What is the evidence that plants and animals had a common ancestor?

Darwin did propose that all extant organisms have a common ancestor:

  Therefore, on the principle of natural selection with divergence of character, it does not seem incredible that, from some such low and intermediate form, both animals and plants may have been developed; and, if we admit this, we must likewise admit that all the organic beings which have ever lived on this earth may be descended from some one primordial form. But this inference is chiefly grounded on analogy, and it is immaterial whether or not it be accepted. No doubt it is possible, as Mr. G.H. Lewes has urged, that at the first commencement of life many different forms were evolved; but if so, we may conclude that only a very few have left modified descendants. For, as I have recently remarked in regard to the members of each great kingdom, such as the Vertebrata, Articulata, etc., we have distinct evidence in their embryological, homologous, and rudimentary structures, that within each kingdom all the members are descended from a single progenitor.

--Darwin, Origin of Species

He probably wasn't the first one; Darwin cites a previous suggestion:

  From a circular lately issued it appears that Dr. Freke, in 1851 ("Dublin Medical Press", page 322), propounded the doctrine that all organic beings have descended from one primordial form. His grounds of belief and treatment of the subject are wholly different from mine; but as Dr. Freke has now (1861) published his Essay on the "Origin of Species by means of Organic Affinity", the difficult attempt to give any idea of his views would be superfluous on my part.

--Darwin, Origin of Species

As you can see, he offers no real evidence for this; he explicitly says it's speculation. Of course, nothing from Darwin is necessary for modern evolutionary theory, and other groups have tried to make this more concrete. Several lines of evidence provided increasing evidence for a universal common ancestor (UCA):

  For a century after the publication of Darwin's bold proposition, before the advent of molecular biology, the UCA hypothesis remained an untested and hardly testable speculation. However, first the universality of the genetic code and later the demonstration of the (near) universal conservation of approximately 100 RNA and protein-coding genes among cellular life forms provided ample evidence in support of the UCA. Although generally considered compelling, this evidence fell short of a rigorous, formal test of the UCA hypothesis.

--The common ancestry of life

A relatively recent approach has tried using information theory to formally test a UCA:

  Here I provide the first, to my knowledge, formal, fundamental test of UCA, without assuming that sequence similarity implies genetic kinship. I test UCA by applying model selection theory to molecular phylogenies, focusing on a set of ubiquitously conserved proteins that are proposed to be orthologous. Among a wide range of biological models involving the independent ancestry of major taxonomic groups, the model selection tests are found to overwhelmingly support UCA irrespective of the presence of horizontal gene transfer and symbiotic fusion events. These results provide powerful statistical evidence corroborating the monophyly of all known life.

--A formal test of the theory of universal common ancestry

Formal positive proof of theories in science, outside of math, are rare to non-existent (what actually happens is that competing theories are disproved) and I don't think that this approach is different. It's not a formal proof, it's yet more powerful evidence that theories not involving a UCA suck.

  A formal demonstration of the Universal Common Ancestry hypothesis has not been achieved and is unlikely to be feasible in principle. Nevertheless, the evidence in support of this hypothesis provided by comparative genomics is overwhelming.

--The common ancestry of life


Quantitative Comparisons of Phylogenetic trees

I don't know whether it's exactly what you need, but there are formal algorithms for tree comparison.

There are basically two approaches: one utilizing tree lengths (branch score distance) and the other one dealing with topologies only (symmetric-difference metric): details and references can be found in the manual to treedist from the phylip-package, which implements both.

PAUP* has a command under the same name (treedist), which calculates the symmetric-difference metric only. This metric is very intuitive: it describes the total number of partitions (= splits) present only on one of the two trees.


Getting xyz co-ordinates from a .map file (CCP4 format) in VMD

Just Download and Install: CCP4: Software for Macromolecular Crystallography


What is the name of this insect? Is it venomous or possess any threat to human life if someone gets stung?

That looks like some kind of lappet moth caterpillar. Although I am no expert in them, especially not species that would appear in India. But hopefully my answer gives you the right direction of research.

You can see some visually similar observations on iNaturalist:

https://www.inaturalist.org/observations/42382365
https://www.inaturalist.org/observations/40958993
https://www.inaturalist.org/observations/40137289


Productive turnover and generations in the fruit fly

What do you mean by you couldn't find anything on the internet? Drosophila generation time is explained here?

Your other question is a bit off-topic here but I'll give all advice I have heard myself:

You can leave out a banana skin and catch some fruit flies, then do the experiment in your kitchen :) Joke aside, unless you perform the experiment independently it will probably take a long time and it's well possible that you won't be able to do it at all (unless you become some famous scientist). I'm not familiar with the experiments you mention, but if you require equipment and/or funding, you will need a qualification and/or a good explanation why people should give you money or let you use their equipment for this experiment.

I don't know what stage of education you are at, but it sounds like you are still at school ("when I'm older")? Most countries have some schemes where students (below uni) can apply for young researcher kind of things, so you could try and google that. Apart from that, the best bet is probably to try and get into a uni with good facilities and research programmes for their students. What you study shouldn't matter so much as long as it's science.

In response to Marta's commment: if you understand the experiment and you think you can gather everything they used at home, nothing speaks against just doing it on your own. Just make sure you don't let those flies swarm your house ;)


Why is an intron (or exon) still called intron (exon) if retained in (excluded from) mRNA?

You must know that:

Introns are non-coding regions of an RNA transcript, or the DNA encoding it, that are eliminated by splicing before translation.
An exon is any part of a gene that will encode a part of the final mature RNA produced by that gene after introns have been removed by RNA splicing.

Now, about the exceptions, alternative splicing: Here,

  particular exons of a gene may be included within or excluded from
  the final, processed messenger RNA (mRNA) produced from that gene. There are numerous modes of alternative splicing observed, of which the most common is exon skipping. In this mode, a particular exon may be included in mRNAs under some conditions or in particular tissues, and omitted from the mRNA in others.

Apparently, this greatly increases the biodiversity of proteins (since there are differences in their amino acid sequence and, often, in their biological functions) which might explain why it is so common.

So in this case, it becomes easier to understand if you use 'coding' and non-coding' as the difference instead of 'spliced' and 'not-spliced'.

EDIT- The coding region of a gene:

  In DNA, the coding region is flanked by the promoter sequence on the 5' end of the template strand and the termination sequence on the 3' end. Although this term is also sometimes used interchangeably with exon, it is not the exact same thing: the exon is composed of the coding region as well as the 3' and 5' untranslated regions of the RNA, and so therefore, an exon would be partially made up of coding regions. The 3' and 5' untranslated regions of the RNA, which do not code for protein, are termed non-coding regions.

I had previously forgotten about the UTR's, so I have included that. Now, if there is a definite sequence where coding regions are found, it points out to the fact that coding regions must be intrinsic. Another point in favour:

  The evidence suggests that there is a general interdependence between
  base composition patterns and coding region availability.The coding
  region is thought to contain a higher GC-content than non-coding
  regions. There is further research that discovered that the longer the
  coding strand, the higher the GC-content. Short coding strands are
  comparatively still GC-poor, similar to the low GC-content of the base
  composition translational stop codons like TAG, TAA, and TGA.


This question is very broad and this would require a lot of calculations, I will focus on the carbon dioxide in the trees, hopefully some other users can add details in respect to the organism and their carbon dioxide storage.

I found an article(R.Jandl et al.,(2007)) which did some calculations, this site does a really good job in explaning these calculations so I will cite that:

  As trees photosynthesise they use carbon dioxide (CO2) from the
  atmosphere with water from rain or irrigation and nutrients from the
  soil to form carbohydrates, which make up the tree’s biomass, but how
  much carbon is made by a tree in this process? Researchers at
  Ecometrica have worked it out! The amount of carbon stored by a tree
  depends on its size, which in turn is influenced by factors, such as
  species, local environmental conditions and the way it is managed. In
  an attempt to find a simple answer to this question, researchers at
  Ecometrica have broken down approximately how much carbon is stored in
  each element of a typical tree (the branches, the leaves, the stem and
  the roots) by percentage for a quick and simple calculation.

  They used standard forestry practices to estimate the amount of carbon
  contained within the stem, branches, roots and leaves of a mature
  sycamore (Acer pseudoplatanus), found near their office in Edinburgh,
  with a diameter of 52 cm and a stem height of 12 m.

  First they measured the various parts of the tree and, from these
  measurements; they calculated their volumes, which were then used to
  calculate the biomass (mass of living matter in plant tissues):  The
  radius of the stem at 1.3 m above the ground (r1 = 26 cm) and at the
  top of the stem (r2 = 20 cm), and The height of the stem (h = 12 m)
  They used known relationships between the biomass of the stem and the
  biomass of roots, branches and leaves to estimate the total biomass of
  the tree: Stem volume was estimated using the equation for the volume
  of a truncated cone:

  which gave an estimated stem volume of 2.0 m3 The wood density of sycamore is approximately 620 kg/m3, so using the equation:

  Mass = Density × Volume  the stem biomass was 1243 kg, or
  approximately 1.2 tonnes  The biomass of the roots, branches and
  leaves of a sycamore tree are known to be around 26%, 11%, and 1% of
  the total biomass, respectively. These proportions were used to
  estimate the total biomass of the tree without having to dig up roots
  or cut down branches.  In summary, the sycamore tree had a stem with a
  biomass of 1.2 tonnes, roots of 0.5 tonnes, branches of 0.2 tonnes and
  leaves of 0.02 tonnes, giving a total biomass of 2 tonnes.

  The carbon content of woody matter (stem, branches and roots) and that
  of leaves is approximately 50% of  their biomass. Multiplying the
  total biomass by the proportion of that biomass which is carbon gives
  an estimate of the total amount of carbon stored in the tree, which in
  this case was exactly 1 tonne! Each tonne of carbon equals to
  approximately 3.67 tonnes of CO2.

Then the further calulations really depends on the density of the trees in the forest (if you know the exact number let me know). There are a lot of atricles which gave some numbers the range is based on these articles somewhere around 30-400(and some even 1200 trees). I used the data from this article, which measured the optimal density for growing. I assumed that the climax forest is just naturally so I just picked 400 trees per acre (this is just guessing offcourse and I just generalized this for all trees, but I saw 400 in an other article):

Then we can just do some simple math for the carbon dioxide for the trees:

  total CO2 for the trees = 400 x 3.67 = 1468 tonnes

Let me know if someone can find the tree density of a climax forest


What is this ornamental, yellow flower that looks like a smooth pineapple skin?

