How to download different kinds of data from NCBI eutils?

Downloading all this using an E-utils search would be cumbersome as you would have to search against multiple databases. For your specific needs, a GTF/GFF3 file would be good. Basically, a GTF/GFF file has genome annotations (positions of features) and includes features like exons, CDS and in some cases even special codons (such as that for selenocysteine). This file would not have the sequences but you can retrieve the sequences from the corresponding genome sequence fasta file using the co-ordinates described in the GTF file. There are several software tools that can do this; for example gffread and bedtools-getfasta (you can even write your own script which would not be very difficult).

You can download the GTF and the corresponding genome fasta files from these sources:

ENSEMBL (many organisms)
NCBI-RefSeq (many organisms)
UCSC genome browser (many organisms)
GENCODE (for human and mouse) and modENCODE (for Caenorhabditis worms and Drosophila)

You should look at the details of the genome assembly. Different releases/sources may have different extents of curation.


First, degeneracy in a basic sense refers to redundancy of the codons in the genetic code.  For example, the amino acid proline is coded for by one of four codons: CCA, CCC, CCG and CCU. The third codon position (the third letter in each group of three) is called four-fold degenerate because it can change without affecting the coding for proline. Phenylalanine is two-fold degenerate because it is coded for by UUC and UUU.

However, this does not account for the alignment part of your question. Without more specific information (such as a reference you saw), I can't be certain of your intent but this paper by Morin et al. (2008) may be helpful. They had a series of small RNA sequences (each about 24 nucleotides long). They wanted to identify DNA sequences in the genome of Lodgepole pine  (Pinus contorta) and rice (Oryiza sativa). To accomplish this goal, they used degeneracy alignment. Here's the relevant section from their methods:

  altered to allow searches against genomic sequence. Alignments were kept if they were no shorter than L − 3, where L is the query sequence length. No more than a total of three mismatches or insertions/deletions were allowed within the aligned region.

Their approach was to find genomic sequences that correspond to the small RNAs. They allowed for some degeneracy, either in the genome or the RNA. The sequences could differ in length by no than three nucleotides or mismatches (an A in the query sequence but a C in the target sequence instead of a T; I'm assuming the query is RNA and the target is the genomic DNA). Their degeneracy alignment allowed for a small amount of freedom in identifying potential matches of conserved RNA clusters (high similarity) in the genomes of distantly related plant species.

  Morin, R.D. et al. 2008. Comparative analysis of the small RNA transcriptomes of Pinus contorta and Oryza sativa. Genome Research 18: 571-584.


Why are mammals unable to produce Essential Fatty Acids?

Well, the essential fatty acids that humans fail to produce are not the same ones that other species fail to produce. For example, while cats produce their own Vitamin C and will therefore never develop scurvy, they can't produce their own taurine and will become sick if they don't consume enough of it.

To answer why a species might lose the ability to produce an essential amino acid, you have to consider what that species is eating most of the time. If its diet is rich in the amino acid anyway, individuals who lose the ability to synthesize it either feel no cost or--possibly more likely--even benefit by not wasting resources synthesizing compounds that may be abundant already in the diet and must be excreted if unused.

Turns out that this loss of ability to synthesize your own fatty acids is a particularly common consequence of evolving parasitic lifestyles, which makes sense: if you're just stealing someone else's acids, why bother to produce your own? Even outside of parasites, there's some interesting discussion on why the nine amino acids essential to all animals might have evolved from a genomics paper here, discussing which amino acids you really do have to make on your own and which you can get away with consuming depending on your species' lifestyle and dietary habits.


Is it possible to exclude article types in a PubMed search?

I believe this will work:
((Acute Kidney Injury[MeSH Terms]) AND (Sodium Chloride[MeSH Terms])) NOT (Review[Publication Type])
Using the advanced search settings on PubMed it was easy enough to set up, here is the link in case you don't have it already:
https://pubmed.ncbi.nlm.nih.gov/advanced/


Is there a difference between polarity and hydrophobicity?

Hydrophobicity means aversion to water which results because of increase in entropy of the system due to the water-"solute" interaction.

As already pointed out in by inf3rno, polarity of a molecule is because of its net dipole moment. It is true that polar molecules can dissolve in water (because they can interact with water via van der Waals' forces especially Keesom and Debye forces).

CO2 is apolar but dissolves in water (it actually reacts with water). Most apolar substances cannot interact with water via van der Waals forces.

