slices of the young rat neocortex. Briefly put: the animal is sacrificed, the brain is removed, it is sliced into about 400 micron thin slices using a vibrating razor blade, and the slices are kept in a artificial cerebrospinal solution that allows the neurons to remain functional for a day's worth of experiments. Then individual neurons are imaged under a microscope and "patched onto" with a glass micropipette that contains a silver wire. Electrical events in the neuron can thereby be recorded into one's computer and plotted as shown in the figure you provided.

In this case, what's shown are what are known as current clamp recordings, in which current is injected into a neuron and the resulting voltage changes are recorded. Here, they are injecting a depolarizing current to make the neurons spike (have action potentials) and seeing that the neurons they sampled vary in their spiking properties. Some are fast spiking, some are slower spiking, some have different spike waveforms or patterns of spiking.


Is this a sentry palm? I "inherited" a plant and was trying to identify it (to understand how to take care of it - plants usually have a hard time with me).

I belive this is a sentry palm (from photo matches gathered on Internet) but my leaves seem much more narrow than the ones on the pictures.

The plant is in France and is probably not a fancy one (in the sense that it should probably be available in Ikea or a general plant store).

I highly doubt that this is a sentry palm. It seems to be a golden cane palm, also known as areca palm or butterfly palm, Dyopsis lutescens.

Here is an image for comparison:

And here is a close up of the leaf:

This whole structure is just 1 leaf. What you called "leaves" in your question are actually just leaflets (or foliolum in Latin).


How can homosexuality evolve despite natural selection? I would imagine that the answer to this question would be population control, especially since even if one sibling is homosexual this does not necessarily mean that the other siblings will be too.

Several years back, results of a twin study (Zietsch, et al., 2008; popular press in The Economist) suggested that genes associated with homosexuality make heterosexuals who carry the same genes more reproductively successful. This would explain the observation that, for example, sisters of homosexual males have more offspring.

  We show that psychologically masculine females and feminine men are
  (a) more likely to be nonheterosexual but (b), when heterosexual, have
  more opposite-sex sexual partners.

So if more sexual partners in heterosexuals is correlated with more offspring, then the genes associated with homosexuality may lead to more offspring in heterosexuals that carry them. So these "homosexuality" genes could easily be maintained in the population by conferring a reproductive advantage to siblings.

The authors conclude:

  Taken together, these results suggest that genes predisposing to
  homosexuality may confer a mating advantage in heterosexuals, which
  could help explain the evolution and maintenance of homosexuality in
  the population.


Basic text/notes on DNA structure (for non-biologists) I am a mathematics grad student researching knot theory, and I've recently discovered that there is a connection between knot theory and DNA structure (if I understand correctly, when DNA strands repackage, they do it in a way similar to what is known as Skein relations in knot theory, therefore tools from knot theory can be applied to DNA research).

The problem is that I have almost no background in biology, therefore it is difficult for me to understand how exactly DNA repackages and what happens on the molecular level.

Could anyone suggest some basic (and preferably not too long) text which gives an introduction to the structure of DNA? I have some basic background in organic chemistry, and I am not really looking to understand the topic thoroughly, just to visualize what's going on so I could see the analogy to the mathematical theory.

Thanks in advance!

this is a special topic, I'm assuming you have looked over the basic Watson and Crick stuff.

Maybe closer to your interests DNA does tangle and needs constant maintenance of the amount of winding to keep it properly ordered.

I would look at topoisomerases and DNA origami to start with.

Topoisomerases are a class of enzymes that help DNA pack up and wind up into the compact forms of the chromosome when its wound into solenoids in chromatin and unwind into the looser forms when it is loose.

DNA origami is a field of study which uses DNA as a self assembling template for making three dimensional structures.

Maybe this helps?  let me know if we can narrow the specifics of your interests.


What is the purpose of DMT in plants? N,N-Dimethyltryptamine (DMT) is found, besides humans and other animals, in many plants(50+).
In humans (in the pineal gland) it is suggested that it is used for our immune system.

  Immunomodulatory activity may contribute to significant anti-inflammatory effects and tissue regeneration. [Wikipedia]

The question is, could it have a same function in plants or it has a more defending function, like other drugs that are derived from plants?

As you guessed, tryptamine alkaloid biosynthesis is generally associated with herbivore deterrence in plants (see e.g. paper 1, paper 2, paper 3), as these compounds can be toxic to animals. I wasn't able to find a reference specifically related to DMT, as it is only one of a family of tryptamine derivatives. For example, the papers just linked to shows that expression of an enzyme catalyzing the creation of the tryptamine precursor of DMT is associated with lower herbivory by insects and nematodes. The second paper also shows that this seems to have little to do with plant morphogenesis via the auxin pathway, which was an alternate hypothesis for herbivory deterrence.

The papers also include a little speculation about the mechanism by which DMT inhibits herbivory on the animal side; it seems to come down again to animal toxicity and behavioral alteration.

