Why do people with Down syndrome get fewer cancers?

This is a great question. Just to make it clear people with DS do have a reduced risk of solid cancers and an increased risk of blood cancers, (B-ALL and AML).

You are correct in picking out DSRC1 because of its angiogenic implications. The current hypothesis centers around people with DS being less capable of driving angiogenesis, and therefore having an internal environment that is less nurturing to metastasized or even developing solid cancers. Current unpublished work I have recently seen shows this very clearly in the eye, where the vasculature in DS is far less branched than in the wild-type population.

Why however they show an increased risk of leukemias is a largely unanswered question, with one exception being AMKL (Acute Megakaryocytic Leukemia). People with DS are at a ~500X increased risk of AMKL over the unafected population, and it appears to be entirely driven by the in-utero introduction of a stop mutation in codon 2 the transcription factor GATA1. This transcription factor is important in driving differentiation of progenitor cells in the bone marrow to become erythrocytes and megakaryocytes. Thus inactivating this transcription factor plays a large role in disrupting normal hematopoiesis such that megakaryocytes are overproduced and become a leukemia.

All that being said, and as you mentioned people with DS have around a 20-50X increased risk of AML and B-ALL. There are certainly some chromosome 21 genes that have been implicated in this like Bach1 (important in DNA repair) Ifngr2 (plays a role in cell death) Usp16 (epigenetic regulator Really important recent Nature Paper) and Runx1 (important in stress response) but the field is entirely unsure why this directly leads to increased risk of leukemias. Many current cancer biologists favor the direct gene-dosage problem that people with DS face in that a some ~120 genes are overexpressed when they shouldn't be, and assume that these gene level cocktail directly leads to this increased risk of leukemogenesis, and this very well may be in part the answer. There is however a great 'contrarian' view, in that hematopoietic stem and progenitor cells will become pro-apoptotic and pro-differentiative when faced with certain stresses like aneuploidy. The effect of this on a global scale would be that many of the stem and progenitor cells in the bone marrow would die or differentiate prematurely. This would then result in teenagers with DS having far fewer blood stem cells then they should, and these cells would then be tasked with pumping out more blood per cell than originally meant for them quite possibly leading to an exhaustive phenotype. In this way the blood systems of people with DS will 'prematurely age', and might thus rapidly increase the risk of cancer.

Make sense?


What is the potential function of ultra-conserved elements in the genome?

Probably development, in particular transcriptional regulation.  To quote each link in turn,

  They are found in clusters across the human genome, principally around genes that are implicated in the regulation of development, including many transcription factors. These highly conserved non-coding sequences are likely to form part of the genomic circuitry that uniquely defines vertebrate development.

and

  [Highly conserved non-coding sequences] are significantly associated with transcription factors showing specific functions fundamental to animal development, such as multicellular organism development and sequence-specific DNA binding. The majority of these regions map onto ultraconserved elements and we demonstrate that they can act as functional enhancers within the organism of origin, as well as in cross-transgenesis experiments

Additionally,

  Here we report that 45% of these sequences functioned reproducibly as tissue-specific enhancers of gene expression at embryonic day 11.5. While directing expression in a broad range of anatomical structures in the embryo, the majority of the 75 enhancers directed expression to various regions of the developing nervous system.

These regions tend to be highly clustered in around 200 areas, and most of them are non-coding.  ncRNA is often regulatory, and those UCE clusters are associated closely with developmental genes.  That being said, not all of them are clustered near known genic regions, which might be a good indicator that there are heretofore unknown genes in those areas; UCEs might be useful for discovery.  And here's a paper trying to give a role to one in cancer.


Animals can be generated with genetic defects similar to Down Syndrome, but not that exact condition, except in the case of great apes.

Down Syndrome is a kind of defect called a chromosomal abnormality, meaning that either there is an extra chromosome or an excessive repetition of the same genes on a particular chromosome. In the case of Down Syndrome, that repetition in on a region of the 21st chromosome. Similar abnormalities in other chromosomes are possible, such as the abnormality which causes Klinefelter Syndrome.

Although animals do have chromosomes, they have different chromosomes than human beings do. For example, a horse has 32 chromosomes whereas a human has 23. Apes are most similar to humans, having 24 chromosomes. Therefore, if trisomy is to be found, apes would be most likely to have it. Researchers have attempted to answer this exact question and there is a paper on the subject entitled "Conservation of the Down syndrome critical region in humans and great apes".

The result of this study was that the area on chromosome 21 in humans that is responsible for trisomy is found analogously on chromosome 22 in apes and that apes can, indeed, get Down Syndrome, if they have duplication of this region. There do appear to be apes that suffer from this condition. The band diagram for both chromosomes is shown below:

where "H" indicates human and "C" indicates chimpanzee.


Those are just ordinary hairs growing in your ear, like the kind you find in your nose and, if you are fortunate, on the top of your head. The "hair cells" of the inner ear aren't really "hairs" at all, they are totally different, and you would never find them falling out of your ear.

Hairs like on your head are protein filaments produced by follicles in the skin.

Hair cells in the inner ear, on the other hand, are sensory epithelial cells with stereocilia, which are protrusions of the cell membrane. Those membrane protrusions have mechanically gated channels which are coupled to nearby protrusions; when the whole cell is pushed one way or the other, that influences the mechanical stress on those channels and they open and close, which produces an electrical signal that can be sensed by the auditory nerve.

These special 'hair cells' are way way deep in your ear, past your ear drum, past three little bones that conduct sound into your cochlea. If you are touching those, you are in bad shape indeed - this is very very unlikely under normal circumstances.


Short answer

Receptor cells are specialized neurons

Background

There are, globally, three types of neurons (Eckert's Animal Physiology):

Sensory neurons: these cells transmit information from external stimuli (e.g., sound, light, pressure), or from internal stimuli (e.g., blood oxygen level or head orientation);
Interneurons: these cells connect other neurons within the central nervous system;
Motor neurons: these neurons carry effector signals to effector organs, causing contraction of muscles or secretion by gland cells.

To illustrate these classes of neurons let's consider the visual peripheral system. Fig. 1 shows a schematized representation of the retinal circuitry, connecting the photoreceptors to the ganglion cells of the optic nerve (interneurons):

Source: Instituto Balseiro

The photoreceptor's response is graded. Notably, the bipolar cell, being an interneuron has also a graded response. The bipolar cells convey the signal, in turn, to the ganglion cells that translate the analog, graded signals into a binary, neural spiking code that enters the optic nerve.

Receptor cells are considered neurons, but they are highly specialized. Although interneurons may come in various shapes and sizes, they are not so specialized as receptor cells. The photoreceptor, for example, has a highly specialized dendritic region containing the photosensitive pigment and membrane stacks that capture light.

Another receptor is the Pacinian corpuscle, a vibrotactile mechanoreceptor of the skin:

  Source: Pixgood

In this case, the receptor cell is in fact a myelinized and spiking neuron that functionally much resembles an interneuron. Just as the photoreceptor, the dendritic part does not connect to another neuron, but is highly specialized structure designed to sense a physical external stimulus. In case of the Painian corpuscle, it is an onion-like structure consisting of many lamina. These lamellar structures substantially change the receptor's response to mechanical stimuli. Specifically, it allows the corpuscle to respond rapidly to pressure changes and allow it to faithfully transmit vibratory stimuli.

Reference

Eckert, Animal Phsyiology:
 - Chapter 5 - The Physiological basis of Neuronal Function
 - Chapter 7 - Sensing the Environment


What are the different types of helices in protein secondary structures and how do they differ?

This DSSP page makes it clear that:

Helix-3 = 3-10 helix
Helix-5 = π-helix

The α-helix is described in every biochemistry text book and widely on the web. It has 3.6 residues per helical turn and has 13 atoms in the ring formed by the hydrogen bond and so can also be called a 3.6-13 helix.
The 3-10 helix is less common than the α-helix, but is still widespread. By analogy with the alternative nomenclature just described for the α-helix, it has 3 residues per helical turn in a 10 atom ring.
The π-helix is even less common. It is a wider helix with 4.6 residues per turn.
A comparison of the three can be found in this proteopedia article, from which I have taken the illustration below.

There is also the collagen triple-helix, but that is specific to collagen, whereas the others are general examples of secondary structure found in many proteins.
Standard Nomenclature
There is no such thing as a “full scientific name” in this area of molecular biology. Names tend to get standardized by unofficial agreement when ambiguity becomes a problem. Helices other than the α-helix are not very well known, but the terms 3-10 helix and π-helix are certainly more common than Helix-3 and Helix-5, which I suspect may have been a computational convenience. However, an internet search indicates that for scientific journals 310-helix is generally preferred to 3-10 helix or 3(10)-helix, these latter perhaps reflecting work in a plain text environment or the word-processing or HTML limitations of writers.


Do findings on promoter methylation of the serotonin transporter gene and amygdala activity contradict the established view of serotonergic function?

I don't think there is an obvious contradiction here.

(1) Mapping neuronal function to the perception of threat (or emotions in general) is often advertised as well-understood, but in fact it is not. Serotonin-concentration-based models (such as the monoaminergic theory of depression) are unavoidably imprecise because ”the brain is not soup”. Additionally, it is also impossible with current technology to measure actual serotonergic signalling in vivo with whole-brain comparability (though progress is being made, e.g. via: fMRI contrast-agents and stimulus-evoked opto-fMRI for monoaminergic systems).

(2) Numerous pharmacological interventions which increase signalling at the serotonergic synapse have been documented to cause widely varying effects (compare e.g. monoamine reuptake inhibitors, monoamine release agents, and monoamine receptor agonists). While selective serotonin reuptake inhibitors (SSRIs), such as fluoxetine and citalopram, are commonly reported to decrease anxiety, serotonin receptor agonists, such as LSD, are reported to induce acute anxiety (though interestingly small numbers of LSD administrations, in conjunction with psychotherapy, have also been reported to reduce anxiety in the long term).