To sum up, usually polar substances are not-hydrophobic (i.e they are hydrophilic), however some polar molecules such as nitriles, ketones and esters can be hydro-neutral (midway between hydrophobic and hydrophilic. See here). Even large polar molecules are insoluble in water such as 1,2 dichlorobenzene and nitrobenzenes (For something to be soluble the solute-solvent interactions should be stronger than solute-solute interactions. "Water insoluble" may not be equivalent to "hydrophobic").

Conversely, apolar substances are hydrophobic (unless they are reactive solutes such as Cl2 and CO2).


Books on population or evolutionary genetics?

TL;DR
I'd recommend Population Genetics: A Concise Guide (Gillespie) for an introduction to population/evolutionary genetics (thanks AGS for highlighting this big miss of mine on the first version of my answer).
I'd recommend A Biologist's guide to mathematical modelling in evolution and ecology (Otto and Day) if you want to ensure your knowledge in mathematics by learning their application to evolutionary biology.
General Entry Books to Population Genetics
There are several books that offer an introduction to population genetics. I read Principles of Population Genetics (Hartl & Clarke). I appreciated it but if I were you I think I would rather try Elements of population genetics (Charlesworth) or Population Genetics (Hamilton). There is also Genetics of Populations (Hedrick). I would tend to think that this last book presents lots of empirical population genetics data and doesn't take as much focus as the others in theoretical concepts (but I might be wrong). Gillespie's book Population Genetics: A Concise Guide is a classic. It is short, very easy to follow and pleasant to read. Gillespie's book might eventually be a little bit outdated but I would still highly recommend it.
Emphasis on Analytical Modelling
A Biologist's guide to mathematical modelling in evolution and ecology (Otto and Day) is a very good and very accessible book. It makes a good review about all subjects that are usually taught to first year students in Biology such as linear algebra for example. It is highly accessible and in the meantime it goes pretty far as it ends up talking about the application of diffusion equation in population genetics (Kimura's work among others). This book presents some important models in population genetics but as it aims to provide the tools for mathematical modelling in ecology and evolution it may under-considerate some fields of ecology and evolutionary biology. For example, the book does not talk about population structure nor about evolutionary game theory and there is little about Coalescent theory.
Other books treating specific subjects within population genetics
Coalescent Theory: an Introduction (John Wakeley) is a good book. I haven't read it completely for both time issues and because the math are a bit complicated for me. Coalescent theory offers a very important set of mathematical tools in evolutionary biology.
There's also Mathematical population genetics (Ewens). I am currently reading it. It is definitely not an introductory book and it really doesn't cover much of the most common fields in population genetics.
If you are particularly interested in age-structured population, Evolution in age-structured populations (Charlesworth) is a very good book.
Modeling evolution (Roff) offers some discussion on how to mathematically define fitness from phenotypic traits. While it is interesting I would not counsel you to buy it. Moreover, all the mathematics are quite basic and it aims to explain how to perform mathematical modelling with R which is to my opinion not essential to learn as other languages make a better job at dealing with math (Mathematica for example).
Evolutionary Conservation Biology (Ferrière, Couvet and Dieckmann) is a very good book of conservation and conservation genetics. It develop some mathematical models that are of special interest to conservation of populations and communities.
Ecology, Genetics and Evolution in Metapopulations (Hanski and Gaggiotti) is a book that may interest you as well. However it focuses much more on ecology than the other ones I cited above. Note: I haven't read it entirely.
If you are interested in kin selection and level of selection, you might want to have a look at Major Transitions In Evolution (Maynard Smith and Szathmary) which is a classic (I have not read it though) or The Major Transitions in Evolution Revisited (Calcott and Sterelny) who encompass the opinion of many authors on the subject. Evolutionary Dynamics: Exploring the Equations of Life (Nowak) is also of interest esp. for those interested in epidemiology. Finally, you might want to have a look at the extremely well written and easy to read books by Dawkins such as The extended phenotype (Dawkins) for example. The Dawkins book are very popular and very very introductory. It offers more a way to think than the actual science behind evolutionary biology.


Species Identification: Snake, New Mexico

It's difficult because the image quality is low, but there are some key features that can be made out which suggest it to be a Western Coachwhip, or "Whip snake", Masticophis flagellum testaceus.

There is not a huge number of species in New Mexico, and most have quite clearly different patterns and coloration, which brings it down to just a couple of species. With respect to colour and pattern, the main candidates are Western Coachwhip, New-Mexico Ridge-Nosed Rattlesnake, Mojave Rattlesnake, and Prairie Rattlesnake.