So, as with other cases, likely the reason that plants express many secondary metabolic compounds is the same reason that humans use them, namely that they can have strong physiological effects on animals. But I wasn't able to find literature specifically about DMT in plants.

Hope that is helpful.

Update: found an entomology paper that goes into more detail about the effects of a variety of tryptamine derivatives on leaf-cutter ants. The compounds are toxic, but also there are some interesting insights about effects on insect behavior.

Update 2: Looking at question again, realized that I didn't address immune system response.

What's important to note is that plants don't have something homologous to animal immune systems, e.g. antibodies and so forth. They instead substitute various chemical responses, many of which are mediated by signaling factors such as jasmonate and salicylate, that have strong effects and sometimes e.g. kill off pieces of infected tissue (sort of a scorched-earth strategy). This part of plant biology is quite complex and bears further reading.

So in this sense, yeah, sure, tryptamines could be thought of as an immune system, in that their production facilitates resistance to their biotic environment. But that mechanism is completely different from any immunomodulatory effect of DMT or similar compounds in humans.


What are most common natural causes of death? What are most frequently occurring natural causes of death?

The WHO has data from 2002 where they have classified and counted causes of death. I have treated the following as natural causes:

Cardiovascular disease (29.34%)
Infectious & Parasitic disease (23.04%)
Cancers (12.49%)
Respiratory disease (6.49%)
Perinatal conditions (4.32%)
Digestive disease (3.45%)
Neuropsychiatric disorders (1.95%)
Diabetes (1.73%)
Genitourinary disease (1.49%)
Maternal conditions (<1%)
Congenital abnormalities (<1%)
Nutritional deficiencies (<1%)
Endocrine disorders (<1%)
Neoplasms (<1%)
Musculoskeletal disease (<1%)
Skin disease (<1%)

I treated the following as non-natural causes:

Intentional injuries
Non-intentional injuries

The sum of the groups explains 96.7% of deaths. I think the remaining 3.3% would be other or undetermined causes, and rounding errors in the data. The natural causes accounted for 87.9%, and non-natural causes were 9.1%. The most common causes were cardiovascular diseases, infectious/parasitic diseases, and cancers.

It is difficult to assess how natural the cause of deaths are. For example, many cancers, cardiovascular, and respiratory diseases are more common in obese people and smokers (often self-inflicted damage), nutritional deficiencies are often caused by failing welfare and social systems.

Additionally, among the recorded causes of death in England and Wales in 2011, of the total 484,367 deaths recorded, 17,590* deaths were from extrinsic sources (accidents, homicides etc.). This is around 3.6% of deaths. In this data, the most common causes were cancers (29.6%), circulatory diseases 28.8%, and respiratory diseases (14.0%).

According to the CDC, in 2013 there were 2,596,993 deaths in the US, and 92.5% were of natural causes. Of those, the principle causes were heart disease (24%) and cancer (23%). There's a good table at the bottom of this site.

Rates of natural and non-natural causes of death will likely vary greatly by country given different health risks (e.g. malaria in Africa vs Europe), health care services, extrinsic risks (e.g. traffic accidents in Sweden vs India).

$*$ The table in the article features a potential mistake, it seems the columns are incorrectly labelled


Does E. coli survive at any pH level? Does E. coli survive at any pH level? If I was to incubate it in agar of different pH, would it still form a bacterial lawn as it's called?

I assume you are asking if E. coli can survive extreme pH conditions and according to this study E. coli K-12 W3110 survives at pH 1.2 – pH 2.0 under low oxygen. This study cultured different strans overnight and exposed to pH 2.0 for 2 hours before diluting 1:80,000 and 1:400,000, under anoxic and aerated conditions. Dilutions where then plated allowing colonies to grow up overnight at 37 oC so this study measured survival as far as I can tell. E. coli can demonstrate robustness and E. coli survives and grows 'accustomed' at pH 7-8 based on the paper here. However it would be great if you clarified your agar pH and the E. coli genetic background you are interested in if you have a specific question about its particular limits (growth or survival).


phylogenetic analysis of gene enrichment? Are there any tools to do phylogenetic analysis of gene enrichment? This is, I have a list of genes from an experiment performed in several species, with a z-score that can be described as "enrichment" associated to each gene in each species. It's not gene expression, it's enrichment of a certain marker n the gene. I would like to compare these lists, that are not fully overlapping, across the phylogeny of the species, to see significant changes in the trend of enrichment at the gene level, or at the branch level. What tools could I use for this?

Species1 Z-score
Gene1    0.532
Gene2    0.531
...

Species2 Z-score
Gene1    0.51
Gene3    0.505
...

Phylogenetically analyzing genes that are not present in every species may present you with some problems, but it is completely feasible to simultaneously analyze the relatedness of the species (based on your enrichment score), and the relatedness of the scores themselves.

Forgive me if this is too 'simple' an analysis, but you have not said what you have tried.