This is a beehive ginger, Zingiber spectabile.

Its inflorescence will become a bit different sometime soon:

I believe the one in your image is not yet fully developed, like this one here:

Source of the images:

http://www.geneticjungle.com/2008/08/deceptive-petals-7-orchid-mimics.html
http://specialflowersintheworld.blogspot.com.au/2015/04/zingiber-spectabile-flower.html


Which was the last significant event in human evolution? What's next?

Background

I'd like to start by saying that phenotypic (loosely speaking phenotypic mean morphological) traits evolve because their variance in the population is correlated with some genetic variance. If most of the phenotypic variance is genetically coded, you'd expect that the trait will change through if different variant of the trait influence fitness (which is a function of both survival and reproductive success). Stated differently and more accurately the change in mean value of a given trait $R$ in the population is given by:

$$R=S\frac{V_{Ga}}{V_{P}} = S\frac{V_{Ga}}{V_{G}+V_{E}} =  S\frac{V_{Ga}}{V_{Ga} + V_{Gd}+V_{E}} $$

, where $S$ is the selection differential, $V_{G} = V_{Ga}+ V_{Gd}$ is the genetic variance where its two components are the additive and dominance genetic variance respectively. $V_P  = V_G + V_E$ is the phenotypic variance which two components are the genetic and environmental variances. The ratio $\frac{V_{Ga}}{V_{P}}$ has a name; it is called the heritability in the narrow sense symbolized by $h_N$ Note: I present here a simplified version of the reality!

So, if the trait you consider has genetic variance in the population and that this trait influence the fitness with a given selection differential you can provide estimates of how the trait will change through time in the human population. Now if the variance does not already exist in the population but you have to wait for mutations to occur, then you cannot really provide an estimate of when will this occur.

Discussion on the future evolution of nail size

Also, when you think about some traits such as our nails. You may consider that they are of no use but do you really think that those people that have no nail would really have a better fitness. At first I would tend to think that I would rather chose a partner that have nails, it is much more sexy! If many people are like me and appreciate nails, nailless people will have difficulties to reproduce or in other words, they will have a lower fitness that nailed people.

I don't think we have data on what loci (positions on the chromosomes) influence the size of the nails and about how much of the variance in nail size is explained by the genetic additive variance. And how do the size of our nails influence fitness. So we don't know about how this trait will evolve through time.

Future evolution of other traits

There are several traits that we can/could more or less predict their evolution. Those are the traits for which we know the ratio of the genetic additive variance over the phenotypic variance and how it influences fitness. I can think of genes that are linked with resistance to new diseases such as HIV for example. If malaria comes to a new area you might expect the allele (=variant of a gene) allowing a better resistance to malaria will increase in frequency (note that this allele is advantageous in heterozyotes (protects from malaria) but it is highly disadvantegous in homozygote because it causes sickle-cel disease). We could estimate the change in frequency of alleles linked with obesity in some countries also. Probably several studies exist on the subject but I don't know them. One might improve this answer by giving some information about how HIV resistant variants is likely to change in frequency through time.

What were the last evolutionary changes in human history?

You can think of the impressive frequency of the Tay-Sachs disease in french canadian due to a bottleneck effect. Or you may think of the evolution of height, about the evolution of the shape of the skull or the evolution of feet. You can think of the reduction of our gut. etc… Your question is not well enough define so that we know if you consider the raise in frequency of Tay-Sachs disease is sufficient for you to be called a significant evolution.

Hope that helps!


To which negatively charged components of the cell envelopes do the crystal violet complexes bind in gram staining?

The gram staining relies on the differences in the bacterial membranes. The gram positive bacteria have a thick peptidoglycan layer on top of the cell membrane, the gram negative bacteria have a lipid layer on the outside followed by a thin peptidoglycan layer and then the cell membrane. See the image for clarification (from here):

Crytall violet dissociates into a positively charged dye molecule (CV+) and chloride (Cl-). The CV+ travels between the membrane layers (outer and inner membrane) and is trapped there by the addition of iodine. This is used to form large crytal violet-iodine complexes which are retained during the destaining process.

In the destaining process, the peptidoglycan layer of gram positive bacteria is dehydrated and therefore shrinks which prevents the staining from being washed out. In the gram negative bacteria, the outer lipid layer is removed and the peptidoglycan layer (which is much thinner) exposed which allows the removal of the stain. The teichoic acid is important for the rigidity of the membrane but not for the binding itself.

References:

Gram staining
The Gram Stain after More than a Century
Use of the Gram stain in microbiology


This is not as hard, as it first seems. Lets have a look at the single enzyme digests first: The digest with enzyme A and B only leads to products which are 5kB (5000 bp) away from each other. Since they are of the same size, both equally sized restriction fragments appear as one band. So each enzyme cuts the plasmid exactly in half.

The double digest is a bit more tricky, but not much. You get two products from it, with 2kb and 3kB. This means that enzyme B cuts between the restriction sites for enzyme A, resulting in these two fragments. Have a look at the sketch I made below (only a quick one and not to scale):

A1 and A2 are the cutting sites for enzyme A, B1 and B2 the sits for enzyme B. The numbers on the outside are the positions on the DNA sequence. You can see that a single digest leads to two fragments of 5kB (doesn't matter which) and that both A and both B sites are located 5kB from each other.

A1 is at position 100, A2 has to be at position 5100, B1 is located 2kB behind A1 (and therefore at position 2100), and B2 2kB behind position A2 (and therefore at position 7100). To get the same restriction pattern it is also possible that B1 and B2 are located 3kB behind their respective enzyme A position (so at 3100 and 8100) and you still get the same pattern of 2kB and 3kB on the gel.


This is more a biological (immunology, serology) question, than one about gardening. It is possible that mosquitoes vary in 'toxicity', however I think the greatest part of the reaction is caused by yourself (no offense, I am prone to allergic reactions to mosquito bites too). So the chemicals that enter your body can vary per mosquito species (or even individual), which can trigger a milder or worst reaction. Just like different pathogens (bacteria, viruses) can also trigger different reactions (influenza can be innocent or deadly). But it is more likely that your own immunological 'state' is causing a worst reaction. For instance if you also have hay fever, levels of immunological molecules (etc. cytokines, chemokines) are already high in your blood and cause a larger or more intense reaction than in periods when less of these molecules are present in your blood.


What is the difference between alarmones and riboswitches

First time I actually hear the word alarmone so bear with me okay?

"An Alarmone is an intracellular signal molecule that is produced due to harsh environmental factors. They regulate the gene expression at transcription level" <- this probably refers to activating/inhibiting transcription factors and stuff like that. Looking at bit further into the wikipedia article from whence you copied the description, we see that ppGpp is considered an alarmone.

According to the wikipedia article on ppGpp (https://en.wikipedia.org/wiki/Guanosine_pentaphosphate) we see e.g. this line "When (p)ppGpp associates with the promoter it affects the RNA polymerase enzyme's ability to bind and initiate transcription", so this alarmone can act by inhibiting RNA polymerase's ability to bind to the promoter.

A riboswitch on the other hand is a structural element INSIDE an RNA molecule that causes a conformational change upon binding a ligand. This conformational change then has an effect on transcription or translation etc. Thus, an alarmone could probably bind to a riboswitch to exert its effect, but a riboswitch is a quite specific thing.
You can read about some of the mechanisms in the wikipedia article https://en.wikipedia.org/wiki/Riboswitch

So basically, think of alarmones as signalling molecules and riboswitches as structural elements in transcripts that regulate gene expression upon ligand binding.


Is transition more common than transversion during the evolution of duplicated genes?

If we consider that the biochemical impact of transitions vs transversions is constant across the two scenarios, then the only discrepancy can be due to the level of purifying selection, or the level of positive diversifying selection, or both, between the two duplicates.

By far the most common fate to one duplicate copy is for purifying selection to be relaxed, leading to accruing deleterious mutations and eventually loss. This means that fixation of non-synonymous mutations are more common, and as transversions are more likely to be non-synonymous, this implies that the rate of fixation for transversions would increase.

Similarly, one might expect functional change leading to positive diversifying selection, which implies a greater rate of fixation of non-synonymous mutations and, following the same logic as above, a greater rate of transversions.

Whether or not this contributing increase to the rate of fixation of transversions mean that transversions actually outnumber transitions, or instead merely decreases the ratio of transition:transversion, will be dependent on the particular gene and selective scenario.

As a final note, while the first cause I identified (biochemical)  actually changes the rate of mutation, the selection-specific factors are changes to rate of fixation, which is a population-level process. So while the relative rates of transition and transversion may stay the same, the fixation rates of these two categories of mutation between the two duplicate copies are the important difference.


Why glycoproteins are better than non-glycoproteins in fulfilling biological tasks?

The central reasoning is flawed because it places some intrinsic value on glycoprotein modification. The general intuition is that, if the protein is glycosylated, then it's likely for a reason, whether it be to help fulfil antigen recognition, adopt a correct conformation, or help in molecular tethering. Beyond, that, many (perhaps a majority) of cellular proteins are not glycosylated. Two important examples of cell membrane proteins that are not glycosylated would be endoproteases (eg, furin) and chemical transporters.


Is there an evolutionary explanation for the black spots around a pandas eyes?

As your commenters have suggested, no.

In order for an explanation to be a good evolutionary explanation, it needs to have a testable hypothesis and a mechanism to test it.

The most common mechanism for testing the crypsis (camouflage) hypothesis is to take a large number of closely-related species, and see if their coloration differences are correlated to a particular habitat. Since pandas have few black-and-white relatives, there is no statistical power in this analysis.

Another option is to take a large number of pandas, create a treatment and control group and bleach the treatment group (or their eyespots) white, and compare survival or visual acuity. Unsurprisingly, this has not been done.

Here's a nice article to animal coloration for those that have access:

Caro, T. I. M. (2005). The adaptive significance of coloration in mammals. Bioscience, 55(2), 125-136.


What is this insect that has invaded my home in Texas?