We can rule out the rattlesnakes because of the shape of the pupil; like most poisonous snakes, the rattlesnakes all have a "cats-eye" pupil, while in the second picture of yours it's fairly clearly a round pupil, which is a feature of the Western Coachwhip.

The slender head is a very telling feature that suggests Coachwhip.

The length is also about right (I'm going to suggest though that the one in your photo is perhaps more than 2 feet/60 cm - it looks bigger to me using the surroundings as relative measures); Coachwhips are in the region of 1-2 metres (3-6 feet) when fully grown.

The range is also perfect for the Western Coachwhip, though Sonoran Coachwhips are also found in southern areas of New Mexico. However, you list this as central New Mexico, so that virtually rules them out.

It seems, given that your picture is in the daytime, that it is diurnal (unlike many species in New Mexico which are nocturnal).


Once again, this is a  longhorn beetle (Cerambycidae).

The overall appearance fits well with the subfamily Lamiinae (flat-faced longhorns). I would also guess it's in the Batocerini tribe. Though I don't think this is your species, per se, here is an image of a female Batocera rufomaculata with white stripe for comparison:

Once you provide more information about location I can give you a more precise answer.

Monochamus scutellatus is almost certainly incorrect. Notice the lighter coloration , wider body shape, and presence of a lateral white stripe along the side of the OP's insect vs that of M. scutellatus.


Formaldehyde turns plantar region of feet red?

It might be due to livor mortis, also called postmortem lividity, which is the settling of the blood in the lower parts of the body which in your case might have been the limbs. By time the color can be interpreted as either blue or purple, but given, that not much time has passed it can very well be the reddish color you might have asked, as stated here on page 39:

  The first manifestation of livor mortis can be expected 20-30 min following the irreversible cardiovascular arrest, initially as bright-red spots that subsequently become confluent and turn bluish-violet.

Which might better describe your case is the fact, that cold conditions can cause bright red color in livor mortis, as it can also be found on page 39:

  Cold conditions, such as keeping a body in cold storage, cause ... bright-red livor mortis.

You can read more about it here or here.

EDIT

I have added references thanks to @Kendall, who provided them.


Can intron become exon in alternative splicing?

Most of the transcripts you show have different transcription start sites. In other words, this happens because of alternative transcription start sites. So this is not typical alternative slicing. Some genes have different transcriptional start sites, but the case you show has exceptionally many start sites.


How to get taxonomic specific ids for kingdom, phylum, class, order, family, genus and species from taxid?

I'll copy/paste my answer from StackOverflow here also.

The following code:

import csv
from ete3 import NCBITaxa

ncbi = NCBITaxa()

def get_desired_ranks(taxid, desired_ranks):
    lineage = ncbi.get_lineage(taxid)
    lineage2ranks = ncbi.get_rank(lineage)
    ranks2lineage = dict((rank, taxid) for (taxid, rank) in lineage2ranks.items())
    return {'{}_id'.format(rank): ranks2lineage.get(rank, '<not present>') for rank in desired_ranks}

def main(taxids, desired_ranks, path):
    with open(path, 'w') as csvfile:
        fieldnames = ['{}_id'.format(rank) for rank in desired_ranks]
        writer = csv.DictWriter(csvfile, delimiter='\t', fieldnames=fieldnames)
        writer.writeheader()
        for taxid in taxids:
            writer.writerow(get_desired_ranks(taxid, desired_ranks))

if __name__ == '__main__':
    taxids = [1204725, 2162,  1300163, 420247]
    desired_ranks = ['kingdom', 'phylum', 'class', 'order', 'family', 'genus', 'species']
    path = 'taxids.csv'
    main(taxids, desired_ranks, path)

Produces a file that looks like this:

kingdom_id  phylum_id   class_id    order_id    family_id   genus_id    species_id
<not present>   28890   183925  2158    2159    2160    2162
<not present>   28890   183925  2158    2159    2160    2162
<not present>   28890   183925  2158    2159    2160    2162
<not present>   28890   183925  2158    2159    2172    2173


There can be many reasons about why too much candy (chocolate) can cause nausea. Lets talk about them one by one.