The conclusions thus far would be: (1) we can't be entirely sure about how serotonin mediates or counterbalances anxiety (2) but the specific kinetics of activity at the serotonergic synapse seem to be just as relevant as the actual amount of signalling. You may think, however, that the effects of SSRIs are kinetically similar to reduced expression of the serotonin transporter, SERT. This is however not the case, as under SSRI treatment it is generally believed that chronic downregulation of 5-HT1A inhibitory autoreceptors is responsible for the therapeutic effect, rather than the acute increase of serotonin concentration in the synaptic cleft (this being in line with the fact that therapeutic SSRI effects are observed chronically rather than acutely). Further evidence corroborating the notion that constitutively reduced expression of the serotonin transporter increases anxiety can be found from studies on the 5-HTTLPR polymorphism. In these studies the short version of the allele, which leads to reduced expression of SERT, has also been reported (though afaik this effect is not very robust) to correlate with increased activity in the amygdala.


Why do viruses last longer on hard surfaces, like glass, than porous ones

The paper you cited is not about survival on smooth versus rough surfaces; it does, however, mention discrepancies in survival on metallic versus non-metallic surfaces.

From the article you cite (Piercy et al., 2010):

  The lack of recovery of virus from metal substrates may be attributed to several factors; previous work (Sommer et al. 1999; Pawar et al. 2005) has shown the binding of micro-organisms to metal surfaces to be poor because of the high surface energy, high electronegative and hydrophilic properties of metal. Other research has also shown that positively charged metallic ions such as copper and silver have a high bactericidal activity (Friedman and Dugan 1968; Bitton and Freihofer 1977; Slawson et al. 1990) and hence by extrapolation may also have a high virucidal activity.

In short, it isn't exactly clear why viruses in particular might have poor survival on metal, but the electrical and chemical properties of metallic surfaces, as well as biological activity of metallic ions that are constantly leached from alloys like steel are all candidates.

The claim may also not apply to all viruses, and the results are not consistent across labs. For example, Sagripanti et al. 2010 find no effect of surface material (aluminum alloy, rubber, or glass) on Ebola, Venezuelan equine encephalitis, Lassa, and Sindbis viruses.

References:

Piercy, T. J., Smither, S. J., Steward, J. A., Eastaugh, L., & Lever, M. S. (2010). The survival of filoviruses in liquids, on solid substrates and in a dynamic aerosol. Journal of applied microbiology, 109(5), 1531-1539.

Sagripanti, J. L., Rom, A. M., & Holland, L. E. (2010). Persistence in darkness of virulent alphaviruses, Ebola virus, and Lassa virus deposited on solid surfaces. Archives of virology, 155(12), 2035-2039.

Bitton, G., & Freihofer, V. (1977). Influence of extracellular polysaccharides on the toxicity of copper and cadmium toward Klebsiella aerogenes. Microbial ecology, 4(2), 119-125.

Friedman, B. A., & Dugan, P. R. (1968). Concentration and accumulation of metallic ions by the bacterium Zoogloea. Dev. Ind. Microbiol, 9, 381-388.

Pawar, D. M., Rossman, M. L., & Chen, J. (2005). Role of curli fimbriae in mediating the cells of enterohaemorrhagic Escherichia coli to attach to abiotic surfaces. Journal of applied microbiology, 99(2), 418-425.

Slawson, R. M., Lee, H., & Trevors, J. T. (1990). Bacterial interactions with silver. BioMetals, 3(3), 151-154.

Sommer, P., Martin-Rouas, C., & Mettler, E. (1999). Influence of the adherent population level on biofilm population, structure and resistance to chlorination. Food microbiology, 16(5), 503-515.


The RNA expression level is an estimate of the amount or proportion a given gene's RNA found in a sample of cells (such as a tissue sample) or even a single cell.

Expression is used because the RNA sequence is translated from DNA to RNA according to the signals within the cells.

There are various means of estimating this.  They often involve a sequence specific probe - a short length of DNA usually - which will bind specifically to the RNA in question.  The exclusiveness of the probe sequence, which is usually 20-45 bases long, to the RNA in question can vary and so this is a bit of an art sometimes.

Examples are qPCR (quantitative PCR), expression microarrays.  Both of these technologies have  many flavors and variants.

Another category of expression estimation include RNASeq - which will sequence all the RNA polymers in a sample and estimate all the sequences at one time.  The result is similar to a microarray, but RNASeq does not necessarily require the use of specific probes to an RNA to measure it, though it can.

These estimates are usually relative - except for careful qPCR perhaps.  The numbers are not usually interpreted as "X copies of the RNA" in the sample.


Is there a physiological reason why direct lightning strikes are not lethal for everyone or does it all come down to dumb luck?

To be lethal a lighting strike has to do enough damage to a critical organ that the injury is not survivable.  Since electricity can take highly variable paths through a body, the amount of damage inflicted is also highly variable.

For example, current entering on the head and exiting on the foot stands a good chance of passing through both the brain and heart.  This is likely to be a very severe injury.  Conversely, current entering on the left hand and exiting on the left foot does not cross the body and may leave superficial burns but limited internal injuries.


How would I explain different properties of the same protein in different species?

As nobody has answered this good question, I'll have a go.

Firstly, let me state that I have little-or-no knowledge of heat-shock
proteins. What follows are some general observations and thoughts.

It would not be unusual for the same enzyme from different
species to have different kinetic properties. For example, yeast and
horse liver alcohol dehydrogenase (EC 1.1.1.1) vary quite dramatically in this regard
(see below).
It is  to be expected that the same
protein from different species will have different amino acid sequences.

Even the sequence of cytochrome C (~104 amino acids), one of the most
conserved proteins, differs between species. There are 44 amino-acid differences
between human and yeast cyctochrome C, for example (although there is no
difference in amino acid sequence between the human and chimpanzee
proteins) [see Creighton, 1993, p116, quoted below].
This fact alone could explain the kinetic variation, but it might be
very difficult (and require a lot of work) to pinpoint what differences
in amino acid sequence (if any) account for the observed differences in
kinetic constants.
In the case of hsp104, a quick alignment (out of curiosity)
of the amino acid sequence of the  Saccharomyces
cerevisiae and Candida albicans enzymes showed quite a number of amino acid differences between these obviously homologous proteins.

I used the
TCoffee
sequence alignment algorithm (a new version of ClustalW) at the
xPASy server. (I received an alignment score of 98).

For the record, the accession numbers used are the following:

hsp140 from  Saccharomyces cerevisiae, 908 amino
acids, Accession Number AAA50477

hsp140 from Candida albicans, 899 amino acids, Accession
Number AAK60625
Of course, the observed kinetic differences may not be due to
amino acid sequence differences at all, or may not be
only due to such differences.  Post-translational
modification (such as phosphorylation) and differences in quaternary
structure are other possibilities.

I notice from this
reference (Parsell
et al., 1994)  that hsp104 from
Saccharomyces cerevisiae forms oligomers in the
presence of ATP, and this might be very important in any explanation of
kinetic differences. (My whole knowledge of hsp140 does not extend
beyond this excellent paper).
Yeast and horse liver alcohol dehydrogenase (ADH) are
homologues and catalyze an identical reaction.  Both also contain zinc.

However, the yeast enzyme is a
tetramer, whereas horse liver ADH is dimeric.

Another difference worth
pointing out is that in vivo yeast ADH functions as
an aldehyde reductase (making ethanol), whereas liver ADH functions as
an ethanol dehydrogenase (in alcohol elimination). [I am aware there are
other isozymes of yeast ADH, which may have different functions].

As an ethanol dehydrogenase, the yeast enzyme has a
kcat value of 455
s-1 (pH 7.05, 25oC;
Dickinson & Monger, 1973) whereas the horse liver enzyme has a
kcat value (for ethanol
dehydrogenation) of only 1.67 s-1 (pH 6.0,
25oC; Dalziel, 1962, 1963).

In the reverse direction, the
kcat for acetaldehyde reduction is
3850
s-1 for the yeast enzyme (pH 7.05,
25oC, Dickinson & Monger, 1973), whereas it
is only 125 s-1 for the liver oxidoreductase (pH
6.0, 25oC; Dalziel, 1962, 1963).

How can we explain these kinetic differences from an analysis of
structure? In my view this is a very tough question.  It may be due to some or all or none of the differences I have highlighted.
Perhaps the question needs to be rephrased as follows: Is there any fundamental
difference, at any level, in the catalytic mechanism, or in the form of the enzyme in
solution, or in the amino acid sequence, or in the tertiary or quaternary structure, that can reasonably account for the observed kinetic variation?
Are the differences worth explaining?  Perhaps one needs to go no further than to record the individual variation under rigorously-defined reproducible conditions?

Before such questions may be answered, it is important to establish the nature of the observed kinetic differences.  What follows are merely some guidelines, most of which you are probably aware of.

Is the velocity versus enzyme plot linear in all cases at both high and low substrate concentrations? That is, in kinetic jargon, is the   ν vs [Eo] linear?  As the enzyme is known to form oligomers in the presence of nucleotides (see above), this might be an important control.  Does doubling the enzyme concentration exactly double the rate, and does halving the enzyme concentration exactly half the rate (at both high and low substrate concentrations)?

An example of an enzyme where the ν vs [Eo] is often not linear is phosphofructokinase.
I notice you are using a coupled assay with two coupling enzymes.  What effect does doubling the amount of one and/or both of these enzymes have on the observed rate?  It should have none, otherwise the assay is not valid.
The substate is ATP.  Almost certainly, the 'true' substrate for the enzyme is MgATP2- (correct me if I am wrong about heat-shock proteins). How much Mg++ do you have there?

In determining kinetic parameters for ATP-utilizing enzymes one needs to be aware of ionic equilibria during experimental design. Failure to do so may give rise to spurious kinetic effects.

A solution containing ATP and Mg++ will contain many ions, probably only one of which is the substrate for the enzyme, and whose proportion will vary with concentration.  It is essential that this is taken into account. The problem and posssible solutions are explained very well by Cornish-Bowden (2003, pp 86 - 89) and by Storer & Cornish-Bowden (1976).

One experimental design is to keep the concentration of MgCl2 in constant excess over total ATP concentration (CB recommends 5mM).  This is an important one.
Are Michaelis-Menten kinetics obeyed in
all cases? Is there any evidence for substrate inhibition, or substrate
activation?

Are the double-reciprocal plots (Hanes plot,
Lineweaver-Burk plot, Eadie-Hofstee plot) linear in all cases?.  Non-linearity may be an indicator of kinetic complexity, or of poor experimental design.