My choice of approach would be to use R (open source stats package) to generate a heatmap of your matrix of data. There are plenty of options for the method of clustering, but the defaults tend to produce quite a nice heatplot, with hierarchical cluster analysis performed on both dimensions of the data (you can specify only 1, or even none, if you prefer). I have used the following code to simulate some data to generate the below heatmap;

# generate 10x10 matrix using random data
x <- as.matrix(data.frame(rnorm(10),rnorm(10),rnorm(10),rnorm(10),rnorm(10),rnorm(10),rnorm(10),rnorm(10),rnorm(10),rnorm(10)))
# use heatmap function on the data. "labRow" and "labCol" simply remove the labels.
heatmap(x, xlab="Genes", ylab="Species", labRow="", labCol="")

Because it is randomly generated data there are no patterns really, but if you were to stick you real data in there it would look better no doubt. (In an actual analysis you will want to leave the labels on, I was just simplifying the plot). The function can handle missing values, so you could put all the genes you want to analyze in there, even if not all species have them.

Using this method you could see the most closely related species by gene enrichment, and also which are the most closely related genes (in terms of enrichment for your TF).


Should corn be considered an invasive species in the Midwest? Per the United States Department of Agriculture (USDA) an invasive species is defined as:

  non-native (or alien) to the ecosystem under consideration

  whose introduction causes or is likely to cause economic or
  environmental harm or harm to human health

Corn in the Midwest, USA (often referred to as the Corn Belt) would seem to satisfy the first requirement as an invasive species as it is not native to this area.  Regarding the second requirement, it could be argued that corn in the Midwest causes environmental harm because it is in place of many indigenous plants that many other animals rely on to survive.  For example, habitat loss is considered a cause in the decline of the regal fritillary (Speyeria idalia) butterfly.

A Google search brought me to this Q&A site where many argued that corn is not an invasive species because it cannot survive or spread by itself without human intervention.  I tend to agree with this logic but it does not seem to be within the scope of the USDA definition.

Should corn be considered an invasive species in the Midwest?

Should corn be considered an invasive species in the Midwest?

I agree with commenter Bryan Krause in that this question requires opinion -- but I think it only requires opinion as to the definition of what we consider "invasive".

The concept of an "invasive" species is highly contested among biologists. It is often used interchangeably with the terms non-native, non-indigenous, and alien.

Some people think we should consider a species as 'invasive' even if it is native to the region but is causing "economic or environmental harm or harm to human health". For example, the USDA considers Juniperus virginia a native species, despite its spread from plantings and its economic and ecological impacts in 'invaded' regions.


Do de-husked seeds germinate? As simple as that, lentils beans and other legumes are sold both with and without husk, and often I make beans with the husk germinate in a jar.
Do those without husk germinate as well? Or are they simply dead?
I'm asking this because my girlfriend told me she's using de-husked legumes, but that they take longer and less of them actually do sprout.

De-husking and industrial storage reduces the germ's longevity quite a lot, although quite a lot of germs will still be viable if the humidity and microbial conditions are very stable, perhaps even a year.
De-husking will accelerate this graph:

The husk is designed to keep the germule in peak condition in the wild until whichever season it is supposed to germ, through droughts, rains, cold weather, changes in humidity, predation, infection.
If the germ is de-husked and left in natural conditions, it rapidly loses vitality and deteriorates. In storage it's kept in conditions made to discourage microbes, so it will last longer, but it will absorb ambient humidity changes and deteriorate much faster than with a husk.


Bee Identification, Rochester NY bee I found in Rochester NY, any guesses what species?

It is a bee in the genus Megachile, in the family Megachilidae, not Halictidae.

Megachile are leafcutter bees, and have scopal (pollen carrying) hairs on their bellies (ventral side of their abdomen).

Most bees in the family Halictidae have scopae for carrying pollen on their legs, though they may have hairy bellies with substantial pollen carrying capacity.


How is it possible for a new species to evolve? Suppose a new species is created from a random mutation that happened during an instance of reproduction in an existing species. How can that new species survive and flourish if there only exists one of it's kind and therefore it's not able to reproduce? By definition a species can only reproduce with others of the same species, no? It seems to me the only way it could is if a mate is created due to a separate occurance of a similar mutation, and the chances of both mutations occurring at around the same point in timespace must be very close to zero. And even if it were to happen, it seems to me the offspring wouldn't be able to reproduce due to problems with inbreeding.

Suppose a new species is created from a random mutation that happened
  during an instance of reproduction in an existing species.

No honest informed person would define species in this manner.

This is a better analogy


Can frogs see clearly under and above water? If humans attempt to see underwater, the image is blurred due to refractive differences in air and water that disrupt the normal refractive effect of the lens in the eye. A diving mask overcomes this issue. How then do frogs accommodate their lenses in both air and water? Are their images clear in water and blurry above, or vice versa?

As far as I know, their lenses are made up of epithelial cells and fiber quite similar to the human eye lens, or am I incorrect here?

Short answer
Frogs are nearsighted on land and farsighted under water.