Hyperglycemia - chocolate contains sugar, and too much sugar consumption can cause high blood sugar levels i.e. hyperglycemia. When blood sugar levels remain high for some time, it can cause nausea and vomiting, among many other symptoms including dizziness, itchy skin, dry mouth, thirst, etc. If left untreated, it can lead to diabetic ketoacidosis or diabetic coma. See this article for more information.
Artificial Sweeteners - often chocolates contain artificial sweeteners instead of table sugar or glucose to prevent risk of hyperglycemia without compromising with taste. But many times, these artificial sweeteners can cause side-effects too. For example, there have been reports that sucralose causes nausea and vomiting in some people. Other alernatives, like mannitol, sorbitol, xylitol, maltitol, isomalt, etc. can also cause nausea and similar symptoms.
Dumping Syndrome - sweet foods, like chocolate, are hyperosmolar i.e. have high osmolarity. When these are ingested in large amounts, they cause the small intestine to expand quickly, due to which the ingested food passes too quickly through the stomach, largely in undigested form. This condition is called Rapid Gastric Emptying (RGE) or Dumping Syndrome. The initial symptoms of dumping syndrome include nausea, dizziness, diarrhea, fatigue, etc. See the Wikipedia page for more information.
Fats - chocolate contains cocoa butter, and cocoa butter is a source of saturated fats. Ingestion of large amounts of fats can lead to indigestion, and indigestion can become a cause of nausea and vomiting. This also explains why greasy foods can cause nausea; because they have high fat content.

Some other factors could include candy allergy, pregnancy, etc. or something I failed to mention. But I hope this much would help too.


How do plants prevent infection from retroviruses?

Virus are extremely host-dependent because they need to enter the host, move inside of it, use its replication mechanisms and codon usage. There are virus that cross the family boundry (ToMV for example) but crossing the kingdom boundry is less probable.  For example, animal cells don't have a cell wall, which is a major change and requires a change in strategy for entrance to plant cells.
For retrovirus, they simply are virus that can integrate into the host genome.  Several articles [1, 2, 3] describe retroelements that have been classified as retrovirus, retrovirus-like particles, and retroelements encoding coat proteins. This can lead to the conclusion that there are retrovirus in plants.
It is worth noticing that virus are not the major pathogens of plants (fungi are) and resistance to virus can be acquired even without understanding the mechanism.   This leads to a lower level of interest, funds, and researchers in the area, which leads to a lower rate of discovery of new virus.
In conclusion, we have not found a virus that crosses the kingdom barrier but have families of virus that contain both plant and animal virus.


Why do some trees have a life span, while some don't?

The answer to this could be that there are many factors contributing to the length of the life of tree species.

Climate: You can see that trees that have a reputation of becoming really old live in environments that have low moisture levels and much sunlight over the course of the year.

For example, you can see that the most long-lived trees in America are located in California, where the temperatures are relatively high, while moisture levels are low. If you have one without the other trees don't tend to live that long. Cold climates make growth
harder for each individual, yet hot and moist climates tend to help trees grow easier, but also die easier. Think of the amazon. It is one of the richest forests in the world, yet the growth of bacteria and high competition in the areas of the equator make life a lot harder for the longest living and slowest growing species.

As you can see, the vast majority of the longest-living trees are located in California, or other regions of the same latitude!
http://en.wikipedia.org/wiki/List_of_oldest_trees

Other species and the life around it/Its Ecosystem: Individual trees tend to be less likely to be destroyed by a fire, as they are less likely to catch fire. At some instances, forest trees or dried-out grass can catch fire and pass it on to other individuals.
Microbes and bugs found in some parts of the world are known to their abilities to destroy trees!

Current size of the tree: Larger trees are generally less likely to die of causes like drought or damage to their trunks, as they have greatly extensive nets of roots and thick trunks and thus are able to, even partly, recover these incidences.

If a rockfall for example causes damage to one side of the tree, some of the brunches will probably die, but the rest of them, that have their own network to the roots, will probably survive.

This means that luck is involved and if the tree is lucky enough to avoid dying for a certain amount of time, regular fluctuations in the environment do not kill it as they would kill a younger, less robust tree.