If you plot the kinetic data for all three enzymes on a single double-reciprocal plot what sort of a pattern do you get?  Competitive? (no
differences in kcat, but
differences in Michaelis constants).
In comparing enzyme kinetic parameters the Michaelis constant has the big advantage that it is independent of enzyme concentration.  Thus any differences are likely to be 'real' and not due to errors in, say, protein concentration.

But what about Vmax? If, say, you determine that the maximum velocites differ by a factor of 1.4, can you be certain that you are not inadvertently adding slighly more enzyme in the higher case, and that the catalytic constants are in fact identical?
As I said above, these are just personal thoughts.  Most you probably already aware of.

References

Creighton, T.E. (1993) Proteins. Strutures and Molecular Properties. 2nd Edn. W.H. Freeman & Company.
Cornish-Bowden (2004) Fundamentals of Enzyme Kinetics 3rd Edn. Portland Press, London.
Dalziel, K. (1962) Kinetic Studies of Liver Alcohol Dehydrogenase. Biochemical Journal, 84, 244-254.[pdf]
Dalziel, K (1963) Kinetic Studies of Liver Alcohol Dehydrogenase and pH
with Coenzyme Preparations of High Purity.  J. Biol. Chem., 238,2850-2858. [pdf]
Dickinson, F.M. & Monger, G.P. (1973)  A study of the kinetics and mechanism of yeast alcohol dehydrogenase with a variety of substrates. Biochemical Journal,  131, 261-270.  [pdf]
Parsell, D.A., Kowal, A.S & Lindquist, S. (1994) Saccharomyces cerevisiae Hsp104 Protein. Purification and Characterization of ATP-Induced Structural Changes. J. Biol. Chem.,  269, 4480-4467. [pdf]
Storer, A.C. & Cornish-Bowden, A. (1976) Concentration of MgATP2- and Other Ions in Solution. Calculation Of the True Concentrations of Species Present in
Mixtures of Associating Ions. Biochemical Journal 159, 1-5 [pdf]


can a protein recognized by antibodies not be immunogenic?

Pure proteins are often poorly immunogenic because you need to have some kind of "adjuvant" effect to induce a strong effect. Bacterially-produced proteins may well have some bacterial LPS or other immune stimulants still present after purification which would drive a much stronger response than the same protein produced from eukaryotic cells. There are many other possible explanations -- one or the other protein may have aggregated or misfolded, which could drive a different response, for example.

In other words the effect you're seeing may be annoying but is not particularly shocking, and you have no choice but to do some routine troubleshooting at this point. Is your protein more immunogenic when administered with an adjuvant? Are the two versions identically folded? Are there antibodies present to a misfolded form that you're not detecting? And so on.


I'm thinking this is a Taxus brevifolia, otherwise known as a "Western Yew". They're most commonly found in the northwest region of the United States; so, even if the tree was planted, it's quite probable that it was still acquired (somewhat) locally.

I had a difficult time finding an image that so directly matches the bark image you provide, just from where that tree is so young, but I was able to find a matured version of the tree, which still has a similiar color and bark pattern. I believe that when the tree matures, the vien-like bark sheds, which results in the "scarring" that can be seen in the following image.

And then here's a few images that show the foliage. Notice the similarities in how the pines flare out, and the coloration of the branches. Once your tree matures, it'll get darker in color and develop small red berries, as can be seen in the following images.

The mature tree is on the left, and the right is still developing (which is most accurate to your images).

There is a small chance that the species provided by this answer is inaccurate, but I'm sure it's at least within the Taxaceae family.


What percentage of protein isoforms have different functions?

It seems that most functional annotation these days is inferred from sequence similarity to previously annotated genes/proteins: this is certainly true of high-throughput functional annotation. It's hard to know how many layers of inference there are between your query sequence and an actual experiment verifying the (possibly tissue- or condition-specific) function of a gene/protein. But alas, I digress...

One confounding factor for is that alternatively spliced isoforms share a lot sequence in common, which means that they might share best hits when searching against a database of annotated transcripts and end up getting assigned the same GO terms.

But as others have mentioned, I think the biggest limiting factor you will encounter is the low-throughput step: in many cases the experimental work required to characterize the functions of alternative isoforms simply has not yet been done.


@kate has what is probably the more correct answer for the observed pattern.

But as an experiment, I set up a basic simulation to approximate the conditions that you lay out:

Starting mean heights of 5'8" (172.72 cm) and 5'4" (162.56 cm) with standard deviations of 2.8" (7.112 cm). I used cm, because it's easier than dealing with inches.
Males will not mate with females that are taller than themselves.
Females will not mate with males more than 8" taller.
Males will not mate with females more then 8" shorter (follows from #3 above).

The problem that I quickly ran into was that, by truncating part of the normal distribution, the variance in height at each generation gradually decreased. After about 20 generations, the means weren't evolving because there was so little variation in height.

Human height is one of the most studied quantitative traits, going back over 100 years to some of the very first statisticians (Fisher, Galton). Height is a polygenic trait with very high heritability (h2 = 0.8)1. Genome-wide association studies have reported 54 genes involved in determination of human height2.

Imagine that each of these 54 genes has just two alleles: a and b. a gives a +1 to height. b gives a -1 to height. So aa would be +2, ab or ba 0, and bb -2. The sum of all those alleles is correlated to height. So if all 54 were aa, then the height would be +108.

The problem comes in when people only mate with taller people. Over time, the proportion of b's will decrease, and the proportion of a's will increase, but only to a point. Once all the alleles are fixed at a, there won't be any room left. The genetic variation will be exhausted. Without the input of new alleles, height will cease to evolve.

1 Lettre, G. 2011. Recent progress in the study of the genetics of height. Hum Genet 129:465–472.

2 Visscher, PM. 2008. Sizing up human height variation. Nat Genet 40(5):489-90.


Your observation is right.

In females( having  XX mammalian germ cells), Oogenesis starts with
the process of developing primary oocytes, which occurs via the
transformation of oogonia into primary oocytes, a process called
oocytogenesis. Oocytogenesis is complete either before or shortly after
birth.(1)

The "germ cells" are called oogonia. Ovum is not a direct product
of meiosis I, the oocyte forms a primary oocyte in meiosis I, which
undergoes meiosis II after fertilization to give an ovum.

The ootid is the immature ovum formed shortly after fertilization, but
before complete maturation into an ovum. Thus, the time spent as an ootid is
measured in minutes.              ....(2)

(In oogenesis, the ootid doesn't really have any significance in itself, since it is very similar to the ovum. It matures into an ovum.)
This diagram sums it up very well:

Oogenesis in Eukaryotic Cells.(A) oogonium where the mitotic division
occurs (B) differentiation and meiosis I begins (C) primary oocyte (D)
meiosis I is completed and meiosis II begins (E) secondary oocyte (F)
first polar body (G) ovulation must occur and the presence of the
sperm penetration (fertilization) induces meiosis II to completion (H)
ovum (I) second polar body               ...(3)

It is commonly believed that, when oocytogenesis is complete, no additional primary oocytes are created, in contrast to the male process of spermatogenesis, where gametocytes are continuously created.

In males, again, as you say, Spermatogenesis is the process by which haploid spermatozoa develop from germ cells in the seminiferous tubules of the testis. The germ cells here are the spermatogonia. But here, initiation of spermatogenesis occurs at puberty. So, males start producing sperm when they reach puberty, which is usually from 10-16 years old.(4)

(The process is almost similar to oogenesis, I would recommend you to start with the wikipedia page if you want to understand this in detail.)
Take away points:

The first haploid cell formed from a diploid germ cell is not an ovum/spermatogonia.

Ovum is formed after fertilization, whereas sperms are formed at puberty.

Oogenesis starts after birth, whereas spermatogenesis starts at puberty.

1- https://en.wikipedia.org/wiki/Oogenesis
2- https://en.wikipedia.org/wiki/Immature_ovum#Ootid
3-https://upload.wikimedia.org/wikipedia/commons/1/1a/Oogenesis.svg
4- https://en.wikipedia.org/wiki/Spermatogenesis


Protein structure prediction from amino acids sequence

what is the accuracy we can predict tertiary protein structure

That depends on the protein.  If the primary sequence closely matches the sequence of a protein for which the structure is already resolved, then template-based methods to model 3D structure can be used (a.k.a homology modeling).  These methods tend to be accurate, as assessed by template-modeling score, though crystal structure confirmation is only available for a minority of models (1%, per this 2010 paper).
For proteins without structurally-resolved homologs, ab initio folding is often used, which relies on molecular mechanics assessment of iterative peptide chain folding to find structures that minimize the Gibbs free energy. Popular software for protein molecular mechanical modeling include CHARMM and AMBER.  Ab initio methods are computationally intensive and are more difficult to validate.

'why a cell can make exactly the same protein structure thousands of time using known to us physical laws, but we have to guess it using machine learning'? Why is it difficult?

It's hard to know all the cellular factors present when a particular protein is synthesized and how those factors affect the folding of the protein.  What is the temperature and pH proximal to the ribosome?  Are chaperone proteins involved?  Is the lowest-energy structure the true structure, or does the native structure fall in a local, stable minimum with a functional potential selected by evolution?  A good discussion of that last point can be found on Quora.


Would we know about a virus that causes no symptoms?

With the modern rise of meta-genomics, symptom-less viruses can be identified by the presence of their genomes. Certainly, there is more interest in pathogenic viruses than in harmless passengers, but today it's not necessary to have symptoms to identify viruses.  For example:

  Investigators can now go beyond pathogenic viruses and have access to the thousands of viruses that inhabit our bodies without causing clinical symptoms. By studying their interactions with each other, with other microbes, and with host genetics and immune systems, we can learn how they affect health and disease. This article reviews current knowledge of the composition and diversity of the human virome in physiologically healthy individuals. It focuses on recent results from metagenomics studies and discusses the contribution of bacteriophages and eukaryotic viruses to human health.

--Metagenomics and the Human Virome in Asymptomatic Individuals.

Even prior to metagenomics, some "silent viruses" were identified:

  Viruses are the most abundant obligate intracellular entities in our body. Until recently, they were only considered to be pathogens that caused a broad array of pathologies, ranging from mild disease to deaths in the most severe cases. However, recent advances in unbiased mass sequencing techniques as well as increasing epidemiological evidence have indicated that the human body is home to diverse viral species under non-pathological conditions.