Background
Frogs are reported to be nearsighted on land, but farsighted underwater (source: Chegg Study). Nearsightedness (myopia) is a condition in which near objects are perceived clearly, but objects farther away are blurry. Farsightedness (hyperopia) is the reverse. The human counterparts of these conditions are shown in Fig. 1. Humans focus images on the retina by changing the shape of the lens; to focus on near objects, light is more strongly refracted by making the lens more spherical in shape. For far-away objects the lens is flattened such that light is less refracted.

Fig. 1. Near- and farsightedness. source: Hyperphysics

In humans refractive errors are common and can usually be successfully treated with corrective lenses.

The cornea adds substantial refraction to the optical system of the eye, namely about 43 diopters. As a comparison, normal prescription glasses often have only a few diopters worth. In water the refractive index of the cornea is mitigated, as water and the cornea have about the same refractive index (source: lasikmd). Hence vision is blurred for humans under water, because images are focused far behind the retina, resulting in hyperopia.

Frogs have another way of correcting their retinal image. They focus on objects at different distances by using specialized (lentis) muscles to move the lens closer to or farther from the retina (Fig. 2), like the focusing mechanism of a camera (Douglas et al., 1985). However, the lentis muscles can adjust the focus only for approximately 10 diopters worth, with an accompanying shift in lens position of about 150 μm. Hence, because of the huge effect that water has on the corneal refraction (~40 diopters), a frog's lens cannot sufficiently correct the refractive state of the eye to achieve normal vision (emmetropia) both above and below water. Apparently it settled evolutionary spoken somewhere in the middle, namely myopic on land, and hyperopic under water.

Fig. 2. Cichlid eye. Accommodation results from the movement of the lens in the pupillary plane using the lentis muscles; the musculus retractor lentis, and the antagonistic ligamentum suspensorium. source: Vision in cichlids

Reference
- Douglas et al., J Comparative Physiol (1986); 158(1): 33–143


What is that insect? I was bitten by this insect (no big deal, but I cannot identify it). I took a picture of it (with my phone, so the picture is not great). I was sitting under some sort of vine tree (downtown though), and I think it fell from it. If that helps it happened in mid July 2016, in Montreal, Quebec, Canada.

I looked on several resources for biting insects in Montreal but I could not identify it. It was very small and yellow.

Also, the insect bit me, took some blood, and left me with a light burning sensation for about 10 mins. I am not a specialist at all in this, and I know nothing about insects, so I apologize for what I am going to write, but if I was to describe it, I'd say it was a weird mix between a very small yellow lizard (for the shape of the first half of the body) and a quite furry(for how it looked under). The head was shaped like a sharp triangle.

That's all the information I have, I hope that helps you identifying it!

The shape looks like a leafhopper for sure. There are several species that are known to bite humans though it is not very common. Without a better photo however it may difficult to say what species it is for sure.


Macrophage pathogen fixation Overly simplified, macrophages recognise pathogenic patterns and endocytose anything that matches them.

That also works on bacteria, which are quite often very mobile. What if a bacterium was just randomly twitching around when a macrophage recognised it - would it be possible for it to "swim away" (as a reaction to the macrophage or just randomly)? Or do macrophages employ some sort of fixation mechanism to keep anything they recognise close until it is engulfed? Or is engulfment in itself just so quick?

The explanation one of my tutors offered was this:

In cell recognition, it is very common for interactions between proteins to be based on weak interactions, but a certain degree of binding can trigger a (conformational) change which will instead establish a very strong interaction between the proteins involved.

In other words, if the contact is specific enough to 'count as a recognised pathogen', the interactions will immediately change to strong forces and the pathogen will not be able to move away.


Why are lions the only social cats? We know that almost all cats are solitary.
How did the Lions (Panthera leo) end up social animals? Do we have an explanatory evolutionary path describing how the Lions became social while the rest of the felines remained solitary?

I'm not asking what general rules apply to evolution, but, rather - what evolutionary path has led to this specific outcome.
I know a bit of evolutionary game theory. No need to reiterate the obvious. I'm asking if we know the mechanism or the evolutionary pressure in this particular case.

This is not a direct answer to your question, but I want to point out that your basic premise is partially incorrect. Other felines also form social groups. For instance, male cheetahs form coalitions (also see Cheetah outreach at http://www.cheetah.co.za/c_info.html), often for life, which generally makes them more successful in defending territories. Female feral cats also form social groups in some environments (see e.g. Natoli et al, 2007), where females sometimes co-rear kittens. There is even evidence that tigers share kills with related or unrelated individuals (see Wikipedia: Tiger for examples), and tiger home ranges can overlap in complex ways. On the other hand, lions (both males and females) are sometimes solitary, and this partially interacts with their living environment.

My point is mainly that sociality (in general or in felines in particular) is not either/or for a particular species, and other felines also show social behaviours and sometimes form groups (so sociality should be viewed as a sliding scale). Granted, lions are definitely the feline with the strongest social behaviors, and they form the largest social groups. It is therefore interesting to think about why that is the case, and what group dynamics and tradeoffs that determine the social behaviours of lions.