Biology of tree species: Debate is held as to whether tree cells have telomeres working the same way as they do in animals. Research published in 2001 suggests that telomeres don't work the same way, as plants developed without telomeres after six generations continue living and growing without problems. But even if they do use telomeres, they may use them in a different way. This is an area where research is still being conducted, though, and you may find controversies in the bibliography!
For example in the paper "Analysis of telomere length and telomerase activity in tree species of various life-spans, and with age in the bristlecone pine Pinus longaeva"
Barry E. Flanary & Gunther Kletetschka which can be found in the rep

http://www.google.com/url?sa=t&rct=j&q=&esrc=s&source=web&cd=2&ved=0CCgQFjAB&url=http%3A%2F%2Fwww.researchgate.net%2Fpublication%2F7709949_Analysis_of_telomere_length_and_telomerase_activity_in_tree_species_of_various_life-spans_and_with_age_in_the_bristlecone_pine_Pinus_longaeva%2Ffile%2F9c96052bcf0a51be49.pdf&ei=zzrCU9OcMIjV0QXmt4CwCQ&usg=AFQjCNH7853fvZ8yneznSfIQQPsxtIDQag&sig2=-PELK5RCQlAGTvQODoyZ2A&bvm=bv.70810081,d.d2k

we can see that sometimes, short lived trees have longer telomeres than long lived ones!
(Look in the second paragraph of the section "Results"). This means that actually, nobody really knows!! It may be the telomeres, it may be something else, it may be a combination of factors.

http://www.madsci.org/posts/archives/2002-04/1019349924.Bt.r.html
(notice that this post has links to pages that are no longer available).

Distillation and the most important point: The way that the tree is adapted to its environment determines its longevity in it. Planting an olive tree in the amazon is a great way of making sure it will not survive! Some trees are better at surviving in a certain climate (even if it is at your own garden) simply because they have evolved to live there.

That means that the trees probably don't have a defined lifetime in general, but the life expectancy is defined in each environment, depending on the circumstances!

This means that species we currently think of as short-lived can reach get really old:
http://www.ncbi.nlm.nih.gov/pubmed/11295506

What some companies may have done is   try to combine characteristics of individuals through selective breeding - and yes, it works for trees as well!- to match the climate and terrain characteristics found in the certain country or region! Or they may have selected for resistance against the most common pests in your area!

I hope I answered you question adequately!


dermatophyte fungi

Ringworm is caused by a several species of Trichophyton fungi (T. rubrum, T. tonsurans, T. interdigitale, and/or T. mentagrophytes); and a couple others are well known (Microsporum canis, and Epidermophyton floccosum).

The ring pattern is not unique to ringworm causing fungi. (Fairy) Rings are totally common with fungi because mycelium grows outward from the center; and as the mycelium grows, the inner mycelium often dies (from starvation, age, attack by immune system?, or it is cannibalized) leaving only the outer ring of mycelium, which may continue expanding.

Unfortunately the medical world doesn't spend much time on the problems that they can already solve (like with an antifungal ointment or pill), so there hasn't been much effort devoted (to my knowledge) toward answering the mechanistic questions of ring formation of dermatophytic fungi. But it is known that some Trichophyton species sexually reproduce and Trichophyton rubrum also probably does reproduce sexually (ie., plasmogamy, karyogamy, and gametangia). I don't have any grounds for mentioning it (besides logic), but sexual reproduction is probably "age" related in fungi as is growth- so, a ring may be more pronounced in an area where fungal hyphae conjugate... much like the expression of fruiting bodies of other mushrooms.


Why cancer disease is named after sun signs ?

It isn't. The name of the constellation/zodiac sign and of the malignant cell diseases comes from the Latin word "cancer", which means "crab".

This name for the disease dates back to the Greeks and Hippocrates, who used the word "karkinos" (the Greek equivalent) because the veins around the tumors they observed made the disease look like a crab 3.


Do squirrels and blue jays play a role in oak tree distribution?

In case anybody is curious this paper seems to answer this question.

  The obvious conclusion to follow from these summaries is that acorns
  of RO have a significant dispersal advantage. RO acorns are dispersed
  greater distances from their sources, cached more often in a wide
  variety of environments, and even show the ability, under some
  circumstances, to escape partial predation. Acorns of WO, in contrast,
  should show short dispersal distances and may be in fact adapted for
  rapid germination near or under parent trees.


What causes inhalation during breathing?

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


Usually, toxicity is given in the units of mass of the substance per unit mass of body mass of the organism that will kill 50% of the organisms in a species if those organisms ingest the toxin at that dose (e.g. mg/kg, ng/kg). This measurement is called the median lethal dose, and is often abbreviated as LD50.

In your table, they only provide the mass of the (average) dose of the substance needed to kill the organism listed, as can be seen by the (mg) after the words "Toxic dose". They likely multiplied the LD50 of the toxin by the average mass of the organism to obtain those numbers. Based on Google's estimation that a mouse has an average weight of 0.68 oz (0.019 kg), and on this table of murine LD50 measurements, I calculated that for tetanus toxin, the lethal dose in the average mouse is 3.8x10$^{-8}$ mg, which is basically what your table provides, which supports my guess on how they obtained their numbers.