--Describing the Silent Human Virome with an Emphasis on Giant Viruses


Plants grow only from regions at the tips of the roots and shoots called meristems.

Within the meristem areas there are stem cells ("blank" unspecialised cells).  Unlike animal stem cells, plant stem cells are totipotent - meaning that they can differentiate into any type of cell.  Therefore when the cutting is taken from the end of the shoot, the stem cells can differentiate into root cells or shoot cells depending on their conditions.

Because the meristems (therefore the unspecialised stem cells) are only located at the tips of shoots, you cant grow a cutting from the middle of a branch.


What are the differences between cancer and tumour?

A tumour is simply a space-occupying lesion (something that should not be there, that is; a "lump") caused by abnormal cell replication.

(In medicine, the word "tumour" literally means "swelling", and can sometimes refer to that instead, but that's a different story).

Cancer is a disease in which cell replication is totally out of control. What causes cancer is damage to the genes (DNA) which normally stop cell replication when it needs to be stopped.

There's no such thing as an "ordinary tumour"; all tumours are abnormal. However, what makes a benign (harmless) tumour different from a cancerous tumour is that there is still some mechanisms stopping the cells inside the tumour from replicating; they are doing it more than they should, but they are not totally out of control. When those last mechanisms are broken too, the tumour is cancerous.

(This is a simplified explanation; the actual explanation is a semester-long university course. It's mostly accurate for the layman, though)


If crocodiles are k-selected, why do they supposedly "not age," as in avoid senescence?

Comments

You seem to use the term evolutionary advantageous vs disadvantageous for the species rather than for individuals. It is a very common misconception from the general public. You might want to follow an introductory course to evolutionary biology such as Understanding Evolution (UC Berkeley) for example.

  younger crocodiles with more slightly more fit genes

"fit genes" does not mean much. Again an introductory course to evolutionary biology should help you there.

Answer

You'd right though that absence of senescence causes longer generation time and therefore lower response to selection pressure (such as those caused by an environmental change). But populations don't evolve in order to maximize the probability of the survival of this population (related to first comment above).

Those that live longer, leave more offspring and therefore long-lived individuals are expected to dominate the population in the long run. The evolution of senescence is not exactly that easy though otherwise no species would show any sign of senescence (see Why does evolution not make our life longer?).


Reduction of size in diatoms due to asexual reproduction

The ability to reproduce sexually is closely associated with cell size
  of the diatom. It is the most prevalent method of restoring cell size,
  and it is often triggered when the size of a cell is less than a
  critical level (usually smaller than half of the original size for
  most species).

Source : Sexual reproduction in diatoms


Why spin live fruit flies in centrifuge?

Correction of Poster’s Source

The article cited mistakenly refers to centrifugation, however the actual procedure used in the work — Karageorgi et al. Nature, 2 Oct 2019 — is vortexing, as illustrated in Fig. 3 of the paper below.

What is meant by standard lab procedure?

  There is no such thing as standard lab procedure. There are standard
  lab procedures for performing certain kinds of experiments or processes.

In studying the effect of mutations on the behaviour of live fruit flies one devises laboratory procedures that are, if at all possible, cheap and easy to perform on many animals. All laboratories have vortex mixers of the type illustrated, as these are used to speed up dissolution of solutes and to disperse (resuspend) solids which have been precipitated by centrifugation — perhaps the source of confusion as the flies would likely have been put in centrifuge tubes as these would be appropriate (although the flies were not subjected to centrifugation).

Why vortex flies?

The vortexing is what is apparently called a ‘Bang’ assay — a means of testing flies for neurological seizures. The authors state:

  To investigate this, we phenotyped monarch lineage knock-in flies for neurological seizures upon shaking (bang sensitivity), a common phenotype in hypomorphic Na+/K+-ATPase mutants29,30

Without consulting references 29 and 30, it seems clear that the authors were expecting cardiac glycosides to produce neurological seizures, and used a simple technique that had been used previously by others to assay this.

So, yes, if you are interested in these aspects of fly physiology vortexing may be a standard laboratory technique, but, no, other fly labs (e.g. those studying the gut) don’t start the morning by saying:

  “Lets take the new mutant for a spin”.


How dissimilar are the fingerprints of identical twins?

Identical twin fingerprints are different, but generally more similar than to random people.  For example:

  Fingerprint recognition with identical twins is a challenging task due to the closest genetics-based relationship existing in the identical twins ... Srihari et al. [6] analyzed the similarity between twins' fingerprints in a study using fingerprint images from 298 pairs of twins. The authors analyzed this similarity using two-level features. With the features of level 1, they found that twins' fingers are much more likely (55%) to have the same pattern type than non-twins' fingers (32%). With the features of level 2, they concluded that the similarity between the fingerprints from twin fingers is higher than from two arbitrary fingers.

Fingerprint Recognition with Identical Twin Fingerprints

  Dermatoglyphic asymmetry and diversity traits from a large number of twins (MZ and DZ) were analyzed based on principal factors to evaluate genetic effects and common familial environmental influences on twin data by the use of maximum likelihood-based Variance decomposition analysis. ... The present results are similar with the earlier results of finger ridge count diversity in twin data, which suggested that finger ridge count diversity is under genetic control.

--Inheritance of dermatoglyphic asymmetry and diversity traits in twins based on factor: variance decomposition analysis


Found it. It's a Sarcodes or snow plant:
http://en.wikipedia.org/wiki/Sarcodes


Help on reconciling seemingly contradictory evidence about fetal experience

I know close to nothing about the subject of self-awareness in fetuses.

But learning —and certainly interaction— can occur without anything close to human "awareness", as evident by the fact that systems without a brain (and even without neurons) can learn. Any system that can process and store information is capable of learning. Does your definition of awareness include anything more than this? Conversely, organisms with a very simple brain can display aversive behaviour.

For an example of memory without neurons, see the Wikipedia article on immunological memory.
For examples of aversive behaviour without a proper brain see Zhang, Lu, and Bargmann 2005 and Babin et al. 2014

References
Zhang, Y., Lu, H., & Bargmann, C. I. (2005). Pathogenic bacteria induce aversive olfactory learning in Caenorhabditis elegans. Nature, 438(7065), 179–184.
Babin, A., Kolly, S., Schneider, F., Dolivo, V., Zini, M., & Kawecki, T. J. (2014). Fruit flies learn to avoid odours associated with virulent infection. Biology Letters, 10(3), 20140048–20140048.


How can succinylcholine cause myorelaxation?

Succinycholine, as its name might suggest, is a cholinergic agonist indeed. It acts on the neural plate of skeletal muscles, where it activates the muscle cholinergic receptors.

Phase 1 block due to succinylcholine thus occurs by activating so many receptors at once, that the whole muscle gets desensitized and therefore paralyzed. A corollary of that is that muscle will twitch during activation, thus accounting for the reason why people twitch shortly before becoming paralyzed after a succinycholine iv injection. This phase 1 block will resolve in 2-5 minutes.

Now an interesting phenomenon is that if you go on stimulating the muscle with more cholinergic agonists (for example, a second iv dose of succinylcholine), you may end up provoking endocytosis and degradation of the cholinergic receptors. This is called phase 2 block, and in contrast to phase 1, it will take at least several hours to resolve. This is why we never use a second dose in the clinics, except in very special cases.
You can also read about it all on wikipedia


You are right about the cDNA 341 nucleotide deletion.
It is an exon deletion, meaning that the deletion is part of a gene that encodes to a protein.
This corresponds to the second part - the protein level (annotated with p.).
The mutation that is caused on the protein level is a frameshift mutation (corresponds to the fs).
A frameshift mutation changes the reading frame of the protein.
You can find more information on frameshift mutations annotations on the HGVS nomenclature website.

In your case (p.Thr114Lysfs*37) the annotation indicates that the cDNA 341 nucleotide deletion led to a frameshift mutation of the protein with a Thr amino acid residue being replaced by a Lys amino acid residue. Furthermore, this also altered when the protein terminates: there is a new translation termination (stop) codon after 37 amino acid residues instead of terminating at the end of the protein where it normally does.


Did any warm blooded animals evolve back into cold blooded?

Secondary ectothermy has been suggested in living crocodylians by Seymour et al. (2004). Their rationale is based on:

Presence of a 4 chambered heart (otherwise only found in endotherms)
Post-cardiac shunting via the foramen of Panizza and "cog-tooth" valve, which develop secondarily in crocodylians
Lung structure and ventilation during locomotion

Thus ectothermy in extant crocodylians is associated with being aquatic or semiaquatic. These authors suggest that endothermy may have been ancestral for dinosaurs as well.

Seymour RS, Bennett-Stamper CL, Johnston SD, Carrier DR, Grigg GC. 2004. Evidence for endothermic ancestors of crocodiles at the stem of archosaur evolution. Physiol Biochem Zool 77:1051–1067.


Plants are oxygen generators. Plants plus decomposition (i.e. the whole system, plants plus bacteria and fungi and fire and cows and termites) are oxygen neutral. So the statement is literally wrong, but may be functionally correct in the current environment.


Which of the following is NOT a type of tropism?

The answer is #5, Leaflets folding after losing turgor pressure. This refers to a phenomenon called plasmolysis.

1 - positive phototropism, incorrect

2 - negative phototropism, incorrect

3 - gravitropism, incorrect

4 - thigmotropism, incorrect


Fitness

Fitness is a trait which, when high is pretty much always attractive to potential mates in all species. However, fitness is definitely not an "aestetic characteristic".

Traits that are often correlated with fitness

There are some "aestetic characteristics" that are correlated to fitness in many species, such as body weight. Such trait are therefore often correlated with what individuals find appealing.

Body weight is a standard examples. Heavier individuals often have better competitive abilities, better foraging abilities and therefore have a higher fitness. As a consequence body weight is often used a s a proxy for fitness.

Relative body characteristics

Novel traits in a population can be evidence of parasitism and therefore would tend to be considered as non-attractive. However, counter to this intuition, it has been shown typically in birds having high sexual selection, that individuals having novel traits are more attractive.

Why is there a lack of generalization?