Myodocha serripes

http://www.americaninsects.net/ht/myodocha-serripes.html

Nice picture! Generally, the body plan of this guy indicates Hemiptera (the 'true' bugs), but the long neck is a bit strange, so a google image search for "Hemiptera + long neck' brought up this strong candidate. It looks like it's distributed in Texas, and is in fact, named for that distinctive neck: "The Long-Necked Seed Bug".

See also the BugGuide.net page for Myodocha


What are the best plants to cultivate yeast from?

Yeast colonize the surface of many plants — for example they are a typical part of the normal surface flora (microbiome) of fruits such as grapes1 and pears2.

As you can see from the second reference, yeast can compete with other microorganisms to delay rotting of the fruit.

You might also find the "Uses" section of the wikipedia article on yeast and this article on winemaking to be of interest.

References:
1: Zahavi, T., Droby, S., Cohen, L., Weiss, B., & Ben-Arie, R. (2002). Characterization of the yeast flora on the surface of grape berries in Israel. VITIS-GEILWEILERHOF-, 41(4), 203-208.
2: Benbow, J. M., & Sugar, D. (1999). Fruit surface colonization and biological control of postharvest diseases of pear by preharvest yeast applications. Plant Disease, 83(9), 839-844.


Is carbohydrate an important part of phospholipid?

Your thinking is correct based on typical carbohydrates, but glycerol, the backbone of the phospholipid, is a 3-carbon carbohydrate that is usually derived from glucose.  It is not a sugar, but it does fall into the general class of polyols (aka sugar alcohols) that are a type of carbohydrate.

A carbohydrate definitely is an important structural part of the phospholipid, but your instructor probably should have been more clear in describing why that is the case; I can definitely understand your confusion here.


I think they are called "Red Bugs" (really), otherwise known as Antilochus conquebertii (aka Antilochus coquebertii).

The black coloring changes from location to location. These were found in India. They were even described by the querent as eating black seeds.

Viet Nam Red Bugs are pretty as well:

  The family Pyrrhocoridae is commonly called the Red Bug family, and the family includes the Cotton Stainers as well as the Firebugs, so Red Bugs is the more general family name that includes the other genera and species.


Analysis of post transplantation lineage tags

I can't find a reference to a "TARIS model" in the paper you linked, but we can break down the molecular circuitry of this lineage tag tracking system step-by-step.

The authors use a type of Tet expression system in order to tightly control the expression of a hyperactive Sleeping Beauty (HSB) transposase.  In the absence of doxycycline, the reverse tetracycline-controlled transactivator M2-rtTA does not bind the TetO operator. Jackson Labs has a very good summary of Tet-On (and Tet-Off) systems:

  ... rtTA is a fusion protein comprised of the TetR repressor and the VP16 transactivation domain; however, a four amino acid change in the tetR DNA binding moiety alters rtTA's binding characteristics such that it can only recognize the tetO sequences in the [tetracycline-responsive promoter element (TRE)] of the target transgene in the presence of the Dox effector. Thus, in the Tet-On system, transcription of the TRE-regulated target gene is stimulated by rtTA only in the presence of Dox.

In the presence of doxycycline, the transactivator drives expression of HSB from the constituent promoters of the TetO operator.  HSB contains DNA binding motifs that specifically recognize the direct repeats (white triangles) and a catalytic domain that excises the direct repeats and the DNA they flank, which contains a transcription stop signal (Tn-STOP).
Excision of the Tn-STOP signal allows for expression of DsRed driven by a strong synthetic promoter (CAGGS, first described here).  The excised sequence is then inserted somewhere else in the genome.
Because successful Tn-STOP excision is concurrent with transcription of DsRed, red fluorescing cells can be selected and prepared for NGS.  HSB transposition is "random", so two different transposition events are unlikely to target the same insertion locus.  The specific insertion site can then be used as a molecular fingerprint to identify the progenitor stem cell after replication and differentiation.


Is stereo olfactory ability restricted to humans?

Moles and rats also smell in stereo (Catania 2013 and Rajan et al 2006), as do desert ants (link).  The latter is rather interesting, given that ants "smell" using their antennae, which suggests multiple sensory structures, not necessarily nostrils, are required for stereo olfactory ability.

EDIT: Hammerhead sharks have two nares and also stereo olfactory ability (here).  Dolphins have one spiracle, as do a number of other cetaceans.

It's actually not clear whether humans have stereo olfactory ability, (see edit below)  as the "stereo" aspect derives from having nostrils that are sampling from different spatial locations.  However, the research in the eastern mole suggests that this is not so far-fetched an idea, as their nostrils are not so far apart.

EDIT of EDIT: I take that back about humans: we do appear to have stereo olfaction.


Let me begin in the sample preparation to explain you the index primers.... and let me assume please that you want to sequence amplicons like 16S. Let me further assume that you have 96 samples, which means that you have one complete PCR plate full of samples. First you prepare your samples. You are doing a amplicon PCR, clean that PCR, attach the adapters which are necessary that the sequences can bind to the glas slide and at last you are attaching indexes.
You are attaching these barcodes individually for each sample.
Looks like that image:

source: https://www.neb.com/~/media/Catalog/All-Protocols/C411AB12AFB04000BED567FC17B2A4AA/Content/PCRPlate.jpg

Let's call such indices barcodes (index = barcode). As you can see, each sample gets its own combination of a indexing primer as you are using always to primers (i7+i5) for each sample. Whats important is, is that all these primers are individuals like:

Line:
1: AAAAAT
2: AAAATT
3: AAATTT

and:
A: TTTGGG
B: TTGGGG
C: TGGGGG

(In reality these primers are longer and more complex!)

After you have done such a indexing PCR and also cleaned your PCR (get rid of the polymerase, something like this) you have to pool your samples (put them all together) before you are sequencing. And thats the point why such indexes are important. Without indexing you would have no chance to get your samples separated (=demultiplexed) again after sequencing.

When you are sequencing paired-end then you are sequencing one time forward (barcode + adapter + the sequence you want to have) and one time reverse (barcode + adapter + the sequence you want to have). One big amplicon of e.g. 500 bps gives you two sequences: the forward sequence (also called forward read) and the reverse read.

Let's call the forward read: R1
And the reverse read: R2

After sequencing you have one big pool of sequences. What you are doing first is to demultiplex your samples. As you know now you have for each samples hundreds of thousands of sequences: each consists of two Parts: The R1 read and the R2 read. What you are doing now is to separate your sequences again: You know that you used for example the indexing primers AAAATTTT and CCCCGGGG (just examples!) for your first sample. So you know that AAAATTTT belongs to the forward (R1) read and CCCCGGGG belongs to the reverse (R2) read. This means, that, when you separate all sequences which contains at the "barcoding/indexing-position" these sequences, you know that these are sequences which belong to your sample 1. For sample two you used for example the barcodes AATTAATT and CCGGCCGG and then you know again: AATTAATT belongs to the R1 read and CCGGCCGG belongs to the R2 read. Filtering that sequences out and save them in an additional file you will get your sample 2 separated. And that's why such indexes are important and that's also the reason why you always have to indexes: one is used for the forward read, and one for the reverse read.

Additionally: Why basically we have to use primers is the following: If you want to sequence an amplicon you (or at least the machine) is only able to sequence about 250 bps in each direction. When you are attaching indexes (which are in each case needed) then you are able to sequence in both directions: forward and reverse. And afterwards, when you have demultiplexed your samples you can run an assembly to put the forward and reverse reads together again.


What proportion of proteins require chaperone-assisted folding?

I'm reminded of a lovely review in Trends in Biochemical Sciences that discusses chaperone independent, partially dependent, and fully dependent proteins in prokaryotes.  The conclusion was that smaller polypeptides are less likely to require chaperone assistance. This is their figure:

That principle still holds to a certain extent (in prokaryotes), but folding assistance is now more broadly understood to include much more than just specific proteins identified as molecular chaperones. The Anfinsen postulate (that the final tertiary structure of a protein depends only on its primary structure) may still hold for small globular proteins, but folding in vivo is almost certainly always assisted. Since you're coming from the perspective of a chemist, don't think of it as a reaction between two molecules in solution. It's a reaction in a gel packed with complex sugars, lipids, proteins, and nucleic acids.

If you're skeptical of the perspective of a crowded cytoplasm, read the review I linked. It's an important but often under-appreciated aspect of in vivo biochemistry. There is much more to read about it. You might try looking up Allen Minton (AP Minton) and macromolecular crowding in your favorite database.


What is membrane-partitioning free energy? Can it be simulated?

In the biological context, membrane-partitioning is usually referring to the stage in which the transmembrane-destined region of a protein moves from interacting with the water, to interact with the interface of the membrane.

In the diagram below showing a four step thermodynamic cycle, the partitioning free energy can be referred to as-is ΔGwiu in terms of free energy where w is water, i is the interface, and u is unfolded. The image comes from the same paper that introduced the famous Wimley and White octanol-interface scale from 1999.

Note that in a more recent 2015 article, they comment that the partitioning phase ΔGwiu is generally the only experimentally accessible step. With that in mind, simulating ΔGwif where f is the folded helix becomes necessary. This 2014 Nature Comms paper use folding-partitioning molecular dynamics simulations to estimate the free energies that are experimentally inaccessible. They used Gomacs 4.5. In fact, a study using a simulation from 2005 suggests that folding isn't necessarily required for insertion of the helices.

Note that all the information here is behind a paywall. Feel free to ask me for clarification or expansion in the comments.


Why is there smooth muscle in our bronchioles?

There are at least two things to consider.

First, ability to limit airflow is a defense mechanism for animal. Imagine getting into area of some sort of toxic evaporation, e.g. CO2 cloud near volcano , then it makes sense to decrease delivery of toxin via lungs to minimum. As I understand, that is what an allergic asthma attack. (Sorry for not providing good enough source of that)

Secondly, you are incorrect in assuming that normal state is "dilated". Dilation of branchioles is sympathetic ("fight-and-fly") response of the nervous system to something like danger, that requires short-term boost in energy production. That is, by default, your airflow is limited. Probably, to limit amount of energy you effectively burn via oxygenation. But most importantly, you leave yourself a reserve in terms of oxygen supply for critical moments.

Some more information you might find here.


Why does an increased heart rate mean increased blood pressure?

In good approximation, the arterial blood pressure PA depends with

PA = PV + R x dv/dt,

on central venous pressure PV, total peripheral resistance R (also referred to as TPR or PVR) and cardiac output dv/dt (aka CO) – the usually cited equation MAP = CO * PVR is an over-simplification. Since cardiac output is defined with

dv/dt = RH * VS

as a result of heart rate (RH) and stroke volume (VS) the blood pressure should increase if heart rate increases.