The other values listed under "Lethal toxicity compared with" appear to be ratios, given by the formula [lethal dose of toxin above]/[lethal dose of toxin on left]. Using Wikipedia's LD50 for Strychnine in mice (2 mg/kg) and the tetanus toxin LD50 from my previous source, I obtain the exact ratio that they do (1x10$^6$). The lack of units makes sense, as ratios are unitless.

Source on LD50


What is the subcellular location of synthesis of non-essential amino-acids?

There are several enzymes involved in amino acid biosynthesis. These some of thse enzymes are encoded in the human genome. You can check out KEGG for a detailed pathway in different organisms.

The green arrows denote reactions (and enzymes) that are present in a given organism (Homo sapiens, in this case). If you click on the arrows you can know the details about the enzyme.

These enzymes are present in the cytoplasm as well as in mitochondria. Moreover, the reactants for synthesis of certain amino acids are produced in mitochondria (TCA cycle intermediates). See this article on the role of mitochondria in amino acid metabolism.

  Overview of the amino acid metabolic network in human mitochondria. Shaded areas represent the cytoplasmic segments of the pathways.


What is the mechanism behind "acquired" alcohol tolerance?

The subject of alcohol tolerance is broader than it might appear. However, in most cases people refer to what is called metabolic alcohol tolerance. Based on your response to the comment made by Alexander Galkin, I assume that you also refer to metabolic alcohol tolerance.

Metabolic alcohol tolerance is the result of drinking significant amounts of alcohol over a period of time as you describe. Both the amount of alcohol and the duration that it takes to develop an increased metabolic tolerance towards alcohol differ from person to person.

When most people drink alcohol, the liver will responds by activating alcohol degrading enzymes that break down the alcohol molecules, which results in the elimination of the intoxicating effect. The activation of those enzymes occurs much faster with people who have developed metabolic alcohol tolerance and the concentration of those enzymes is generally higher. This means that those people can break down alcohol faster than you and me, that is, they can "tolerate" more alcohol in the sense that they simply get rid of it much quicker.

On a final note, being more alcohol tolerant is not exactly correct as metabolic tolerance doesn't necessarily mean that the organs affected/intoxicated (such as the brain) by alcohol aren't necessarily more tolerant. The alcohol is simply broken down much faster and can therefore have a limited impact.


How many proteins on PDB have unknown function?

The article cited in the question indicates that the authors searched the PDB with the term “unknown function”. There is nothing special about this — you just type in the standard search field and hit ‘Go’. I conducted a search of this type myself:

http://www.rcsb.org/pdb/results/results.do?tabtoshow=Current&qrid=91CA3A5F

Which returned 4384 structures out of approx. 149,600 in the data bank.

Of course, it is evident from the first page of the results that the number of unique proteins is smaller than this because a single study may examine different forms of the same protein.

I admit that I was surprised to find that people had spent time and money determining the structure of so many proteins of unknown function, but it appears that there is at least one blanket initiative to determine the structures of bacterial proteins of unknown functions because of their roles as potential pathogens. The idea would seem to be that they even if their mechanism of pathogenicity is unknown they could still be targeted on the basis of their structure.


Here's a paper in Current Biology1 on the discovery of a species of bee (Anthophora pueblo) in Utah (US) that burrows through sandstone. Pretty cool!

Sandstone is harder than limestone, so I suppose it could be possible for this type of bee to get through your wall material, though Utah is a long flight from Israel.

Perhaps you have discovered a related species of Anthophora local to where you live (perhaps this one?), except that it is unclear if the bee in your picture has the same large mandibles that would help it dig through stone:

  As sandstone is harder than other substrates bees excavate (e.g., sand or soil), higher energy and time costs are expected. Mandible wear is consistently seen in older females, a consequence of excavation that likely limits their further use.

Unless you have a lot of similarly-sized and -shaped holes in your wall material, with large-mandible-d bees coming and going, it seems reasonable to infer that this hole came from something else and that these particular bees are just reusing it.

1. Orr, M.C., Griswold, T., Pitts, J.P. and Parker, F.D., 2016. A new bee species that excavates sandstone nests. Current Biology, 26(17), pp.R792-R793.


Google image search gave me answer as "Plumeria"


Your updated question is still very vague, but I'm going to assume it is basically: "Why would the ancestral version of a gene be mistaken for a more recent version than the modern gene?"