To build the intuition I would just say that given the gigantic phenotypic diversity that exist among all species that perform some level of mate choice, it is pretty clear that you will not find a simple morphological trait that will be attractive to all species.

Mating preferences evolves. Individuals that are attracted toward individuals that will yield to a high progeny (and low sexual conflict and low transmission of parasites) have higher fitness their preferences increase in frequency in the population. As a consequence, individuals like whatever is (should rather say 'was') favoured in the population. Now, in some population individuals are selected to be small, or to be big or any other things. This is the process of natural selection applied to mating preferences.


I think this partially depends on the timeframe. Endemism is usually divided into paleoendemism and neoendemism (see e.g. Kier er al in PNAS for use of both terms). Here, neoendemism is referring to the result of recent adaptive radiations that have led to new endemic species. This is then in contrast to paleoendemism, which refers to previously widespread species that are now confined to isolated areas.

Neoendemism is clearly related to your question, but whether dingos should be labelled as neoendemic depends on if it can be seen as a unique subspecies. If it is, it might be more suitable to view it as neoendemic and not exotic (nothing prohibits neoendemic species to be ecologically "problematic" to the previous fauna though).

In the literature (from what I've seen), neoendemism is usually used to describe historical events though (the result from adaptive radiations etc), so timeframe is obviously important (see e.g. Mishler er al, 2014). Even so, all taxa that has led to neoendemic species (through adaptations to local conditions) was by definition exotic at one point in time (e.g. when the most recent common ancestor of the Galapagos finches colonized the Galapagos islands). The same goes for the relatively recent adaptive radiation of Drosophila on Hawaii.

To me, neoendemic and invasive are not mutually exclusive terms, while the division between neoendemic and exotic may depend on time since colonization and whether the population now forms an independent taxon (e.g. subspecies) instead of a subpopulation still connected to its host population. I cannot find a reference or definition to support this interpretation right now though.


This refers to the turnover number (a.k.a kcat or k2) of an enzyme and is usually calculated using Michaelis-Menten kinetics. Jump to the summary at the end if you want a simple answer. If you want a more thorough answer, consider the following chemical equation:

  [E] + [S] ⇌ [ES] → [E] + [P]

This says that a certain concentration of enzyme mixed with a certain concentration of substrate will first combine and form a complex depending on the enzyme's affinity for the substrate. Then the enzyme complex will generate a product depending on the enzyme's ability to convert the transition state into product. The k1 constant is the arrow moving from [E] + [S] → [ES] and the k-1 is the arrow moving from [ES] → [E] + [S] (they oppose each other). The k2 constant is the arrow moving from [ES] → [E] + [P].

  Vo = [ES]k2

Vo - this is the rate that product is being formed, which can be measured.
[ES] - this is the concentration of enzyme-substrate complexes.
k2 - this is a constant value comparing the two.

This can also be expressed in terms of maximum rate:

  Vmax = [E]Tk2

Vmax - Vmax is catalytic rate when [E]T = [ES] (when all of the enzyme present is bound to substrate/saturated).
[E]T - [E]T is the total enzyme concentration. [E]T = [E] + [ES].
k2 - the kcat is the catalytic constant. It is a constant indicating how quickly an enzyme can convert substrates into products. It is easily observed by this equation.

Summary

So k2 is basically an indicator of how efficiently or quickly an enzyme operates. Not all enzymes follow standard Michaelis-Menten kinetics. For example, the allosteric properties of some enzymes cause a non-linear saturation curve. Because of this, the turnover number is commonly referred to. The turnover number's units of s-1 indicate one product molecule per second, so a turnover rate of 3000 means you can create 3000 products in 1 second at Vmax.


What is this thing? It is hairy mostly a cocoon, and i saw a white worm pop out of it. It is spreading rapidly

Bagworms?
https://en.wikipedia.org/wiki/Bagworm_moth
I don't know how destructive individual species are. They probably aren't more than an aesthetic concern.


Question about enveloped RNA virus viral genome

Your image illustrates the replication cycle of a negative-sense single-stranded RNA virus, where the viral genome needs to be "inverted" by an RNA polymerase into mRNA before being translated by the host. There are many examples of (-)ssRNA viruses, including filoviruses (Ebola, Marburg), paramyxoviruses (measles, mumps), orthomyxoviruses (influenza), rhabdoviruses (rabies), deltaviruses (Hepatitis D), and others.

These (and all) viruses evolved alongside their hosts, and consequently the hosts evolved various protection mechanisms. One primitive component of the so-called innate immune system in humans and other organisms (going back at least to plants) are proteins known as pattern recognition receptors (PRRs) which bind to conserved motifs found in microbes, including possible pathogens. The types of molecules recognized by these PRRs include certain types of carbohydrate moieties like LPS, peptidoglycans and other components of bacterial cell walls, fungal glucans, bacterial peptides, some types of microbial nucleic acids (such as single- and double-stranded RNA, more on this in a bit), chitin, and others.

One class of PRRs are the Toll-like receptors (TLRs), named after the Drosophila Toll protein. They recognize a wide variety of microbial patterns and activate downstream signaling to stimulate an immune response, including production of pro-inflammatory cytokines and anti-viral interferons. In our case, two of them are particularly important - TLR3 and TLR7. TLR3 recognizes double-stranded RNA, which occurs transiently during (-)ssRNA virus infection when the negative-sense genome is being copied to positive-sense mRNA. However, dsRNA is much more common in retroviral infections. TLR7 recognizes single-stranded RNA in endosomes, which would occur after macrophages, dendritic cells, or B cells consume dead virally-infected cells.

Unfortunately for the host cell, once it has been infected there isn't much that can be done to save it. Viruses evolved to hijack the cell's machinery and make more copies of themselves. This hijacking is generally one way, so the only way to fight the infection is to kill the cells producing the viruses. This is, for example, why you often get a sore throat during an influenza or rhinovirus (one of the most common causative agents of the common cold) infection - epithelial cells lining the throat get infected, and are killed by the immune system to prevent the spread of the infection. This leaves a "raw" area that must heal over time.


What is the reason for cats not liking water?

First, some cats do like water. But it seems true (from personal observation and most people's opinion) that most cats don't.

The question has already been asked many times online. Just Google your question!

I doubt one will find peer-reviewed papers on the question but below is a summary of what seem to be the most often mentioned possible reasons I could find. Of course, these bullet points are very hypothetical and I don't know of any research presenting evidence for or against these hypotheses.

Their fur is not really adapted for the water and will very quickly become waterlogged and heavy making it uncomfortable.
Cats are generally speaking quite skittish
Cats may not like the odour of chemicals we put in the water.
Cats love to groom themselves. It is an aweful lot of work to do the grooming after a bath.

Note also that domestic cats are descendent from cats living in very arid areas. The most closely related species with cats are the African Wildcat living in Northern Africa, the Near East and around the periphery of the Arabian Peninsula.

Source

My non-peer reviewed sources are

http://www.petful.com/behaviors/why-do-cats-hate-water/
http://www.animalplanet.com/pets/healthy-pets/do-cats-really-hate-water/
http://www.petguide.com/blog/cat/why-do-cats-hate-water/


Does leaving land alone actually help nature conservation?

I'll give you an example, because this question is pretty case specific. In Delhi, my hometown, they kept areas of the forest, the 'Sanjay Van' free from construction and people and only very recently started cleaning it up. As a result, an invasive variety of the Acacia tree (known locally as keekar) more or less took over the forest and has basically wreaked havoc on the wildlife.
I think better than just letting Nature take it's course, humans should help get abandoned areas back to a sustainable point, where it can integrate with the wildlife, but again, it depends on each area.


After reading Satwik Pasani's comment to the original problem, I tried using the hypostatic locus as the common locus in the epistatic relationships, instead of the locus causing the onions to be white.  The following solution fits the answers supplied in the book.

Three loci can be used to determine the colors of the onion, the alleles of which can be denoted by C, D, and E.  Suppose that C and D are each epistatic to E, such that the phontypes of the onion are given as:

cc---- white
--D--- white
C-ddE- red
C-ddee yellow

Then the first crossing in the problem can be given by CCDDEE x CCddee.  The second crossing could be ccddee x CCddEE.


Resemblance between parent and offspring is certainly true. Some traits are more obvious than others, for example skin colour would be very obvious. As babies mature they will gradually begin to look more and more like their parents, the features of babies often change rapidly, for example pretty much every baby has a little nose, but by the time they are a fully grown adult it probably resembles that of one the parents fairly well.

More obvious example would be height - imagine being presented with a baby and two males who are identical in every way, except one is two metres tall, and the other is 1.5 metres tall. As a baby it would be very difficult to assign paternity on the criteria of height/size, but as the child develops it would likely become easier and easier.

The resemblance between parent and offspring relates to the heritability of a trait but, because there can be temporal variation within an individual, heritability can only be properly determined by measuring the traits in parent and offspring at the same time point (e.g. father's height at 18 years old and son's height at 18 years old), otherwise it will introduce noise in to the estimation, likely reducing the estimate of heritability (and specific to your question, making it harder to assign paternity based on phenotypic characters).

In the context of your question: Ability to assign paternity would depend on a) the resolution with which the traits available can be distinguished among all individuals in the test and b) the variance among all individuals in the test. E.g. If the only trait available was number of fingers per hand, and all potential fathers and the child had five then the lack of variance would make it impossible to use this as a criterion, while if both one of the potential fathers, and the focal baby, had six fingers on one hand then there would be pretty good clue.

Whether babies more resemble their fathers more than mothers (which I think is the true question you are asking here) there is evidence from Drosophila that within-sex heritability is much higher than cross-sex for lifespan and aging, i.e. the lifespan of males (females) far more resembles the lifespan of the father (mother) than the mother (father). This would suggest that there is a sex specific element. Meanwhile there is evidence of high cross-sex genetic correlations in humans preventing males and females from becoming more different (thus maintaining resemblance to opposite sex parents). I would think that resemblance to the father could offer some benefit in assigning paternity by care giving males (stopping males devoting resources to other males offspring) but some of the resemblance could be generated by genetic correlations to sex-specific genetic variance, for example, males (females) will look more like their father (mother) in many ways purely because they are of the same sex, so it will heavily depend on the traits you look at to judge resemblance.

For a related answer about heritability on biology SE see:

Is it possible for a child to grow taller than their tallest parent?