However, in reality, the conditions are more complex. In exercise body temperature increases, which leads (via the thermoregulatory system) to vasodilation, so that the total peripheral resistance R decreases, which is able to reduce the blood pressure again.

Decreasing PV in exercise should occur on a very slow time-scale and only be relevant in long-time endurance training.

Concentrations of some hormones change in exercise. Levels of some stress hormones (catecholamines) rise and therefore increase cardiac output, but their action on peripheral resistance is heterogeneous. It goes up, if alpha receptors are stimulated, but decreases after stimulation of beta receptors. Similar to (and partly mediated by) beta adrenergic action classic thyroid hormones (e.g. T4, T3 and 3,5-T2) increase heart rate but decrease total peripheral resistance. It depends on the type of exercise if thyroid hormones rise or drop. They are increased in short-term or endurance exercise (representing type 2 allostasis) but decrease in exhausting exercise (leading to type 1 allostasis).

In summary, it depends on many factors, if blood pressure increases during exercise. In ergometry the blood pressure usually slightly rises.

References

1: GREENE BA. Cardiac output and total peripheral resistance in anesthesiology;
clinical applications. J Am Med Assoc. 1958 Mar 1;166(9):1003-10. PMID
13502096. https://www.ncbi.nlm.nih.gov/pubmed/13502096 https://doi.org/10.1001/jama.1958.02990090011003

2: Mayet J, Hughes A. Cardiac and vascular pathophysiology in hypertension.
Heart. 2003 Sep;89(9):1104-9. PMID 12923045. https://www.ncbi.nlm.nih.gov/pubmed/12923045/ https://doi.org/10.1136/heart.89.9.1104

3: Silva AS, Zanesco A. Physical exercise, β-adrenergic receptors, and vascular response. Jornal Vascular Brasileiro. 2010 9(2). https://doi.org/10.1590/S1677-54492010000200007

4: Chatzitomaris A, Hoermann R, Midgley JE, Hering S, Urban A, Dietrich B, Abood
A, Klein HH, Dietrich JW. Thyroid Allostasis-Adaptive Responses of Thyrotropic
Feedback Control to Conditions of Strain, Stress, and Developmental Programming.
Front Endocrinol (Lausanne). 2017 Jul 20;8:163. doi: 10.3389/fendo.2017.00163.. PMID 28775711. https://www.ncbi.nlm.nih.gov/pubmed/28775711 https://doi.org/10.3389/fendo.2017.00163


Is it possible to use two forward primer and one reverse primer?

Well, technically yes but no. Why yes is because on paper this looks simple enough but think about the technicalities. Your FP1 and FP2 will have different TMs, meaning the temp required to make the complete fragment with FP1 and RP1 will be different than to the MP of FP2. Effectively when the temp for FP2 reaches it might cause FP1 and RP1 to detach.Or the opposite might happen, where FP1 and RP1 are attached whereas FP2 might not.
Another problem I could think of is that as the PCR is cycling, the difference will lead to random length amplifications if at all you get any. The maximum amp product you might see will be of Frag-2.
If you want to fuse such fragments, I suggest going for OE-PCR (Overlap extention PCR).
This is a highly effective method to join two pieces of DNA using PCR. the concept is similar to what you have proposed.
Look at the wiki page- https://en.wikipedia.org/wiki/Overlap_extension_polymerase_chain_reaction

This image also explains the process...


Small non-coding RNA (sRNA) vs. micro RNA (miRNA)?

Small non-coding RNAs are NOT generally abbreviated as sRNA but as sncRNA, if anything. I say "if anything" because the "small" part is subjective and just a portmanteau descriptor. The straight answer to your question is as Forest has written: miRNAs are a specific type of small non-coding RNA, some of which appear to function in the regulation of gene expression — others remain to be characterized. Another problem with the 'small' epithet is that miRNAs may only be 20 nt in length, but are formed from pre-miRNAs of up to 1000 nt.

Other categories of small non-coding RNAs include:

tRNA (transfer RNA) - originally abbreviated sRNA (for soluble RNA) - involved in protein biosynthesis.

5S rRNA - a component of the ribosome

7SL RNA - a component of the signal recognition particle involved in recognizing the signal peptide of secreted and membrane proteins.

snoRNA (small nucleolar RNA) many of which act as guide RNAs in ribosomal RNA modification.

snRNA (small nuclear RNA) many of which are involved in the splicesome, the ribonucleoprotein complex which removes introns from precursor mRNA (these have names like U1, U6 etc.)

SINE RNA: RNA transcribed from the short interspersed nuclear repeats (SINEs - Alu sequences in humans) which are thought to be 7SL signal recognition particle pseudogenes.

And, no doubt, there are some I (and science) have missed.


How are micelles formed from the byproducts of emulsification in fat digestion?

Fat (triglyceride) enters the small intestine in the form of an emulsion of droplets which are stabilised by surfactants from the diet including proteins and phospholipids.

Bile salts (BS) bind to the surface of these droplets, displacing proteins. The BS-stabilised droplets are the substrate for pancreatic lipase which can adsorb to the BS-stabilised surface and convert the triglycerides to monoglycerides and free fatty acids.

The products of lipolysis then enter micelles that are formed by BS and phosphatidylcholine (PC: also in bile). The prevailing view is that these micelles take the form of discs of bilayer-like structure with BS situated both around the edges protecting the exposed acyl groups, and also embedded within the PC bilayer.

I think that the mechanism by which the products of lipolysis move from BS/PC micelles into enterocytes is not known. However, once they have entered they are re-esterified to form triglycerides which are packaged into chylomicrons (a class of lipoproteins) and exported into the lymphatic system.

Maldonado-Valderrama et al. (2011) The role of bile salts in digestion. Adv Colloid Interface Sci. 165:36-46 doi: 10.1016/j.cis.2010.12.002


Calculating Rate of Growth without a Population

The breeding lifespan of an individual is (maximum life span $L$ - age of sexual maturity $M$).
Call the time between pregnancies $\tau$ and the gestation period $g$. Then the average number of pregnancies per (female) individual is then $(L-M)/(\tau+g)$.
If the average number of individuals per pregnancy is $N$, then each reproducing individual produces $N(L-M)/(\tau+g)$ offspring in their lifetime.

If this species has males and females (gonochoric/dioecious), and a 50/50 sex ratio, then the number of females per female is $N(L-M)/(2(\tau+g))$.

This is a growth rate per generation: the generation time is approximately (mean time between birth of mother and birth of offspring) = $(M+(L-M)/2)$ (it's a little more complicated than this); the growth rate per unit time would be approximately equal to the ratio (growth rate per generation)/(generation time).

Other things you might need to take into account: survival of juveniles up to $M$; menopause (unusual).


Protocol for checking pipette calibrations using absorbance readings of a dye in solution?

I see what you are getting at however this would be a very WRONG way of calibrating such an instrument. If dyes varied among trials it would throw off your calibration. Also, you would need to generate some sort of standard curve to equate absorbance to weight, since true calibration of these instruments is done by weighing the volumes they dispense (1g = 1ml water). The weight of water and the weight of your dye solution will not increase the same in terms of moles/g. Also a scale is far easier to calibrate that the detector in any spectrophotometer. Calibrate pipettes by weighing the volume of water they dispense. It should be done in a chamber that inhibits evaporation and you need a precision scale.

Here's a reliable guide for pipette calibration

enter link description here


The reason that UV light causes sunburn, while normal light does not, is not founded in the energy carried by single photon. As stated on wikipedia:

  Importantly, both sunburn and the increase in melanin production are triggered by direct DNA damage. When the skin cells' DNA is overly damaged by UV radiation, type I cell-death is triggered and the skin is replaced

The UV light can cause reactions in the DNA of the skin cells that directly damages the DNA. A low amount of this damage can usually be repaired by the cells, but a lot of DNA damage will lead the cells to die and cause inflammation reactions in the skin (the sum of which is then what we experience as sunburn).
[Here is a citation also explaining this, the paper is behind a paywall though].

  What area of skin is necessary to absorb one single photon? How many photons of visibile light per cm2 are required in order to produce burns to the skin?

A single UV photon has no measurable size and can therefore in principle be absorbed by any arbitrarily small patch of skin. In practice only those photons that interact with the DNA in your skin cells are relevant for sunburn (that will be a very small fraction of all UV photons). Additionally the melanin in your skin will also absorb photons and therefore protect the DNA from the UV radiation, which is why people with darker skin get sunburn less easily. This also means that the amount of radiation/skin area required to cause sunburn varies from person to person and can be influenced by the ability of your skin cells to repair the induced DNA damage.


There are a lot of differences, you can check the companies that sell competent cells for guides on how to choose (NEB, Sigma Aldrich). But there are only a few things that matter for the really common uses of competent cells.

The most important part of selecting your cells is choosing cells suitable for protein expression or for plasmid preparation.

The cells meant for plasmid prep carry certain mutations like endA that inactivate nucleases that would otherwise degrade DNA. Typical choices here would be DH5$\alpha$ or XL1-Blue.

Cells meant for protein expression have some proteases mutated, and can often use different promotors like T7. A typical example are BL21 cells, and BL21(DE3) which can use the T7 promotor.


What is it called when a dead flower is rotted away and only the veins remain?

Retting could be a valid term. But I think that the term "skeletonization" is more common. For instance here is a link to the University of Arizona showing how you would take a flower or a leaf and remove all components, leaving the veins:
Skeletonization

I think that "retting" is confined to the industrial harvesting of plants like flax. I would use the term "skeletonization" to include acts of botanical science in which the veins alone were sought. For instance in the above link the botanist Frederick Ruysch published a method of chemical skeletonization in his book Adversariorum Anatomico - Medico - Chirurgicorum Decas Tertia in 1723.

It also became a form of art and craft in the late 1800's in the United States; "Skeleton Leaves & Phantom Flowers" was published by E.Parrish. I would assume that the end result as a craft would be to display the skeletonized flowers or leaves on a display board.

As a natural, observed event the term skeletonization could be used. But if the  underlying causes such as fungus were considered then both rot, or fungal rot, and skeletonization might be used together in the same sentence. The wikipedia entry skeletonization considers animal decomposition. It's a reasonable and analogous step to use the same term for plants that decompose and leave fibres rather than bones.