Can all animals of the same species crossbreed? For example, take Canis lupus, the species of dog and wolf. Within their species, can all dog and wolf types crossbreed? We can forget the logistics and assume this is all done through artificial insemination or in vitro methods (let's assume that the in vitro methods would be feasible).

If yes to the main question, does cross-breeding stop at the species class, or does cross-breeding extend across other taxonomic classes? From what I gathered, the taxonomic classes seem somewhat loose in their definitions. Perhaps I should ask, is there a rule "in general" to cross-breeding?

Let me know if this question ought to be refined in any way.

Species definitions are a somewhat contentious part of biology. There are no hard boundaries in nature that mean "this group here is one species, this group here is another species". Some people don't even believe that species truly exist and there are only gradations of relatedness. That being said, the Biological Species Concept is one of the more popular species definitions.

From the linked website: "The biological species concept defines a species as members of populations that actually or potentially interbreed in nature". Thus, by definition, all animals of the same species can and do interbreed in nature. If two individuals breed in nature, they are considered the same species (under this definition).

Of course, you can already see some problems with this definition. Under the BSC, are a dog and a wolf the same species? Do dogs and wolves breed "in nature"? Of course, fertile half-dog half-wolf animals exist, but does it even make sense to ask whether a domestic species breeds "in nature". I suppose you can say they can "potentially" breed in nature. But how do you define "potentially" breeding? Asking questions about species can lead to many exciting debates.


Difference between ‘tagging’ and ‘conjugating’ a fluorochrome to an antibody? The Wikipedia entry on fluorescence repeatedly states that “a fluorochrome must be tagged or conjugated to the antibody”.

How is tagged or conjugated different? Is this a mistake or are these indeed different concepts?

Conjugated and tagged mean the same thing here, although I would advise against using tagged here.

In the context of antibodies, tagging means the addition of a (short) peptide sequence to a protein. Either to do something useful (degradation tag, HHHHHH-tag) or just as an epitope for an antibody.


Why was disease transfer to the Americas one-way? It is well known that the European colonists brought many infectious diseases to the Americas, and that these had a deadly effect on the native populations, because they had no immunity to them. Were there any local infectious diseases to which the colonists were not immune? I’ve never heard of such. I’m not aware that the colonists suffered any epidemics, or that they brought any new and unusual diseases back to Europe.

Why not? Is this merely an accident of history, that there were no infectious diseases in the Americas which did not already exist in Eurasia? Or is there some explanation?

In "Guns, Germs, and Steel" Jared Diamond includes quite a bit on this topic. His conclusion is that Europeans, and old world humans in general were much more exposed to their farm animals, often living in the same buildings. This allowed a much greater number of diseases to jump from animal to human, forcing us to development immunity against these pathogens.

The native americans never domesticated as many animals, and weren't exposed to as many pathogens. As a result the foreign pathogens could freely move through their populations.

So why did it only go one way? A lot more Europeans came to American than vice-versa, so there just wasn't as much opportunity for American pathogens to move to Europe. Additionally, the Europeans brought a lot of animals here, including cattle, horses, and pigs. These would have carried pathogens as well, again, very few American animals were taken to Europe.


Is the colour of a chrysalis predetermined? Usually, chrysalis of butterflies camouflages with the surface it is attached to, for protection, as I understand it. There are exceptions, though; For example, the golden chrysalis of Euploea core is reflective and literally pops out of its background. My point is, what is the evolutionary advantage of that?

Edit: user -personjerry pointed out that shiny colours indicate poison.
So the main question now is,  if the aim was to scare off predators, why aren't they red/black in colour (as red means impending danger in the animal world)? Also, wouldn't developing a red pigment be much easier?  In these cases, is the colour predetermined?

Generally, in biology nothing is designed but if something is working it is saved for the future generations. Chemistry of colors is a complicated field, you can't just slightly modify single "color" molecule to get any color you want. Maybe in chemical sense the material of this shell can be easily modified to get shiny. Suppose it happened occasionally once due to sporadic mutation and no one dared to eat this chrysalis, which gave abundant progeny.


Human evolution: Where *exactly* did the first human come from, whose parents were not? Layman here. So I have never really quite understood this facet of human evolution, (or any other for that matter), in that, I understand the evolutionary process, but I get lost on the 'border' cases.

For example, we, as humans, evolved from monkeys, (to use the colloquial term, I am not a biologist by any measure).

My question is, doesn't this mean that at some, discrete point, there had to have been a human, whose parents were not? If that is true, how does that work, in the sense that we now have species1 giving birth to species2.

If not, then how exactly does this border case work? The only other alternative I see, is that the borders are 'fuzzy', but then that necessarily means that the definition of a species is itself fuzzy, which I understand is not the case.

Thanks!

but I get lost on the 'border' cases.

Not surprisingly, since there are no borders, and this is probably the greatest misunderstanding: Evolution is gradual. It’s not generally possible to say where a complex feature (or a species) starts and another one ends. We could in theory say, for individual mutations on the genetic level, in which generation they first occurred, or when they became fixed in the population. But we cannot infer from these atomic changes where our ancestors started becoming humans. So the whole concept of “first human” is not biologically meaningful.