Why most small organisms seem not to be interested in any organic matter which has all moisture removed?

TL;DR
If it doesn't last forever this is some organisms consuming it. It is a matter of ecological niches, what are the requirements (humidity, temperature, etc.) to live and reproduce
I believe we should separate the discussion in two: small organisms and microrganises
Microorganisms
Microorganisms that consume our food need to get there, either they got there from the air or they are already there. Other vectors can be insects, animals, water and soil but since this discussion is about food and we tend to keep our food protected from those vectors I'm going to ignore them.
Most of the microorganisms of interest (Bacteria, Archaea, Fungi & Oomycetes) exist in air as spores. This are analog to seeds, they are alive but inactive and need to arrive to a good environment to sprout. Spores can survive for many years, even millions of years("Revival and identification of bacterial spores in 25- to 40-million-year-old Dominican amber". Science. 268 (5213): 1060–1064.). This survival mechanisme includes dehydration and therefore rehydration is necessary for sprouting.
In addition some of these (mainly oomycetes) need free-water to live & reproduce while others require some levels of moisture.
Dehydrated organic material tends to be hygroscopic. Thus if the non-spore form of the microorganism lands on it the organism will probably loose water and die.
Microorganisms, like every organism, have niches they occupy. One of the characteristics of these niches is the temperature. Freeze-drying includes freezing which lowers the temperature below the survival temperature of many microorganisms and preserves the food. Microorganisms that grow in low temperatures grow slower so it will take more time for us to notice their presence. They still require water so the combination of freezing and dehydration provides a good protection.
Honey has a antibacterial activity in it preventing growth of microorganisms. In addition honey contains a lot of sugar and other molecules making it hypertonic to most microorganisms causing them to loose water if they land on it. Also his high viscosity prevents the free movement of microorganisms.
Small organismes
Many small organismes still need water to live and reproduce (like nematodes)
Insects are highly specified to their environment and food intake. They might not be able to consume dehydrated food.
In addition, as mentioned in the comments by Kal

a lot of these small organisms who are not interested in completely dehydrated "food" would also be ones who
don't explicitly drink water (at least, not enough).[...] For organisms that
don't explicitly drink water, their major source of water would come
from the food. So if the food doesn't contain enough water, they don't
bother.

Ants and other insects do eat dehydrated organic material like seeds, but it still has around %10 moisture
Oil is not hydrated but liquid, since it is oil and not water


What risk to DNA does long-term exposure to low-dose radiation pose?

I agree with @Kevin - there are no ultimate statements in science. The answer is 'its all relative'.

With radiation and risk, more radiation means more risk of cancer or any number of other types of damage that can result.  The question is is this significant?  And this is a somewhat subjective question.

When someone says:

'there is no health risk from XYZ'

what they mean is..

"to the extent that we can determine, we can't see any more chance of adverse health if you are exposed to XYZ conditions than if you weren't"

DNA damage happens all the time.  The frequent flier study you cite is trying to see if the additional exposure to cosmic radiation while flying, which is largely blocked by the atmosphere, causes a change in the rate of some cancers.

Radiation and cancer is like a lottery.  If you buy just one ticket you might win.  If you step outside, the thousands of extra gamma rays you get outside might start a cancer that will eventually take your life.  If you buy 20 million tickets you will very likely win.  If you hang out next to high levels of radiation, even for a short while, you will get so much damage you will not live long.

Its difficult to study the effect of low levels of radiation. The lower the levels of radiation we are asking about, the longer you will have to wait to see if there is an effect.  If 10% more people get cancer, you have a very real concern that some of these folks might have done something else, like sunbathe or live in a poorly ventilated basement for too long.

The real question is, what is significant?  I once saw a 60 minutes segment where a dermatologist said that she simply never directly exposes her skin to direct sunlight.  I'm betting she never got a melanoma.  She carried a parasol and wore light gloves outdoors.  (sorry I can't find the link)  She was at least in her 50s and she had the skin of a teenager.  I still go out in the sun.  I assume my risk of melanoma is 5-10 times more than hers was (this was a pretty old broadcast).  (mine is 0.03% in the next 5 years btw).  Its just not worth it to me.


Does destroying a virus envelope make the virus inactive?

Enveloped RNA viruses will get inactivated quickly without a membrane. RNase is a ubiquitous enzyme that would quickly digest any exposed genetic material.
Via https://www.neb.com/tools-and-resources/usage-guidelines/avoiding-ribonuclease-contamination:

RNases are found in all cell types and organisms from prokaryotes to eukaryotes. These enzymes generally have very high specific activity, meaning tiny amounts of contamination in an RNA sample is sufficient to destroy the RNA. The major sources of RNase contamination in a typical laboratory include:

Aqueous solutions, reagents used in experiments
Environmental exposure, RNases are in the air, most surfaces and dust
Human contact with hands and skin

Without a membrane (and any associated receptor-binding proteins), the genetic material of an enveloped virus would not normally have a way to get incorporated into and infect the host cell, in any case.
Your question is about enveloped viruses, specifically, but there is an interesting exception of a kind, so-called viroids that infect plant cells. These have no capsid or protein envelope, but are still infectious.


Telomeres are at the end of the chromosomes and get shorter with every cell division, since the lagging strand is missing a start point for the DNA polymerase. This limits the number of cell divisions to 40 to 60 before the cells go into senescence and stop dividing (they are not dying at this point). This phenomenon is called the "Hayflick limit".

Cell populations which need to divide more often or cells which need to maintain a long telomer status (stem cells) because they give rise to other cell populations, have an enzyme called telomerase which has it's own (RNA) template and can enlarge the length of the telomere. See the figure how this works (from the Wikipedia article on Telomerase):

To answer your question: Younger cells have longer telomeres (compared to older cells). Usually cells stop dividing, when their telomeres get too short to avoid chromosomal damage, due to the progressive shortening of the chromosomes. In cancer cells the pathways controlling this (for example p53 and the retinoblastoma pathway) are often mutated, so that the cells divide forever. This leads to chromosomal instability, further mutations and chromosomal disarrangements, which can cause real havoc.

It also happens for some cancers that they manage to reactivate their telomerase, thus keeping their telomers at a healthy length and preventing chromosomal damage. By this activation they get around reaching the Hayflick limit for the maximum number of cell divisions and are truly capable of living forever. The famous HeLA cell line for example is telomerase positive.

The activity of the telomerase in one cell has no effect on the neighboring cells.


This question has a related issue that should be addressed first: what is a species? To some extent, if you want to understand how speciation can occur, then you have to consider how you are going to define a species. There is no species concept that applies to all species, past or present. The most widely applied concept is the biological species concept (Mayr 1942), which applies (imperfectly) to sexually reproducing species. Of course, Taenia does not always reproduce sexually. I think the discussion of species concepts is beyond this question but I encourage those that are interested to check out references [2-4] as well as a series of papers published in Systematic Zoology in the mid-70s. Here, I'll focus on genetic differentiation with a subtext of reproductive isolation.

Genetic differences can accumulate between populations$^1$ of Taenia in two different ways. The first is non-adaptive evolution via genetic drift. Drift is when allele frequencies change by random processes. For example, just by chance, tapeworms in a particular host may not live very long because the host was killed in a mudslide. Those tapeworms don't produce as many proglottids over their interrupted life so they don't leave as many copies of their alleles. Tapeworms in a host that lives a long time produces lots of proglottids and therefore produce many more copies of their alleles.  The key point here is that the process of genetic drift is random. Allele frequency changes in one population of Taenia will be different from allele frequency changes in another population. Thus, over time, different populations of Taenia can become genetically different solely by chance. It's called non-adaptive evolution because natural selection is not evolved.

Adaptive evolution by natural selection can still occur on individuals that are asexually reproducing. Genetic differences will accumulate in a population over time to due mutations. Some mutations may be beneficial, some may not. Selection can increase the frequency of beneficial mutations and decrease the frequency of very mutations. Note that non-lethal but harmful mutations can accumulate in asexually reproducing species (see Muller's Ratchet) but I am assuming survivorship is decreased by harmful mutations for this example. If we assume that Taenia in different populations are subject to different selective pressures, then genetic differences can accumulate, leading to speciation. Note that drift will also affect the allele frequencies of both beneficial and harmful alleles because drift is random.

That brings us to the "mixed-up genes". I assume you mean the new genetic combinations that occur via sexual reproduction. Even if a host typically has only one individual of Taenia (not always the case), I suspect the opportunities for sexual reproduction in a population of Taenia are frequent, especially over evolutionary time. Consider places where tapeworm infestation of humans is high. Such places often have poor sanitary conditions so the opportunity for mixing of fecal material from different human hosts is high, and therefore the opportunity for mating among different individuals of Taenia is also high. If you have many humans living in squalor over long periods of time, then you have conditions very favorable for sexual reproduction of Taenia. Remember too that Taenia produce lots of proglottids, each with the chance for reproduction. Each reproductive opportunity creates new genetic combinations potentially subject to natural selection.

The final point to consider is population size. If the population size of Taenia is small (relatively few individuals) then genetic differences can accumulate fairly rapidly by genetic drift but the accumulation of beneficial mutations in the population will be low. If the population size is large then new mutations including beneficial ones can occur relatively often, increasing the rate of adaptive evolution among different populations.

Footnote

I'm assuming some sexual reproduction among individuals of the same population and individuals from different populations do not interbreed. Without sexual reproduction, we have to think about the individual as the species and that makes my head hurt.

References

Mayr, E. 1942. Systematics and the origin of speceis from the
viewpoint of a zoologist. Columbia University Press, New York, USA.
Howard, D.J. and S.H. Berlocher (eds.). 1998. Endless forms:
Species and speciation. Oxford University Press, Oxford, England.
Wheeler, Q.D. and Meier, R. (eds.). 2000. Species concepts and
phylogenetic theory: A debate.  Columbia University Press, New
York, USA.
Coyne, J.A. and H.A. Orr. 2004. Speciation. Sinauer Associates,
Inc., Sunderland, Massachusetts, USA.


Bird identification: song two low, two high, five short

Best guess is that the bird is a Song Sparrow, Melospiza melodia. Cornell Lab of Ornithology has a good website for basic facts about birds. Here is the account for Song Sparrow. There is a sample of typical song, but there can occasionally be some variety.