Why do human eyes glow red on a photo and dog's eyes green?

Short answer
In humans it is basically the red choroid plexus in the back of the eye you are seeing on a flashed photo, while it is the green-reflecting tapetum lucidum in dogs.

Background
The red-eye effect in humans was explained nicely by Yale Scientific Magazine, and I adapted the following text from that source:

The human eye can effectively adjust to different light conditions, but this adaptation is also what leads to the red-eye effect. The eye regulates the amount of entering light by contracting or expanding the pupil. At night, your pupils will accordingly enlarge to extract more light from their surroundings. However, this dilation also leaves your eyes unprepared for the sudden burst of light from a camera flash.

When light from the flash enters your eyes under these conditions, your pupils are unable to contract fast enough (full constriction takes a few seconds) to prevent the light from reflecting back, off of the red blood vessels of the choroid. The choroid plexus nourishes the retina, and therefore contains ample blood supply. As a result, the camera will pick up the red reflection, resulting in the red-eye effect. Interestingly, due to their increased “dark adaptation,” children more commonly have red eyes in photographs.

The amount of melanin, a light-absorbing pigment in the eye, also has a role in the red-eye effect. Individuals with lower levels of melanin will absorb less and thus reflect more light, explaining the high incidence of the red-eye effect in albinos.

Though the cause of this effect is wired in the biology of the eye, some cameras can reduce red-eye by sending a few preliminary flashes before the final flash to give the pupils enough time to contract and adapt to the increased-light conditions. Another way to reduce the effect is to avoid looking directly into the camera lens, which will reduce the reflection of light. Finally, if all else fails, modern image editing software, such as Photoshop, can remove the red discoloration.

With regard to why dogs and other animals may not have red-eyes but other colors, this was indeed answered in your linked question: some animal species have a tapetum lucidum, which is situated in front of the choroid and reflects light back onto the retina thereby increasing light sensitivity. In dogs it is green, as aptly shown in the linked question's answer. The following figure shows the anatomy and the position of the tapetum in front of the choroid. It was adapted from Pets.SE with the related question "Should I be concerned that my dog's right eye is reflecting green in the dark when his left eye doesn't?"

Hence, the reason why animals with a tapetum lucidum have another eye color is that light does not reach the choroid in these species, giving rise to green-eye effects in dogs and cats (picture taken from Ask Nature):


What determines the thickness of Cornea?

The corneal thickness is genetically programmed. There are multiple genes that induce the final corneal thickness:

USP37, Chromosome 2;
GPR15, 3;
TIPARP, 3;
CWC27-ADAMTS6, 5;
RXRACOL5A1, 9;
LCN12-PTGDS, 9;
FGF9-SGCG, 13;

and at least 6 other genes.

source

other questions had to be asked as separate ones


Why are recombination rates increasing in mammals?

If rates of meiotic recombination DIDN'T vary across species - THIS would require an explanation! After all, evolution creates diversity, not homogeneity.

I can only wonder that more recombination would allow for a faster diversification. The more DNA you shuffle, the more distinct each individual offspring may be (though I'm not 100% sure). The recombination rate has an energetic price, so not all animals recombine so much their DNA like later mammals. I.e. they needed a selective pressure to justify paying that price.

Perhaps it was useful for a group rapidly occupying the "vague niches" left by dinosaurs? This make sense, since the primary mammalian irradiation occured in the beginning of the Cenozoic era, right after the Cretaceous mass extinction that killed most big animals, including the biggest dinosaurs.

Unfortunately I have no references on the subject, it is just what makes sense to me, given evolutionary logic.


A paper was published about a week ago in Nature Biotechnology and adresses your question, Maruyama T et al., 2015. I must say I found the authors' strategy extremely clever.

It is not about increasing efficiency by reducing specificity, but simply increasing efficiency (which is your ultimate goal anyway). What the authors did was to inhibit nonhomologous end joining (NHEJ) to promote homology-directed repair (HDR), two DNA repair mechanisms that compete in cells and of course HDR is the mechanism needed for the CRISPR/Cas9 system.

They achieve NHEJ inhibition using the molecule Scr7, a DNA ligase IV inhibitor which in turns perturbes NHEJ.

Using Scr7 they boosted by 3 to 19 fold (depending on the cell line) the insertion of the target gene. Here the graph showing these results

See paper figures

Moreover using 1μM of Scr7 over 24h on DC2.4 cells increased the % of transfected cells from 4.58% to 58.3%, a neat ~13-fold increase. Here their results:

See paper figures

Hopefully this should give you some ideas.


What does it mean to perform in vitro experiments with mutant bacteria?

Answer clarified based on comment by @DurgaDatta

  What would it mean to say the enzyme activity was tested in vitro on the mutant? When we say the response of the a single gene knock out mutant, the cell should be intact except for lacing one gene, which would mean that the response is in vivo.

The knockouts were performed inside the E. coli cells and, as you noted, the flux measurements were in vivo (in the cell) inside of the chemostat culture. They identified two mutants, Crp and Cya, that yielded much higher biomass. On page 2326, the authors write,

  In the Cya (encoding adenylate cyclase) and Crp mutants that lack the cAMP-CRP complex, in vivo glyoxylate shunt activity was essentially abolished....

I am not familiar with these genes but the implication is that the wild type regulators have the cAMP-CRP complex. Because this complex is missing from the mutants, the enzymes no longer function the same. However, it would be possible that some type of interaction of the mutants with other enzymes caused the observed result in vivo. They therefore verified the result by extracting the Crp and Cya mutant enzymes from the cells and assaying their enzyme activity in isolation from the other enzymes (in vitro). The technique is explained in the answer by @dgg32.

In your comment to that answer, you ask.

  what difference does it make whether the enzyme was taken from wild-type or the mutant one, since it is the same enzyme?

It is the same enzyme in name but not in function. The mutant enzyme lacks the cAMP-CRP complex so it cannot perform the same function as the wild type. In vitro, they first showed that mutant enzyme activity was altered relative to the wild type.  They then added the wild type enzyme to the in vitro test and restored normal wild type activities:

  To verify that the observed changes were not due to polar effects of the still present marker gene or secondary-site mutations, we complemented the Crp mutant with the plasmid-based Crp gene and cultivated the complemented mutant under the same chemostat conditions. In vitro enzyme activities demonstrated that both the isocitrate lyase and isocitrate dehydrogenase activities were restored to the wild-type level

Yes, this was performed inside the chemostat cultures but only with the enzymes, not the living E. coli cells.


The term "function-triggering antibodies" is not standard, these are more widely known as cross-linking antibodies. As you may know, an antibody has multiple "arms", with the antigen binding region or Fab (Fragment antigen binding) at the end. IgG antibodies have 2 arms, IgM can have 10. The Fab portion is generally identical on all the arms, although it's possible to engineer them differently. This allows the antibody to bind to multiple antigens at the same time, drawing them close together.
NCAM is a homophilic binding protein, with an extracellular domain that binds to other NCAM molecules, both on neighboring cells and on the same cell. That binding induces structural changes in the intracellular domain which promotes the binding and activation of kinases, proteins that phosphorylate (and thus activate or inhibit) other proteins. This starts a signaling cascade that induces changes in the cell, typically by controlling the activity of transcription factors in the nucleus.
Receptors are generally not spread out evenly over the surface of the cell, they often exist grouped together in membrane structures known as lipid rafts. When drawn close enough together, NCAM molecules can begin their signaling cascades on their own, as adapter proteins bound or recruited to the intracellular domains get activated – the kinases and their substrates are in close proximity as well. To induce this type of signaling in the lab, cells can be treated with cross-linking antibodies that draw the receptors together. This in effect triggers the function of the receptors, beginning their downstream signaling.

Source


Are microRNAs transcribed from the same DNA strand as their parent messenger RNAs?

The following bear on the question of the relationship of the transcription of microRNAs to that of the pre-mRNAs of protein-coding genes:

Some microRNAs (termed ‘intergenic’) do not reside in a protein-coding gene (e.g. Drosophila mir-31a). Here the question does not arise.

Many (although not all) of those that do reside within a protein-coding gene are found exclusively in introns (termed ‘intronic’) — e.g. mir-11 and mir-998 in Drosophila gene E2f1.

For those microRNAs that reside in a parent gene, the direction of transcription is generally, although not exclusively, the same as that of the transcript (ca. 70%, according to this review).
The question arises whether the intronic microRNAs are generated from the spliced introns of transcripts of their parent genes. One of many papers which consider this is by Ramalingam et al. (2014). It appears that in some cases this may be so, but in other cases this appears to be ruled out by a disparity between the expression profiles of parent genes and microRNAs, and between different microRNAs encoded in the same intron.
The co-directionality or otherwise of transcription of ‘parent’ mRNA and microRNA has no implications for the interaction of microRNAs with their, often numerous, ‘target’ mRNAs. This is because (1) there is no genetic relationship between parent mRNA and target mRNAs — the parent mRNA, lacking the intron that gave rise to the microRNA, is not the target; (2) the hairpin loop of the microRNA precursor (imperfect though it may be) in effect represents both strands, from which may be generated either the 5ʹ portion, the 3ʹ portion, or both, depending on the microRNA. The miRBase site contains information on relative abundance of 5ʹ- or 3ʹ-fragments for individual microRNAs, and the microrna.org resource lists potential target mRNAs.


what are the factors that can be used to compute the probability of getting the coronavirus?

I'd refer you to a couple of papers in Lancet, here and here. They, in fact, have a mathematical treatment of this very question, and in the supplementary material they list some parameters that might be useful to you. Good luck!


This question is not easily answered as there are a multitude of factors involved in the production of proteins.  DNA - the molecule - does not "determine" when proteins will be produced.  The environment (truly environmental, extracellular, intracellular, etc.) of the organism governs this.  If you have not found enough material to satisfy your inquiries I recommend Jim Watson et. al. Molecular Biology of the Gene.  A classic.


All-trans-retinal being converted back to 11-cis-retinal or vitamin A

Short answer
A complex visual cycle in vertebrates involving vitamin A is useful for storage, re-distribution of retinoids to both rods and cones, to improve photosensitivity and reduce noise in the visual system.

Background
The visual cycle in mammalian rods is depicted in Fig. 1.