If this is incorrect, please let me know and modify your question to clarify.

The simple answer to that question is that the mutations that occurred after the Ancestral gene resulted in less apparent divergence than the LCA (last common ancestor), which would cause the Ancestral gene to seemingly have more polymorphisms - and the general assumption is that the more polymorphisms (mutations) that a gene has undergone, the more recent it is.

So let's say you have the following DNA sequences:

5' - AAAT - 3' = LCA (Template)

5' - AAAG - 3' = Sample 1 : # Differences = 1 Nucleotide

5' - AACG - 3' = Sample 2 : # Differences = 2 Nucleotides

The general assumption is that the larger the difference from the LCA, the more mutations have occurred over time. So, under the general assumption, Sample 2 is probably the most recent version of the sequence.

However, and this is what I think is the answer to your question, because mutations can occur in any order and at any place in the genome, it is entirely possible for the third (from left) Nucleotide to have followed this mutation path: A -> C -> A

That would make Sample 2 appear to be more recent than it is because it essentially mutated "back" to the LCA version of the gene, despite being a linearly older version than Sample 1. In this way, an Ancestral gene can be mistaken for a more recent evolution of a gene. This is also why genomic data is never as strong as when paired with fossil records or other corroborating data that also aligns with the genomic data's proposed timeline; though the odds of a mistake being made grow exponentially less as more of the genome is compared and analyzed.

With very recent mutations; on the scale of hundreds to thousands of years, it's sometimes necessary to analyze thousands of base pairs to calculate an adequately confident answer.


Can I use commercial DNA loading dye for my RNA samples without degrading them?

Handling of RNA requires extra care, especially using RNase-free pipette tips, tubes and reagents, to prevent RNase contamination. Common labware and reagents usually indicate whether they are RNase-free certified. If there is no such mention written on the box or label, then you should assume it is not RNase-free and you should not use it to handle your RNA.

Check whether your loading dye is certified RNase-free (this should be written on the tube, or easy to find out on the manufacturer's website using the product reference number). If it is, and you exclusively used RNase-free certified tools and reagents all the way, then maybe the loading dye tube or something else got contaminated by one of your co-workers.


What kinds of bacteria live in water bottles?

In addition to the cracks providing a better place for bacteria to grow, all plastic bottles, when reused, are subjected to high levels of bacteria due to contact with hands and mouths. So your water bottle can potentially host a range of bacteria.
Your water bottle traps humidity inside and provides a perfect growing medium, especially near the threads of the mouthpiece and along/within cracks in the bottle which provide better bacteria accumulation.
Microorganisms that Grow

Overall, most sources I could find remained very vague (numerous News stories) or mentioned bacteria generally:

Staphylococcus and streptococcus species, [Source].

Norovirus [Source].

The seemingly most detailed studies I could find came from Watanabe et al. 2014 and Ohnishi et al. (2012) who examined microbial growth in numerous beverage types. However, I could only find their their abstracts online, which report:

microbial growth was detected in ~20% of poured samples, and in ~51% of drank samples.

225 bacterial strains, 27 mold strains, and 77 yeast strains were isolated

Bacteria: Streptococcus spp. (e.g., S. salivarius) and Staphylococcus spp. (e.g., S. aureus), made up the majority. Enterotoxin-producing S. aureus and Bacillus cereus were also isolated.

Molds: Cladosporium spp., Tramets spp., Bjerkandera spp., and Penicillium spp.

 [I Will hunt down these articles to get more details and will update accordingly when I find them...]
Microorganisms in the Water

Based on a study found here, brand new bottles of water can have fungus spores (typically harmless), but opened bottles can show signs of greater diversity (e.g., fungi, skin Staphylococcus, and yeast.

Igbeneghu & Lamikanra (2014) found Staphylococcus species (notably S aureus) and strains of Pseudomonas in bottled water available in Africa.

Your Livestrong article lists a number of non-human pathogens such as: Ralstonia Pickettii, Acidovorax Temperans, A. Delafieldii, Agrobacterium Rhizogenes, Burkholderia Glumae, and Bacillus Thermoglucosidasius.

Juvonen et al.'s  (2011) "Microbiological spoilage and safety
risks in non-beer beverages" provides a thorough list of organisms found worldwide in different bottled waters and other beverages.

Other Issues

According to Rose State microbiologist, Dr. Amy Hurst:

The plastic materials degrade into the water, so then you're drinking very small plastic molecules. [Source].