The song is kind of complex and the recording you linked to seems to garble or not capture some of the song, but the changes in phrases throughout the duration seem to match as does the pitch of most of the phrases.


Well, first of all 812mm is a pretty precise value to be preceded by the word "about". "Mildly hot", on the other hand, is too vague a term for your question to be answerable. If you update your question with better parameters, you may get more helpful answers.

In any case, according to this page, a tropical savanna has mean monthly temperatures at or above 64°F (~18°C), which may or may not qualify as "mildly hot" by your standards, and annual precipitation averages between 30 and 50 inches which means between 762mm and 1270mm.

So, I what you are describing could be a tropical savanna, but as I said before, I can't tell unless you update your question with more information. Have a look at this site, it may be of help.


If, at a locus, you have several alleles, then this locus is said to be polymorphic or segregating.

A segregating locus is just an untintuitve name for a polymorphic locus.


That is a papaya seed showing vivipary, or premature sprouting. The plant is getting all the sugar it needs from the nutrients stored in the seed so it does not photosynthesize. If it were to run out, the plant would die.


How to check if a population density obeys replicator dynamics

For discrete time replicator dynamics, fitness is defined only up to a multiplicative factor. I.e. if you pick some number $k$ then $(f_1, ..., f_n)$ defines the same fitness function as $\hat{f} = (f_1/k, ..., f_n/k)$. In particular, this mean for any $p$ you can always pick a $k$ such that $\langle \hat{f} \rangle_p$ = 1.

So using your final equation, just let $\hat{f}_i(p) = g_i(p)/p_i$.

Note that the resulting landscape $\hat{f}$ will be a relative fitness landscape and not an absolute fitness landscape. But there is no way to recover an absolute fitness landscape from the data you have. You would need information on how the population size, not just frequencies evolved for that.

As a final note: if you're trying to match this to experimental data, the discrete time approach might not always be necessary. In that case, you can try the method that I describe in this post or depending on your experimental system, you might be able to just do the game assay as we defined in this paper.


Which organs do cats not eat on their prey?

That looks like some sort of rodent.  The rodent stomach, while not as acidic as the human one, is still strongly acidic:

  The mouse stomach pH was 3.0 (fed) and 4.0 (fasted), and the corresponding values in the rat were 3.2 (fed) and 3.9 (fasted).

From this article

Since it's clear from the picture that the organism had just eaten (the stomach had not yet emptied), the pH would be on the lower end of that spectrum.

In humans, acidic foods often taste sour, so it may be that the cat ran into a terrible taste at the base of the esophagus that caused her to stop there, but I don't know whether the taste buds on the cat are comparable to those in a human.


Identify this indoor plant with strange stem-like leaves

Looks like a Pencil Tree (Euphorbia tirucalli), sometimes called "pencil plant", "pencil cactus" or "milkbush." This "leafless-looking" plant is not actually a cactus, but actually a "Euphorbia" (i.e., member of the Euphorbiaceae family), and should present a white "milky" liquid latex when broken.

CAUTION: THIS IS A POISONOUS PLANT [See symptoms here].

Description: A succulent, spineless shrub with round, green branches; leaves clustered at the tip of the branches and soon dropping

Although it eventually can grow into a small-sized tree in its natural habitat, this plant is found more commonly as a medium-sized house plant or landscaping "shrub."

Range: Tropical Africa and India

Euphorbia tirucalli is very well adapted to semi-arid conditions, but also occurs in both dry and moist forest, savanna and shrub land, and withstands salt stress associated with coastal conditions, but no frost. It occurs from sea-level up to 2500 m altitude. It grows well on a wide variety of light-textured, neutral to acidic soils. It is commonly associated with human settlements and becomes naturalized rapidly. It is locally common and often occurs in groups. [Source].


Could a strong magnet field repel the body before damaging it?

While mammalian blood is characterized by diamagnetism (as demonstrated here), as far as I know, the human body as a whole is more or less electrically neutral—that is, with all of its summed components the negative and positive charges balance each other out or there are extremely insignificant differences.

If you want to get strict though, it's theoretically possible to use a super strong magnet to repel or attract someone's entire body to a meaningful degree as long as it's not electrically neutral at a given point in time. But even in the video linked above, the guy is using a super strong magnet to observe its repulsive effects on blood and the blood is just barely moving away; definitely not forceful enough to where someone wouldn't be able to resist moving with just their body weight alone.

So to answer your question: can someone be repulsed or attracted by a magnet practically? No. Can someone be repulsed or attracted by a magnet theoretically? Yes.


Do plants refix some of the carbon dioxide in the Calvin cycle that they produce through cellular respiration?

Gases like CO2 move quite freely in biological systems, approximating the laws of diffusion (note: there are of course some exceptions, especially underwater, as well as with proteins that assist in bulk transport of CO2 like hemoglobin).

If you were to measure the net amount of CO2 coming into the stomata, it would indeed approximate the net CO2 use by the plant. From this, you could make a claim like "the CO2 a plant needs comes in through the stomata": this is true for the net, and that's usually what's most important to a biologist.

However, if you want to get picky about what really happens at a molecular level, the flux of CO2 coming through the stomata is not the same as the net: no one is keeping track of the individual gas molecules, they just float around back and forth. The only reason there is a net flow at all is due to a concentration gradient: because the plant uses some CO2, there is less inside than outside. When molecules move around randomly, that means that a few more end up coming inside than are leaving. When we talk about net diffusion we are talking about the averages of many many molecules over time.

Included in that random motion are not just the CO2 molecules present inside and outside the plant, but also those that the plant is producing through cellular respiration. By chance, certainly, some of these molecules could end up back in the Calvin cycle. Some could even exit through the stomata and come back in (my intuition is that this is quite improbable for an individual molecule but I haven't done the math...the important concept is that it's all one "pool").

If you really wanted to know, you could set up a Monte Carlo simulation (or use differential equations) and calculate probabilities of all sorts of event sequences for individual molecules. You could also tilt the scales a bit if you, say, put the equivalent of a 'plastic bag' over a leaf, either physically or in a model: if there's a limited amount of CO2 in the "outside" space it would be much more likely for individual molecules to be "reused".

From a biologists' perspective, though, and especially for ubiquitous, freely moving molecules like CO2, it's usually only important to think about net flow.


Although this is theoretical a problem, in fact it isn't one. Lets do the calculation around it. EDTA complexes equimolar amounts of bivalent cations (e.g. Magnesium), so 1mM EDTA will complex 1mM Magnesium ions. Lets assume that the PCR reaction contains 2mM Magnesium.

A typical PCR reaction I do has a total volume of 25ul and contains 1ul DNA template in TE buffer (10mM Tris, 1mM EDTA). The final reaction contains 1/25th mM (or 0,04mM or 40nM) EDTA which can complex 0,04mM Magnesium. So instead of running the reaction with 2mM Magnesium, you do it with 1,96mM, which will not be noticable.

Additionally other errors in setting up (pipettes not accurately calibrated, not setting small amounts into the liquid etc.) easily add up to 5-10% error in total, which has a much higher impact in the Magnesium concentration of the reaction than the EDTA. If you use much higher template concentrations (which is usually not necessary), then you can correct for this, but normally this is not necessary.


How to learn molecular biology through pubmed research articles?

Tom Silhavy would use a similar method in the first year graduate Molecular Biology course.

His text was basically a set of papers bound into a book "The power of bacterial genetics: a literature based course".  I'm not sure its in print anymore, but a used copy can be had.  If you find a copy you can just fetch the papers if you like.

You can't do much better than finding excellent papers to read.

Briefly, the class covered the development of selection for mutations and mapping them onto genes - use of bacteriophage and replicate plating.  The papers started in the 40s and went on from there to the heyday of molecular biology.

It was an awesome course to take... an awesome baptism of fire.

As they say... Whatever doesn't kill you, will select you for a distinguishing phenotype.


You mention that you "started in bioinformatics", so perhaps you might feel more comfortable taking such an approach to better characterize where the promoter for HBA2 might be.

As @Bitwise mentioned in his comment, "the promoter" is not a well defined region. Often times "we" take the promoter of a gene to be some arbitrary (2-4) kilobytes upstream from the TSS. With more high throughput data coming online (especially from ENCODE), we are starting to get a better picture of where the functional regulatory elements of genes might be.

By combining data from several different high-throughput assays across a variety of cell types, the human genome has been segmented into broad regions of interest. You might start by looking for where the "Predicted promoter region including transcription start site" segment is for HBA2.

I'd also take a closer look at the DNase-seq data in this "promoter region" across as many cell lines as they have processed for you to look for regions that are differentially occupied in hopes of identifying more precisely which parts in the promoter region might be important for the gene's expression (this would, of course, require you to connect DNAseq data with gene expression (RNA-seq) data).


So i did some more research and found some canon photos of two moth species both found in india and super similar to this

both of them have brown spots around them
both of them are found in india
 So it was hard for me to eliminate one of them
here are both the insects
Sphenarches Anisodactylus

Sphenarches caffer

So now its up to you to decide which one it is???


There are two types of eye movement: smooth pursuit and saccadic. As the name suggests the latter movement involves quick and discontinuous movements of the eyes. Saccadic movement is used most of the time as the eyes move around analysing the current scene.

According to Wikipedia, these saccades are the fastest movements produced by the human body: peak angular speed of 900 degrees of rotation per second (this would be 2.5 full rotations of the eyeball per second, were such a thing possible).

The processing of information by the eye-brain system during a saccade is complex, and may be responsible for the effect that you report: it causes the phenomenon of saccadic masking explained in this quote from Wikipedia:

  A person may observe the saccadic masking effect by standing in front of a mirror and looking from one eye to the next (and vice versa). The subject will not experience any movement of the eyes nor any evidence that the optic nerve has momentarily ceased transmitting. Due to saccadic masking, the eye/brain system not only hides the eye movements from the individual but also hides the evidence that anything has been hidden. Of course, a second observer watching the experiment will see the subject's eyes moving back and forth. The function's main purpose is to prevent smearing of the image.