Fig. 1. Visual rod cycle. Source: Palczewski (2010)

11-cis-retinal isomerizes to all-trans retinal by absorption of a photon.  Your notion that this pathway can involve direct re-isomerization back to 11-cis-retinal is only true for invertebrates. They simply absorb another photon to back-isomerize all-trans to 11-cis (Saari, 2012).

In vertebrates, however, this bi-stable configuration is replaced by a complex visual cycle (or retinoid cycle, Fig. 1). The reason is that the bi-stable invertebrate system is less sensitive, as photons used for regeneration cannot be used to initiate phototransduction. Moreover, the invertebrate system is more prone to noise, as photons can both start the phototransduction or recycle all-trans retinal (Saari, 2012).

In vertebrates it is thought that the visual cycle only emerged after appearance of the cone system (Saari, 2012). Notably, the visual cycle depends on the retinal pigment epithelum (RPE), as shown if Fig.2.

Fig. 2. Rod and cone visual cycle. Source: Saari (2012)

Fig. 2 shows that vitamin A (all-trans-retinol) is present in the RPE. RPE cells are able to store vitamin A by converting it to fatty acids and store it in oil droplets. Moreover, RPE cells can funnel this stored vitamin A to both rods and cones, another reason why the complex visual cycle and vitamin A conversion makes sense (Palczewski, 2010)

References
- Palczewski Trends Pharmacol Sci (2010); 31(6): 284-95
- Saari, Annu Rev Nutr (2012); 32: 125–45


The exact answer to this greatly depends on the lysis buffer used, what you are lysing the cells for (DNA/RNA isolation, protein analysis, etc.) and how you intend to quantify your samples.
https://www.sigmaaldrich.com/content/dam/sigma-aldrich/docs/Roche/Bulletin/1/11814389001bul.pdf
This is a link to a standard red blood cell lysis buffer and handling recommendations. Note the following:

Lysis buffer must be stored at low temps prior to use
Use blood stored in EDTA, citrate or heparin anticoagulants
To obtain RNA use fresh blood only
For best results in DNA applications, use fresh blood or blood stored for less than 3 days.

Here is another paper describing the effects on DNA/RNA extracted from blood in ranging temperatures and storage methods
https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0184692


TL;DR

In a population, directional selection reduces genetic diversity.

Simple scenario

In a population, directional selection reduces genetic variance (at the loci that are under selection and other linked loci). Selection selects for variants that are associated with the highest fitness. Hence, selection reduces the number of variants (or at least the frequency of the variants that are associated with a lower fitness).

Note that, by reducing genetic variance, selection also reduces heritability (see this post for definition) for the selected trait.

Note that, for a correct terminology, you should not say that selection "selects for" low genetic diversity. Selection "selects for" variants associated with high fitness which causes a reduction in genetic diversity. Selection indeed does not "select for" any population-wide statistic but only for specific variants in the population which affect those population-wide statistics.

Selection vs evolution

You say

  Does evolution select against genetic diversity?

Please do not confound "evolution" with "selection". There are a number of "drivers" of evolution other than selection (e.g. genetic drift, mutation, migration). Both selection and drift reduce genetic diversity, however, mutation and incoming migration will typically increase it.

Balancing selection

Note also that there are types of selection that maintain genetic variance such as negative frequency-dependent selection, or heterozygous advantage for examples. Those types of selection that maintain genetic diversity are called balancing selection.

Multiple populations

Imagine a scenario where two populations are present in two different environments. If there is directional selection going into opposite direction in each environment (aka local selection), then selection will still reduce within-population genetic diversity but will increase the among-population genetic diversity.

Definitions of genetic diversity

Genetic diversity is a concept used in population and evolutionary genetics. The term genetic diversity is typically defined as the probability of non-identity by state of two alleles. In a single population, this is identical as the definition of expected heterozygosity. Let $p$ be the allele frequency in a population, the genetic diversity $\pi$ at this locus in this population is defined as $\pi = 2p(1-p)$.

More info about these definitions and their relationship to $F_{ST}$ (a widely used statistics of population divergence) in Nei (1973) and Charlesworth (1998).

Definitions of genetic variance

Genetic variance is typically a term used in quantitative genetics. One could say that genetic variance is defined by the phenotypic consequences of genetic diversity. See this post for the definition

For simplicity, above, I used the terms genetic diversity and genetic variance correctly but without highlighting that they take different definitions.

Intro to evolutionary genetics

Your question is a very introductory question in evolutionary genetics. You might be interested in some intro books (have a look at the post Books on population or evolutionary genetics).


Systematic difference of diversity between sister taxa?

Bond and Oppell address your question points one, two and three empirically by looking for what they call "unbalanced bifurcations" as a sign of adaptive radiations in a well-resolved phylogenetic tree (spiders), and find that the number of unbalanced bifurcations does indeed exceed what they would expect to occur by chance.

As you mention and as I suggested in the comment, there are some serious problems that arise in trying to answer your question. Many of these are well presented in Cracraft, including assuming that higher taxa are comparable with one another, making arbitrary choices about what rank of taxa to compare, ignoring counterexamples, and qualifying rather than quantifying diversity. I think that Bond and Oppell effectively address most of these problems through rigorous, apriori definitions.

There's a diversity of opinions and evidence from biological systems on your fourth question point. Bond and Oppell connect these significantly unbalanced bifurcations to key traits (like orb-weaving) that open up new adaptive zones. I suppose therefore they might say that there's a fundamental factor (a key trait, and therefore open adaptive zones) driving diversification, and therefore might not agree with you that diversification would necessarily beget more diversification (at least, not in the absence of open adaptive zones). For instance, in Hawaiian tetragnathid spiders, ecomorph niches on an island are filled either through immigration from another island or through adaptive diversification (Gillespie). No ecomorph is represented by two sympatric species, so a niche filled by immigration will presumably not spur adaptive radiation. However, species radiations in Andean lupines (Hughes and Eastwood) and plethodontid salamanders (Kozak et al) seem not to have been accompanied by any key traits or particular ecological opportunity, and could theoretically be driven by the self-reinforcing mechanism you propose. As a related point, I suppose more diverse lineages could be less likely to go extinct; which could support diverse lineages becoming more diverse.

 Bond JE, Opell BD. 1998. Testing adaptive radiation and key innovation hypotheses in spiders. Evolution 52: 403–415. (Behind paywall, free pdf here).
 Gillespie R. 2004. Community assembly through adaptive radiation in Hawaiian spiders. Science 303: 356–359. (Behind paywall, free pdf here)
Cracraft J. 1990. Origin of evolutionary novelties: pattern and process at different hierarchical levels. p. 21-44 in Evolutionary Innovations, ed. M. Nitecki, U Chicago Press.
Hughes C, Eastwood R. 2006. Island radiation on a continental scale: exceptional rates of plant diversification after uplift of the Andes.
 Kozak KH, Weisrock DW, Larson A. 2006. Rapid lineage accumulation in a non-adaptive radiation: phylogenetic analysis of diversification rates in eastern North American woodland salamanders (Plethodontidae: Plethodon). Proceedings of the Royal Society B: Biological Sciences 273: 539–546.


Effect of ethanol and detergent on cell membranes problem

Detergent and membranes
Moderate concentrations of non-ionic detergents facilitate lysis of cells. This can be exploited for extracting soluble proteins, often in their native form (ThermoFisher). Detergents affect the membrane at concentrations lower even than those that cause an increase in membrane solubility (Ahyayauch et al., 2010). Two ways this manifests is an alteration of the flip-flop effect (the lipid action caused by flipases) and leakage.
Note that the relationship between detergents and membranes aren't mechanistically well understood, and there aren't yet good general mechanistic rules that explain the relationship between concentration and permeability.
Your experiment

The absorbency rate was higher for the 20% and 40% detergent than it was for the 100%. It seemed as though the results were backwards.

It depends on your specific experiment, but typically the higher concentrations will more readily lyse the cell/make them more permeable. It's hard to say exactly what went wrong here without more information. Unless you were using an exotic detergent, it is quite likely that there was an experimental error and the test should be repeated. Alternatively, the results have been misinterpreted and indeed at lower concentrations, there was no cell lysis, and at 100% there are no cells left intact or something along those lines.


Biology Intuition and Origin of the "facts"

Googling "landmark experiments in biology" came up with a lot of hits, what was wrong with the experiments cited in any of those works?  Mendel's pea experiments should be easy enough to understand.

Honestly I don't see how it will benefit you to know the organic chemistry work that went into determining the chemical structure of adenine.


Is cell wall and cytoplasm an organelle?

Wikipedia gives quite clear and sourced answers in this case:

an organelle is a specialized subunit within a cell that has a specific function. Individual organelles are usually separately enclosed within their own lipid bilayers.
Under the more restricted definition of membrane-bound structures,
some parts of the cell do not qualify as organelles. Nevertheless, the
use of organelle to refer to non-membrane bound structures such as
ribosomes is common.[11] This has led some texts to delineate between
membrane-bound and non-membrane bound organelles.[12] The non-membrane
bound organelles, also called large biomolecular complexes, are large
assemblies of macromolecules that carry out particular and specialized
functions, but they lack membrane boundaries.

To answer our question, the cell wall can be considered an organelle as it is a subunit with a defined (set of related) function(s).
The cytoplasm in itself is difficult to consider as an organelle, but the cytoskeleton can be considered one.


I think the only place you are going wrong is in getting confused about strands ("take reverse complement").