The best analogy remains a gradient between two colours. Going from the left, where does blue end and red start?

By the way, you spotted this very well by yourself:

  [if there is no first human] then that necessarily means that the definition of a species is itself fuzzy

Exactly, that’s the case. For more details on definitions of species, refer to MCM’s answer. But it’s indeed crucial to note that the definition of species (or any other biological classification) is an ever-changing approximation which tries to fit a definitive yes/no answer onto a gradually changing scale.


Why hand washing causes skin to dry? This seems counter intuitive: dry hands mean low humidity, so why when humidity is increased, by washing hands, they become even more dry, eventually?

In particular, why such hand dryness is usually observed in a dry climate?

I will assume the hand washing you speak of involves soap.

The human skin (which also covers hands) is a complex organ with an underlying system of glands.

One of these is the exocrine sebaceous gland which is responsible for the production of a substance known as sebum. This substance is primarily composed of triglycerides, wax esters and other fatty acids. Sebum makes human skin waterproof as it's constituents are not water soluble (oily).

The action of soap on oily substances typically involves increasing their solubility in water so that they can be easily rinsed upon being dissolved. So when one washes their hands with soap they remove the oil layer secreted by the glands under their skin.

Removing the oil layer makes the skin susceptible to drying up as oil reduces the rate of evaporation of water on the skin to maintain a moisture balance. This is the reason why most brands of lotion have a moisturizing effect (or marketing statement).


Why are we carbon-based? Is that because of evolution?
Does it have something to do with its amount in the universe?
Carbon compounds form the basis of all known life on Earth, and the carbon-nitrogen cycle provides some of the energy produced by the Sun and other stars as I know.

We are carbon-based because carbon is the only molecule that is able to form the long, long chains of hundreds of molecules that are required to from proteins, DNA, etc. Absolutely no other molecule will do it. (Whatever you may have heard on Star Trek about Silicon-based life, Silicon doesn't form chains anywhere near as long.) Plus it's very handy in that its oxide is carbon dioxide, which is a gas, so using it and oxygen (another gas) as the end-points of respiration is very handy, you can get rid of a lot of gas very quickly. Silicon's oxide is, well, glass.

If you want to know why only carbon forms long chains, it's because of its size (not too large like silicon), its medium electronegativity (it's in a middle column of the periodic table, so it forms what are called "covalent bonds" very easily, especially with hydrogen, the #1 element in the universe by far; covalent bonds are easy to form and easy to break) and its valence (again, because of its position on the periodic table -- it forms four bonds, the maximum for a smallish molecule, giving it the geometry to form long chains).

For life to be based on anything but carbon, it would have to be made only of smaller molecules, which to our knowledge isn't very likely. Our DNA molecule is made up of billions of atoms; it's difficult to conceive how heredity could work on a small scale.


Is "computational biology" different from "bioinformatics"? Are "computational biology" and "bioinformatics" simply different terms for the same thing or is there a real difference?

I found this post by Russ Altman quite good.  Below is his opinion about the two similar but distinct fields:

  Computational biology: the study of biology using computational
  techniques.  The goal is to learn new biology, knowledge about living
  sytems.  It is about science.

  Bioinformatics: the creation of tools (algorithms, databases) that
  solve problems.  The goal is to build useful tools that work on
  biological data.  It is about engineering.

Just as a note:

This is just one persons opinion and I have heard many other definitions for both of these terms.  For example, one person I know mentioned that he believes computational biology is concerned with very theoretical research such as NP-hardness (ie. articles published in the Journal of Computational Biology). Other people think that bioinformatics is an applied field that is essentially using already published tools.


Did the jackal (wild African dog) evolve independently or with some form of human domestication? The jackal is a wild dog species in Africa that feeds on carrion, much like the hyena.
Pop science, as it were, would make us believe every dog species emerged as a result of human domestication. Was that the case for every dog species? Or might some have evolved independently?
Another way to phrase this would be: Do wild dog species have a completely wild heritage, or did they branch off of some previously domesticated line?

This answer is just for African golden jackal evolution, but this website (sciencemag.org) explains that...
“...researchers compared genomewide DNA samples from jackals, gray wolves, and dogs. They found that African golden jackals diverged from coyotes and gray wolves some 1.3 million years ago...”.
Also, this Wikipedia article about Canis arnensis (the Arno river dog) (I know that Wikipedia is unreliable but it had related helpful information) explains that...
“The Arno River dog has been described as a small jackal-like dog. Its anatomy and morphology relate it more to the modern golden jackal (Canis aureus) than to the larger Etruscan wolf of that time. It is probably the ancestor of modern jackals.”


What does it mean "specialized populations of neurons"? I'm reading now the Campbell biology book (10th), and on page 1063 is written:

  In all but the simplest animals, specialized populations of
  neurons handle each stage of information processing.

What does it mean "specialized populations of neurons"? I always knew that there is a population in biological hierarchy of creatures rather than the cells which assemble the creatures.