It is not possible, that a plant grows without any nutrients. Magnesium for example is needed in every chlorophyll, so there is no photosynthesis without magnesium. Another point is that plants can not get nitrogen from the air, so they have to get it from the soil and nitrogen is present in every amino acid, which build the plants proteins. Proteins are essential for every living organism. This are only two points and there are many many others why every plant needs nutrients like nitrogen phophorus, magnesium...

If it seems that Epipremnum aureum does only need water, maybe the plant gets its nutrients from a place you don't expect. Maybe the water is contaminated. Are there leafs falling into the water for example? Another possibility could be that Epipremnum aureum stored a lot of nutrients before it got only water but this won't last for ever.

I read your comment, thats why i think the nutrients have to come from the water. Additionally I found this publication about Calcium Deficiency Symptoms of Epipremnum aureum

I think you know that tap water or rain water isn't pure H2O. We just measured the tap water in Cologne, by ICP-MS. This is no official measurement, and we measured only once but I think its nice to see whats else in tap water.     Unfortunately we couldn't measure nitrogen, because normally the machine is used for plant extracts and there would be to much nitrogen.

Maybe your Epipremnum aureum gets enough nutrients from the water, I don't know if this is possible and how often you change the water.

Your pot could also be a source for nutrients if its not sealed up.

In conclusion the answer is that in general it is not possible, that your plant grows without nutrients. So there is a source which can be only detected by yourself, because you know the exact conditions under which your plant grows. I hope I could give you some hints.


What physical or mental actions can be picked up by EEGs?

Many EEG responses are swamped in random brain activity, artifacts and background noise. A single movement typically doesn't evoke measurable activity, because its amplitude is so small with respect to background noise.

I think the potentials you are looking for are event-related potentials or ERPs (Fig. 1). During ERP recording, basically a regular EEG is registered, but certain events (presentation of stimuli or actions by the subject) are time locked with the EEG recordings. By repeatedly measuring (e.g., 25 times) the time-locked response to the event, an average EEG can be obtained. Assuming remaining EEG activity, noise and artifacts are random, the averaging process will decrease noise, but will not affect the ERP. The averaging hence leaves you with a clean ERP response (Yordanova et al., 2003).

Fig. 1. ERPs. Left are stimulus-evoked ERPs (auditory, visual) and right are ERPs associated with the motor response by the subject (button-press upon stimulus presentation). Source: Yordanova et al., 2003.

In Fig. 1, the reaction times indicated correspond to the subject's button press, so the intention to press the button in fact precedes the actual motor response. In fact, the covert (imagined) ERP response can be nearly identical to the overt ERP (the motor action), see Fig. 2 (Kranczioch et al., 2009).

Fig. 2. Overt motor-evoked ERPs (top three panels) and equivalent covert (imagined) ERPs (lower three panels). The three panels cover different electrodes. Source: Kranczioch et al. (2009).

By characterizing the exact shape and other characteristics of the ERP, computer software can be deployed to recognize this ERP wave within a normal EEG. This is done in computer-brain interfaces. By filtering the ERG outside the frequency range associated with the ERP a lot of the cleaning can be done on the fly in near-real time.

A list of various stimuli in ERPs can be found in Table 1 in (Goodman, 2010).

References
- Goodman, Atten Percept Psychophys (2010); 72(8): 10.3758
- Kranczioch et al., Human Brain Mapping (2009); 30(10): 3275–86
- Yordanova et al., Brain (2003); 127(2): 351 - 62


What happens when you take a deciduous tree and place it in a climate controlled greenhouse?

It harms the trees, seasonal chemistry in the plant is reduced and weakened they have tried growing apples and decidious fruit trees at the equator and they have to treat them chemically to help them stay stronger:
http://www.actahort.org/books/49/49_14.htm
the tropics have seasonal queues, and in a greenhouse with no temp and light change, the plant would be very disoriented, the critical glucose and leaf cycling would be very degraded, because plants have most of their queues from temps, water and sun.
http://www.madsci.org/posts/archives/2001-02/981072513.Bt.r.html
more infos


This is a very interesting question and I had not thought about it before. I am reiterating the background of your question.

Background

Cas9 cuts the both the strands of the target DNA at the same location thereby making a blunt end cut. Usually sticky ends and microhomologous ends lead to indels because of exonucleolytic clipping and addition of extra bases by pol-µ. The question is how do indels arise during NHEJ mediated re-ligation of blunt ends.

NHEJ may not always lead to indels. Most blunt end cuts can be repaired without error. Some non blunt cuts are also perfectly re-ligated; the best example for this is VDJ recombination. The binding of Ku proteins is essential for a perfect re-ligation (canonical NHEJ/C-NHEJ).

However, there are some variant non-canonical pathways which include alternative-NHEJ, backup-NHEJ and microhomology mediated end joining (MMEJ) (Bétermier et al. 2014). Some studies also refer to all of these pathways as alternative-NHEJ or altNHEJ. These alternative pathways involve resection of nucleotides by exonucleases such as Mre11 to produce overhangs. Imperfect alignment of these overhangs prior to ligation leads to indels. Sometimes non-templated addition of nucleotide happens by the action of terminal deoxyribonuclotide transferase (TdT). Pol-µ can also add random nucleotides at the 3' end (Lieber 2010).

In general, the propensity of DSBR via alternative NHEJ pathways would be higher when Ku activity is lower. Even with a moderate Ku activity, there is always some likelihood of alternative pathways in action. Moreover, it is to be noted that sticky end ligations are more efficient than blunt end ligations.

   Reproduced from Bétermier et al. 2014


How did the introduction of artificial light changed the life cycle of a plant?

According to this study, artificial lighting similar to that provided by streetlights in the UK can reduce flowering in at least one plant, which also affects the aphids that feed on it.

This article discusses it in more general terms - night lighting doesn't affect photosynthesis, but can affect the length of day/night perceived by plants and alter growth accordingly. There are two examples given of how it is harmful:

Young trees grow longer and don't enter dormancy, making them increasingly susceptible to cold temperatures.
The stomatal pores of leaves remain open longer, making some trees more susceptible to pollution and water stress.


How to determine sensitivity in a dose-response curve?

I think you are after the slope of the dose-response curve:

Dose-response curve. Souce: Merck

The slope indicates the change in response per unit dose, which translates to sensitivity.


The title question,

Is there any evolutionary reason why male traits appear in the heterogametic sex and female traits in the homogametic sex?,

suggests that male always is the heterogametic sex, but this is not true.  ("Male" is usually defined as the sex with the small, mobile gametes, i.e. sperm, as contrasted with the large, nutritive gametes, i.e. ova.) There are many species where females are the heterogametic sex, such as birds, most snakes, some fish, crustaceans, and insects.[a] These species use the "ZW" sex-determination system, which is essentially the inverse of the more familiar "XY" system.[a]  Other species don't have a heterogametic sex, but rather use lack of one chromosome as the determiner ("XO", "ZO"), and yet others use lack of one half of all chromosomes as the determiner ("haplodiploidy"). Others don't distinguish sexes by chromosomes, but use environmental stimuli.[b]
All this variety in forms of sex determination suggests that there are not substantial evolutionary advantages to having the heterogametic sex be the male.
[a] "ZW sex-determination system", Wikipedia.
[b] "Sex-determination system", Wikipedia.


What decides the position of the node of Ranvier?

A combination of differentiation site, chemical guidance during migration, and signaling cues form a variety of sources.

  The final step in the generation of an oligodendrocyte is the
  development of a mature myelinating phenotype, and this is largely
  regulated by axonal signals. It seems likely that both soluble and
  cell mediated signals from adjacent axons are integrated into the
  developmental profile of oligodendrocyte precursors resulting in cell
  differentiation, up-regulation of myelin gene expression and formation
  of the myelin organelle. Candidates for axonally derived soluble
  factors include FGFs (Bansal et al., 1996 and Qian et al., 1997) and
  thyroid hormone (Barres et al., 1994a and Barres et al., 1994b), while
  axonal cell surface molecules such as L1, MAG, NCAM and N-cadherin may
  regulate formation of the myelin sheath (Payne and Lemmon, 1993 and
  Trapp, 1990).

http://www.ncbi.nlm.nih.gov/pubmed/12385864

I don't know of any diseases that just mess with positioning but there are diseases that kill oligodendrocytes (like multiple sclerosis).


James Allison's T-cell discovery technique

Well so here's the paper, at least on Dr. Allison's side. Mind you, the discovery is shared by a number of individuals for their combined effort.

So what they did is took mice and immunized them with T-cell lymphoma cells. The mice would essentially produce B cells against the lymphoma cells. And so we know that B cells produce antibodies, and hybridoma methods exploit the B cells to get a lot of that antibody. With their constructed hybridoma library, they could look at reactivity of antibodies produced against the lymphoma cells against the reactivity of the same antibody against other cells. They ended up finding 1/43 antibodies, which they dubbed 124-4O, reacted to their lymphoma line, but not to other cells.

With a pull-down assay, they isolated the receptor and determined it was a heterodimeric glycoprotein. A step further, they looked at both B cells and T cells, then, and were able to detect similar structures in the T cells, but not in the B cells.

Someone correct me If I'm wrong, though.


Do plants take in the same amount of CO2 as they release?

You've made one faulty assumption: that the second reaction is occuring at the same rate as the first.  In fact, plants only burn enough glucose to fuel their activities. Much of the formed glucose is converted into storage forms like cellulose and starch.  In fact, the vast majority of a plant's carbon mass comes ultimately from CO2 which has been converted photosynthetically into carbohydrate forms. (Further reading)

Ultimately, when plants die, those carbon molecules are used as food for other species, such as animal and bacteria.  Ultimately, whether in composted plant material or fecal mater, the carbon is deposited on the ground.  So ultimately it is correct that trees & plants are removing CO2 permanently from the atmosphere.  Although some is being released to the atmosphere catabolically, more is re-absorbed for anabolic processes, and ultimately, that CO2 gets deposited on the ground in more complex carbon forms.


What is the classification for animals with full tube digestive tracts?

Animals with a single hole do not form a monophyletic group: metazoa > eumetazoa >bilateria almost all have separate mouth and anus (except notably flatworms which is one reason it does not form a monophyletic group).

As species are not grouped in monophyletic groups by what they don't have (eg. invertebrates do not form a monophyletic group while vertebrates do) there is no particular group. Eumetazoa before the bilateria have a single mouth-anus.