5'-GGATCGTGCCACCATCCACCATCGTTA-3'   << coding strand
3'-CCTAGCACGGTGGTAGGTGGTAGCAAT-5'   << template strand

The coding strand has the same sequence as the transcribed RNA (apart from T>U), so the primary transcript is:

5'-GGAUCGUGCCACCAUCCACCAUCGUUA

Then, positions of introns:

5'-GG AUCGUGC CACCA UCCACCAU CGUUA

and after splicing:

5'-GGCACCACGUUA


I will go through your list of questions below:

I wanted to know how similar is our nervous system to [the circulatory system]?
They are very different, but as in every comparison of very complex systems, there is some overlap. The circulatory system carries fluids, the nervous system electrical signals so they are functionally not alike. However, both systems run throughout the body and have a more or less central control unit (the brain and heart respectively). So there is a structural similarity. I reckon they are as much alike as a city's sewer system and electricity grid.
I understand we have neurons (please correct me if I am wrong) all over the surface of body.
That is correct
Whenever we feel a touch (stimulus arises) a neuron fires a response, and that response travels through axons (myelin sheath).
Tactile stimulation may result in firing of one or more neurons, dependent on the intensity of the stimulus. Larger stimuli will, obviously, recruit more fibers. Stronger stimuli will evoke stronger responses (increased firing). Axons indeed conduct the neuronal responses, like an electrical wire conducts electrical current. Longer axons are often myelinated (insulated). Not all neurons related to touch are myelinated, however.
So my main question is that what exactly is a nerve?
A nerve is a bundle of axons that carry related functional information. Typically, nerves conduct information originating from locations closely located together in the body, and generally they convey this information to a localized spot in the body as well. For example, the optic nerve carries information from the photoreceptors (related information) from the retina (localized source) to the brainstem (localized target).
Is [a nerve] a long axon?
A nerve contains many axons. 'Long' or 'short' is rather subjective.
How many axons (same thing as neuron body?) are in a nerve? I am sure it depends on different nerves.
Neuronal cell bodies are typically located outside a nerve. Nerves contain varying numbers of fibers. For example, the auditory nerve harbors the axons of the spiral ganglion cells that transmit auditory information from the inner ear to the brain. It contains between 31k - 32k (myelinated) fibers in normal-hearing humans (Spoendlin & Schrott, 1989). In contrast, the optic nerve, which carries visual information from the retina to the brain, contains some 1.3 million (myelinated) fibers in young human adults (Jonas et al., 1992)

References
- Jonas et al., IOVS 1992;33:2012-8
- Spoendlin & Schrott, Hear Res 1989;43:25-38


ID for red millipede swarm near my place

Based on the body structure and double pair of legs per body segment, this is a millipede.

Based on the small size and spacing between body segments, it could possibly be in the Paradoxosomatidae family. You could check by examining the specimen more closely:

  Most species possess a groove or furrow ("sulcus") on the dorsal surface between the keels (paranota) on each segment.

National Geographic ran a story/video on swarming Paradoxosomatidae in Senegal in 2017:

  Some species swarm together during mating season or to hunt for food, and some studies have theorized juveniles swarm together for protection from predators.

Bellairs et al. (1983)1 studied a similar swarming species of millipede in India:

  The adults of Streptogonopus phipsoni (Pocock), an Indian polydesmoid millipede, emerge from the soil at the onset of the monsoon and mate. Eggs are laid in the soil and the adults die. The larvae leave the soil at stadium III and, apart from moulting periods, remain on the surface until the end of the monsoon. The larvae are aggregated in swarms, usually consisting of several hundred individuals. They are active on open ground, including metalled roads, during daylight, but usually spend the night in an inactive state under cover of stones or vegetation. If a swarm is disturbed, the individuals scatter but later reaggregate.

 Source: Bellairs et al. (1983)

I couldn't find any additional reputable (or really much of any) detail about S. phipsoni in English sources online. So I think I'll leave you with this information for you to explore in your native language more closely.

Though, Bellairs et al. cite Hoffman (1980) 2 and Attens (1937) 3 as their identification sources.
Also, Golovatch & Wesener (2016)4 provide a relatively up-to-date species checklist of the millipedes of India, so I'm certain that reference would be a good place to continue learning more.

 Citations:

1  Bellairs, V., Bellairs, R. and Goel, S., 1983. Studies on an Indian polydesmoid millipede Streptogonopus phipsoni Life cycle and swarming behaviour of the larvae. Journal of Zoology, 199(1):31-50.

2  Hoffman, R. L. (1980). Classification of the Diplopoda. Geneve:  Musee d’Histoire  Naturelle

3  Attems, C. (1937). Myriapoda 3. Polydesmoidea 1 Fam. Strongylosomidae. Tierreich 12:1-300.

4  Golovatch, S.I. and Wesener, T., 2016. A species checklist of the millipedes (Myriapoda, Diplopoda) of India. Zootaxa, 4129(1):1-75.


The antibiotic 'kanamycin' in the growing of culture E. coli

According to this data sheet, the genotype of the strain RosettaTM(DE3)pLysS is F- ompT hsdS (r- m-) gal dcm (DE3) pLysSRARE (CamR).

This strain carries certain tRNA genes on the same plasmid as the LysS gene, and these tRNAs boost expression from genes containing rare (in E. coli) codons. The plasmid encodes chloramphenicol resistance (CamR).

If you have a protocol that suggests growing your strain under kanamycin selection then presumably you have an additional plasmid present which carries your gene of interest. Then, as the accepted answer says, you are selecting positively for the correct strain.

I don't know how stable the pLysSRARE plasmid is, but I would have expected that you should also maintain selection for chloramphenicol resistance.


Most tumors are probably not strictly clonal; all cancer cells in a tumor seldom have the exact same set of mutations. Tumors tend to be subclonal, with all cancer cells having a single common ancestor but with later evolution resulting in some mutations shared among all cancer cells but others restricted to sub-populations of cancer cells. This fact and its implications for therapy were noted 40 years ago by Nowell (Science 194:23-28, 1976), and verified by much recent work as reviewed for example by McGranahan and Swanton (Cancer Cell 27:15-26, 2015).

A tumor might need to have a billion ($10^9$) or so cancer cells to be clinically detectable. Thus many years and many cell divisions have passed since the time that a single cell developed the set of mutations originally needed to produce the invasive tumor. With a probability of some uncorrected mutation at each cell division, particularly in cancer cells that often have defects in DNA replication and repair and in chromosome separation, it is essentially impossible for all of the billion cancer cells in the tumor to have identical sets of mutations. See, for example, the work of Bozic et al (eLife 2: e000747,2013). So although there is a clonal origin of the tumor, the tumor is typically a collection of related but genetically distinct populations best considered to be subclones.

Differences among subclones present a major barrier to traditional cytotoxic therapies, to more modern targeted therapies, and to the immunotherapies that presently receive so much attention. Even if most of the tumor is sensitive and responds, a subclone whose mutations somehow provide resistance to the therapy will be able to repopulate the tumor thereafter. Bozic and Nowak (PNAS 111:15964-8, 2014) estimated that a clinically detectable tumor may have 10 or more subclones resistant to any targeted therapy, due to mutations accumulated during the subclinical growth of the tumor.

As examples from immunotherapy for cancer, McGranahan et al recently showed (Science 351:1463-1469, 2016) that responses to immune checkpoint inhibition in melanoma and non-small cell lung cancer were best in patients with clonal rather than subclonal tumor neoantigens for the immune system to attack. Zaretzky et al (New Engl J Med 2016, epub ahead of print) identified subclonal mutations in interferon-receptor signaling and antigen presentation in some patients, mutations enriched in the recurrent tumors following immune checkpoint inhibition and thus likely accounting for relapse following that therapy.

It is possible in principle for a single physical tumor to have multiple cells of origin. Tumors often develop from a region of tissue that has been subject to field cancerization, where carcinogenic challenges have produced many cells with mutations that lead to dysregulated but not invasive behavior. This can lead to multiple independent cancers arising from the same general location, as individual cells later develop the full complement of mutations needed for an invasive tumor. In principle, such multiple cancers might coalesce into a single tumor mass so that the tumor is polyclonal, but I'm not aware of any well documented cases. So it seems that tumors are seldom truly polyclonal with multiple independent cells of origin.


Question about the DNA glycosylase enzyme assay/formamide gel loading buffer

Escherichia coli endonuclease III (which I will now refer to as Nth), and the human homolog hNTH1, has both glycosylase and AP lyase activity. The section of the article you're referring is describing an assay of lyase activity. The assay tested both Nth and hNTH1 as well as HAP1, a human AP hydrolase that cleaves 5' to the AP site. Nth and hNTH1 were found by this assay to cleave 3' to the AP site. HAP1 is dependent on $Mg^{2+}$ for catalytic activity. hNTH1 (and likely Nth, given the high conservation) are dependent on $Mg^{2+}$ for substrate specificity (Eide et al., 2001). hNTH1 and Nth contain an $Fe-S$ cluster that is involved in DNA binding (Thayer et al., 1995).
Originally I thought that the reaction is stopped with EDTA. EDTA is a chelating agent; it binds and sequesters metal ions and prevents their use by enzymes. EDTA would prevent catalysis by HAP1 and DNA binding by Nth/hTNH1.
However, Chris pointed out that the loading buffer contains 1 mM EDTA while the reaction buffer contains 5 mM $MgCl_2$. While the paper doesn't give the volumes of reaction and loading buffer mixed together, it is perhaps unlikely that EDTA chelation of $Mg^{2+}$ is the sole mechanism for stopping the reaction. The high concentration of formamide (80%) in the loading buffer could then be responsible. Formamide is commonly used to denature nucleic acids and, at high concentrations, would likely have an effect on enzyme function.
References

Eide L, Luna L, Gustad EC, Henderson PT, Essigmann JM, Demple B, Seeberg E. 2001. Human Endonuclease III Acts Preferentially on DNA Damage Opposite Guanine Residues in DNA. Biochemistry-US. 40(22):6653–6659
Thayer MM, Ahern H, Xing D, Cunningham RP, Tainer JA. 1995. Novel DNA binding motifs in the DNA repair enzyme endonuclease III crystal structure. EMBO J. 14(16):4108–4120.


The best free and most up to date phylogenetic tree on the internet?

Available ressources

I would recommend oneZoom.org is probably the best ressource. oneZoom.org is based on openTreeOfLife.org (for phylogenetic relationships) and eol.org (Encyclopedia Of Life) (mainly for the pictures I think). If you do not fancy to much the display and links of oneZoom/org, then I would just recommend openTreeOfLife.org.

There is also tolweb.org but it is not as nicely updated as openTreeOfLife.org (and therefore openTreeOfLife.org) and the dates are harder to find.

Particularities of oneZoom.org

I particularly like that for each node oneZoom.org offers links to

wikipedia
encyclopedia of life
the red list
NCBI

, which makes it a very appreciable tool. oneZoom.org has the advantage of a nice display (although a bit slow to load IMO) and is easy to navigate and get time to the Most Recent Common Ancestor of a lineage.

I also like that you can just add the species name after "#" in the URL and it will jump to its node. Here is the Kagu for example.