It's just a specialized group of neurons. You can call a group of cells a population of cells. They are specialized because those particular neurons carry out a specific function.


Is this Quercus coccifera? This specie grows in a dry hilly area in the south of France close to Marseille. I made the picture today. It is quite dominant and grow close to the soil maybe about 50cm.

Yes. That is definitely a Kermes Oak / quercus Coccifera.

It should start blooming in a week or two, in case you're still in the area by then I recommend checking it out.

It is thriving in that area specifically because it's a dry area, otherwise they tend to be pushed out by Holm Oaks / Quercus ilex.

The combination of the area (see below), habitat (dry hills) and picture (especially the acorn cupule) are pretty conclusive and support your original assumption.


How does Australia fit into 'New World' / 'Old World' dichotomy? How are places such as Australia and New Zealand classified when differentiating geographic areas based on 'New World' and 'Old World?'

My understanding is:

New World = North America + South America (+ Central America)
Old World = Europe + Asia + Africa

This is biologically relevant via biogeography:

Ex: neotropical vs. paleotropical (comparable to New and Old World Tropics)

I've seen online sources group Australia / New Zealand in both New and Old World (or in neither). So what's the right answer?

Reputably cited answers only please!

First off - this is an answer without citations. I looked for them, but couldn't find any. The terminology is undoubtedly described in reputable sources, but it is unlikely a paper is dedicated solely to explain this terminology, making literature searches tricky. Having said that -

I discussed this question with an anthropologist and she agrees with my idea that the terminology Old and New World is a historic and Euro-centric one, dating back to the colonial times when Europe viewed itself as the center of the world.

The Americas were discovered relatively early, around 1492. It was designated the New World. Australia wasn't found until around 1606. By that time the New World was already a century old and very likely already solidly associated with the Americas.

The New World, in a biological context, is often used to describe groups of closely related species found in the Americas and not elsewhere, such as New World monkeys. In certain areas of expertise the terminology is baked in in the jargon, .e.g,  monkey and ape behavioral research areas. New World monkeys can be referred to by the Cebidae, as per the Linnaeus's classification. However, due to practical reasons geographical clustering of species can be more convenient.

The term New World means different things in a biological context or in the context of wines, for example (Americas versus Americas + Australia - admittedly Australian wines are pretty good).

In all, I think the terminology 'New and Old World' is confusing, rooted in historical considerations. Australia as well as Antarctica don't fit in this terminology.


Surviving only on another's exhales? While reading this - Surviving under water in air bubble - this question came to me:

How long can an adult person survive on breathing in only exhales of another adult person? Can this be even calculated by not relying on rough approximations or there are too many variables?

In order CPR (mouth to mouth breathing part) to be effective, logic says that exhaled "air" is not poisonous to bring a fatal blow, but for how long?

Ok, I'll bite. Now, I'm going to assume that in this scenario, Alice and Bob are stuck underwater. Alice has a SCUBA tank filled with compressed air (not pure O2) and though she won't share it with Bob, she magnanimously agrees to share her exhaled breaths with him.

Exhaled air contains 13.6–16.0% oxygen and 4.0–5.3% carbon dioxide in addition to other gasses which we'll ignore here. The real question here is: can you survive on that?

13.6–16.0% oxygen is 66%-80% of the amount of oxygen in normal air (which is ~20.1% O2). If we assume that the air pressure of the exhalation is the same as the air pressure at sea level, then the amount of oxygen available to Bob is roughly equivalent to being at an altitude of 2000 - 3500 meters above sea level, which is certainly survivable.

The CO2 is likely to be a bigger problem. CO2 is toxic and, in sufficient quantities, can case asphyxiation even in the presence of sufficient O2. Amounts above 1% can cause drowsiness, headaches, and mild narcosis while higher levels lead to dizziness, confusion, and unconsciousness.

It looks like you need amounts around 7%-10% for death, so Bob will probably survive in the short term, he definitely won't be happy and he won't be doing much. According to wikipedia's page on Hypercapnia, the time one can expect to perform useful activity varies greatly based on the exact amount of CO2:

1 week at 4%,
8 hours at 4.5%,
4 hours at 5%, and
1 hour at 5.5%

If Alice and Bob are just relaxing and waiting for rescue, it's likely that the CO2 in her exhalations will be on the low end of that range and Bob will likely be able to survive (albeit in great distress) for a significant period. If they were exerting themselves, however, Bob wouldn't do well at all.


Duration of selection and survival of the fittest I feel there is a part of the theory of evolution I'm not understanding correctly or maybe I'm missing it, but would like cleared up.

From what I understand, over time random mutations occur which in some cases provide an advantage allowing that animal to survive and reproduce. Its children will have that mutation allowing them to survive and so on over many many years until it evolves into a new species and / or the old ones become extinct.

For example the rock pocket mouse.

The part I'm getting stuck on is that unless these mutations happen instantly and in a large number, given its over such a big time scale how do animals who are not well adapted get enough time to evolve to survive?

Another example is fish that evolve to be able to "walk" out of the sea to escape predators.