Potential issues in oneZoom.org

Of course, oneZoom.org contain a few mistakes! Some of them are unintentional (wrong picture, misrepresentation of what is known from the literature, fail to update information), some of them are caused by lack of knowledge of true phylogenetic relationships. oneZoom.org does not say how certain we are that a given speciation event is correct or correctly dated, it just display the best estimates we have. If a specific node is of interest to you, you will need to go to the scientific literature which will give you much more information about what we know and what we roughly guess.


DNA Topology of two circular chromosomes

Yes, there is an abundance of evidence. I think the following electron micrograph is pretty convincing.

This image is from a review:

Gil-Ramirez G, Leigh DA, Stephens AJ. 2015. Catenanes: Fifty Years of Molecular Links. Angew Chem Int Ed 54:6110-6150.

It was adapted from the first paper to observe naturally occurring catenated DNA molecules, which were isolated from HeLa mitochondria:

Hudson B, Vinograd J. 1967. Catenated Circular DNA Molecules in HeLa Cell Mitochondria. Nature 216:647-652.

You can see this answer for an explanation of why catenanes form during replication:

How do catenanes form when DNA replicates?


Soap molecules are amphiphilic. This means they have parts which are hydrophilic (water-loving, or "polar") and parts which are hydrophobic (water-avoiding, or "non-polar").
Fat molecules are non-polar. They avoid water. This is why a mixture of oil and water will separate into layers. In this mix, oil molecules prefer to hang around other oil molecules, and water molecules prefer to hang around other water molecules. Soap "likes" both oil and water, so it can be used for cleaning, by helping dissolve this mixture. (For a similar reason, this is why vinegar is used to dissolve or emulsify oil in salad dressings.)
The coat of an enveloped virus is made up of layer of phospholipid molecules and proteins. Phospholipid molecules are similar to detergents, made up of polar and non-polar ends. These lipids arrange themselves into a two-layered sandwich called a "bilayer". The polar ends of this sandwich are the "bread", while the fatty non-polar ends are the "filling".
Detergents can help disturb this by pulling or dissolving out phospholipids from the virus coat to form micelles, tiny bubbles of fat and soap that can be washed away. This puts holes in the virus coat and helps dissolve it.
The insides of the enveloped virus particle cannot infect directly and must rely on its envelope to get into and infect a cell, so breaking down the coat inactivates (or "kills") the virus.
Alcohols are also amphiphilic. There are many different alcohols, but they all have a hydroxy group at one end, which is polar, and a saturated or partially-saturated carbon chain on the other end, which is non-polar. Like detergents, this property allows an alcohol — at a sufficient concentration — to disturb and break down the virus envelope phospholipid bilayer, inactivating it.
Non-enveloped viruses lack this phospholipid bilayer coating and are instead protected by a protein capsid. The proteins in a capsid will not dissolve with detergents, but they can be attacked with other disinfectants that chemically denature the proteins. Examples of such disinfectants are chlorine (bleach), iodine, peroxides, etc.
Just as soap can put holes into the phospholipid coating around enveloped viruses, destabilizing them, denaturing agents change the structure of proteins that protect non-enveloped viruses, also destabilizing the capsid. If the capsid proteins are damaged sufficiently, the virus particle is not able to infect a cell and so is deactivated.


Structures of cyclodextrin complexed with small ligands

I looked for relevant publications at Web of Science using 'structur* AND cyclodextrin' in the Title field. For the period 2011-2012 there were 56 hits including:

  Racz et al (2012) Structure of the inclusion complex of beta-cyclodextrin with lipoic acid from laboratory powder diffraction data. Acta Crystallographica Section B 68: 164-170

  Ali et al (2012) Structure determination of fexofenadine-a-cyclodextrin complex by quantitative 2D ROESY analysis and molecular mechanics studies. Magnetic Resonance in Chemistry 50:299-304

  Lula et al (2012) Interaction between bradykinin potentiating nonapeptide (BPP9a) and beta-cyclodextrin: A structural and thermodynamic study. Materials Science & Engineering C 32: 244-253

I looked at some of the papers but I didn't find any specific case where a structure has been deposited in a database. There were, however, several mentions of the Cambridge Crystallographic Data Centre  as a source of small molecule structures.


Why is living muscle tissue seemingly able to restore its shape under force, while dead tissue is not?

Capillary refill time is defined as the time taken for the capillaries to refill after the blood in them has been squeezed out by pressure. It is widely used as a quick way to determine the effectiveness of the circulatory system in humans by doctors.

In a normal living organism, the capillaries will take time to refill after they have been emptied. Muscle volume consists of the cell volume (which is fixed in the absence of lysis), the blood, as well as lymph and other intracellular fluids (which will be displaced elsewhere when it is deformed by pressure).

When the organism is dead, there is no more circulation in both the blood and lymphatic systems, and therefore any fluids squeezed out by pressure will remain elsewhere, and the deformation is permanent without any regulatory effect by the circulatory system.


It resembles Cepaea nemoralis, or commonly called Grove Snail, belonging to the family Helicidae.

Image Source: WikiMedia Commons

According to Wikipedia, these snails were introduced to North America from Europe. These fascinating creatures occur in diverse forms of shell color as well, as shown below.

Image Source: Metodologie di Programmazione

Here I have found a very detailed shell and body markers for Cepaea nemoralis.

Image Source: ResearchGate


How can facultative anaerobes exist without catalase?

There is another class of peroxide decomposing enzymes called peroxidases. These enzymes can catalyze the reduction of $\ce{H2O2}$ to water using an electron donor. However, unlike in the catalase reaction, the electron donor is not another $\ce{H2O2}$ molecule and no molecular oxygen is produced. Thus their presence would not be detected by the typical spot catalase test (which looks for gaseous oxygen generation). For example, NADH peroxidase catalyzes the following reaction to protect cells from oxidative damage:

$$\ce{NADH + H+ + H2O2 -> NAD+ + 2H2O}$$

Thus catalase negative organisms can still have a means of protection against $\ce{H2O2}$. You can read more in this textbook, specifically the section titled "Oxygen Toxicity".


Both cells from unicellular organisms (for example, E. coli) and multicellular ones (humans, for example) divide by mitosis - you are correct. The daughter cells are not just very genetically similar, they are identical (if everything goes right, which it usually does). Both of these instances are called "cell division". It's also called "reproduction" in unicellular organisms because the entire organism just reproduced, in an asexual manner - it went from one to two copies of itself. On the other hand, many multicellular organisms (and some unicellular) can or must reproduce sexually. This involves (generally) at least one partner and a cellular process known as meiosis, which produces haploid gametes, which then meet somehow, one gets fertilized by the other, and the resulting diploid cell begins mitosis again.


Don't know whether it was ever investigated, but I'm pretty sure, that frogs can in principle swim upside down (e.g. when escaping from predator), but they normally do not do it.
One example of alternative swimming styles in animals is provided by some munnopsidid isopod crustaceans. Several genera are pelagic and have very elongated forelegs equipped with rows of setae and paddle-like hindlegs (see Marshall & Diebel 1995 and Giver 1998):

the forelegs are used to "walk" in the water column
the same legs can be stretched out for passive parachuting
the hindlegs are used for backward swimming

Below is a photo of a parachuting specimen. And here is a very nice video of a backward swimming specimen.

Foto by Karen Osborn from here


likely they are trying to sun themselves especially in cold weather. The water is cold and they immediately try to get back on the boat.  becasue they are not as afraid of you as other snakes they are harder to discourage. They also probably can't tell the difference between your boat/dock and a log.

as for following you I can see three possible answers.
D's answer about eddies might be it.

Or they may be doing the same thing birds do with tractors, your kayak and paddles stir up the water and they are after the animals your movement scares up. A lot of small predators have learned following human machines can be a good way to find an easy meal.

Or they might hope you are a crocodile that will scare up small animals or leave scraps they can eat. Answering Hans will help understand what is happening.


What is the difference between nucleotide polymorphism (θ) and nucleotide diversity (π)?

You are also confusing definition of these terms with their expected values (typically computed from coalescent theory). Let's look at an example.

Consider a haploid population of 6 individuals. We will represent these individuals with 5 sites that can take values 0 or 1.

00000
00001
00000
00010
00010
00000

Polymorphism

In this population there are $S=2$ polymorphic sites. In other words, there are two sites for which different individuals take different values in the population. Over these 5 sites, the fraction of polymorphic sites is $\frac{2}{5}$. You use $\theta$ for this quantity but to me, $\theta$ is typically used as a short hand for $2 N \mu$ (or $4 N \mu$ for diploid populations).

Under an infinite allele model, in a single panmictic haploid population (without selection and other assumptions), $E[S] = 2 N \mu a$, where $a = \sum_{i=1}^{k-1} \frac{1}{i}$, where $k$ is the sample size.

Genetic diversity

Genetic diversity is also known as expected heterozygosity. While it is most often called $\pi$, I will call it $H$ to avoid confusion. Imagine, you randomly sample two individuals in the population, what is the probability that there have different alleles at a given locus?

At locus 1, $H = 0$
At locus 2, $H = 0$
At locus 3, $H = 0$
At locus 4, $H = 2 \frac{2}{5} \frac{3}{5} = \frac{12}{25}$
At locus 5, $H = 2 \frac{1}{5} \frac{4}{5} = \frac{8}{25}$

You can average over all loci if you want.

The expected heterozygosity in panmictic population (without selection and other assumptions), $E[H] = \frac{4 N \mu}{1 + 4 N \mu}$. You should notice a relationship between $H$ and $F_{ST}$ here!

Nucleotide diversity

The nucleotide diversity is the equivalent of $D$ from Nei and Li (1979) and is highly related to $D_{XY}$ (Nei, 1987). Once you've managed to demonstrate that the expected coalesence time is $N$ (I won't do the demonstration here), then under an infinite site model, the number of mismatch between two individuals is logically $E[D] = 2 N \mu$ (it is the number of mutations that has happened in both lineages since the the coalescence event). For diploid population, multiply everything by 2.

Relatedness between $D$ and $S$

Under a neutral model $\frac{S}{a} = D$. Actually the standardize difference between $\frac{S}{a}$ and $D$ is what is used in Tajima's $D$ tests.

Source of information

Hartl and Clarck is good IMO but I would also like to recommend reading Population Genetics: A Concise Guide by Gillespie who explain all of that wonderfully.