If moving out allowed them to survive how did they get enough time to evolve and not be made extint in the time they didn't not have these limbs.

Hopefully I have explained myself clearly :)

Could not fit in a comment..

Welcome to Biology.SE! Here are a bunch of comments.

The sentence until it evolves into a new species and / or the old ones become extinct sounds weird and there seems to be some confusion between evolution and speciation. Also it seems that you have a very static view of what is a species, as if species were predetermined categories into which evolution came to show itself!
I am not sure but I think your question has to do with "valley crossing", that is "how can a population evolve toward some phenotypic trait if intermediate phenotypic traits are not fit?" Is that your question? You may be interested in "shifting balance theory" but it might be a bit too advanced.
It is common to overconsider the valley to cross (the deleterious impact of interemediate traits) and those traits are not necessarily so deleterious
Mutations do not always have small effects on traits. One mutation may have some very important impact and therefore, one mutation alone might be enough to cross a whole valley! You amy be interested in Fisher's geometric model. Fisher's geometric model is just some very arbitrary model and is not much inspired by any biological observation but it helps getting the concept of how mutations impact fitness (=function of survival and reproductive fitness).
When you say how do animals who are not well adapted get enough time to evolve to survive? I may use the word animals to refer to populations or to individuals in a population (extinction of genotype is a population and extinction of populations are two different things). If you referred to individuals then, your interest seems to be into "valley crossing" and "mutational effect"(effect of a mutation on phenotype or fitness). If you referred to populations, then you may be interested in "evolutionary rescue" or more broadly speaking in the so-called "theory of extinction".
There are probably other posts (or part of answers) on this site that will help you. A very good answer would be very very long. But maybe a moderately good answer may be relatively short!


What chemicals/substances exist in green capsicum (peppers) that do not exist in red capsicum? I have known 3 people in my life that have incredibly adverse reactions (one called it an "allergy" and his symptoms did resemble such) to consuming any form of green pepper (capsicum) but have no problems with red peppers (also capsicum). Besides the obvious chlorophyll -- which I rule out since none of these friends had issues with green vegetables -- what else is unique to the green peppers that could possibly cause such reactions?

My limited understanding is that green and red peppers (at least with bell peppers) are actually the same peppers at different stages of maturity. If that is true what changes within the plant during the maturation process?

Your limited understanding is indeed correct - the different colours indicate different stages of maturation, even though different colour cultivars exist (e.g. some that remain green even if fully ripe).

It is known that the different maturation states have different vitamin and/or mineral concentrations (see here or here). This indicates that different biochemical pathways are active and that therefore the enzymatic set-up is variable during pepper maturation (which could have an effect on tolerability as it might also affect other plant components).

Moreover, you are right that the green colour is - at least partially - caused by chlorophyll but also non-green bell peppers often have chlorophyll (Lancaster et al., 1997) but that probably is not the cause of your friend's responses.

More likely the cause is 3-isobutyl-2-methoxypyrazine (IBMP) which gives the characteristic (green) pepper smell and has highest concentrations in green peppers (that's why it is called green pepper smell). It has one of the most intense odours that can be detected at very low concentrations, even within the complex odours of wine (Pickering et al., 2007), according to Roth, 2014 perhaps even below PPT concentrations.

So how does this fit together? Pickering et al., 2007 also suggest that one should determine 'consumer rejection thresholds' for methoxypyrazines, indicating that it might be repellent to some people even in low concentrations of 1-2 ng per litre. This could explain your friend's aversion but evidence for the allergy component is dubious.

I did find one paper (Jensen-Jarolim et al., 1998)  about allergen expression in peppers (birch allergy like). However, no green-specific allergens are reported, and it even seems like green peppers would be a better choice to avoid these allergens.


Do the left half and right halves of the diaphragm undergo the same displacement during breathing? Do the left half and right halves of the diaphragm of a normal person move exactly the same distance between inhaling and exhaling?

A short answer is that the displacement of the right and left part of the diaphragm during breathing may not be the same.

ASYMMETRY

Thoracic diaphragm (Wikipedia):

  In humans, the diaphragm is slightly asymmetric—its right half is
  higher up (superior) to the left half, since the large liver rests
  beneath the right half of the diaphragm. There is also a theory that
  the diaphragm is lower on the other side due to the presence of the
  heart.

Genetic specification of left–right asymmetry in the diaphragm muscles and their motor innervation (PubMed):

  The diaphragm muscle is essential for breathing in mammals. Its
  asymmetric elevation during contraction correlates with morphological
  features suggestive of inherent left–right (L/R) asymmetry.

EXCURSION

Excursion (displacement during breathing) of the right and left part of  the diaphragm may or may not be the same, which may differ from case to case.

Manual evaluation of the diaphragm muscle (PubMed):

  In most cases, the diaphragm shows a symmetrical respiratory excursion
  of ~2–10 cm...

Imaging of the Diaphragm: Anatomy and Function (RadioGraphics):

  The excursion may be somewhat asymmetric and there may be a slight
  delay or lag on one side, typically the right.