PET plastics tend to leach when exposed to realistic though extreme conditions, such as exposure to sunlight, heat and storage time. [See UF article]

Bisphenol-A (BPA) and phthalates present in the bottles can leach into the water and possibly cause harm to humans.

Rochester (2013) provides a good review of BPA effects in humans and other test organisms.

New research shows that BPA alternatives such as BPS aren't any safer either; in fact, in some cases they are considered more dangerous to humans. All bisphenols are capable of mimicking the body's sex hormones, says Robin Mesnage, research associate with King's College London.

Al-Saleh et al (2011) found that  76% of the bottled waters they tested in Saudi markets contained measurable amounts of phthalates.

So Reusable Plastic Bottles are Better Right?

Well, from a bacteria standpoint, this isn't necessarily true.  According to a small study  of 12 reusable bottles being used for a week:

Avg bacteria load: 300k CFUs (colony forming units). Ranged between 25 - 900k CFU/cm$^2$.

Notable types found: E.coli, salmonella, and various gram-positive cocci and gram negative rod bacteria.

They found that different bottle types harbored different amounts and kinds of bacteria.


I think this is Cosmos sulphureus which is also known as yellow cosmos or sulfur cosmos. See the image (from here) as comparision:

More information can be found here and here.


Heavy metal toxicity is actually due to the inhibition of the body's natural enzymes as well as the denaturing of proteins that it causes.

Here, Tchounwou et. al go into detail about the mechanics of different heavy metals and how they interact with the human body specifically. It even suggests ways that the heavy metals could be introduced.

A short summary on the damage caused by what was studied:

Arsenic inhibits DNA repair.
Cadmium toxicity isn't well known, but they think it causes single
strand DNA damage.
Chromium causes chromosomal abnormalities thought to be caused by
oxidative damage.
Lead prevents the body from interacting with Calcium which is a key
element in many biological processes. It also competes with other
metals for the active sites in different enzymes.
Mercury depletes the body's antioxidants.

So to answer your question, no, the heavy metals are not all working on the same mechanism. It all depends on what dose, how it was introduced, and the particular metal. Also, anything can be toxic in the right amount (people have died from water toxicity in drinking contests).


Can bacteria release free DNA into their environment?

Natural Transformation
The process of Natural Transformation (Lorenz and Wackernagel 1994) has a very huge importance in evolution of prokaryotes. Definition quoting from (Stewart and Carlson 1986)

Natural transformation is part of the normal physiology of the cell.
It is the only form of bacterial genetic exchange whose functions are
encoded on the chromosome, and competence is a heritable trait,
subject to selective pressure.

This is almost similar to our daily use artificial transformation. You need some chemical like $CaCl_2$ to cell permiabalized, some chelating agents like EDTA and DNA material. You can imagine naturally occurring cell encountering such conditions, like decrease in temperature in presence of certain chemicals and proteins.
This concept of one cell externalising, and another internalising DNA got stronger when researchers observed free DNA in culture media (Catlin 1959, Sinha and Iyer 1971).
The Creation of eDNA
The release of eDNA (extracellular  DNA) can occur via spontaneous excretion or autolytic action.
There are known mechanisms for the release eDNA like formation of blebs (Dorward and Garon 1990). This extracellular DNA production is affected by many physiochemical factors than biotic (Paul and David 1989). There are many in detailed reports which shows such DNA can be passed through cell wall without any cell damage (Hara and Ueda 1981). Half life of such eDNA in various environment is reported in following table from (Lorenz and Wackernagel 1994)

Now there are even more novel ways of production of extracellular DNA like in Neisseria gonorrhoeae secretion of chromosomal DNA occure via new type IV secretion system (Hamilton et al 2005). Not just experiments, mathematical models also shows novel role of such process in gene-level selection (Draghi and Turner 2006). I haven't touched upon uptake of these DNA, which itself has lot of literature and unique mechanisms like this.


It is not necessarily about special (psychrophilic) genes, but rather about psychrophilic variants of their mesophilic and thermophilic homologs.

In general, lower temperature means lower rate of enzymatic reactions.

To cope with this problem, psychrophilic bacteria encode enzymes with highly mobile surface loops (higher mobility, higher catalytic rate).

Thermophilic bacteria have a different problem: enzymatic reactions are fast, but the enzymes are unstable; to cope with this problem, thermophilic bacteria encode enzymes with more rigid surface loops (more rigid, more stable).

Sočan et al. (2018) Catalytic Adaptation of Psychrophilic Elastase. Biochemistry 57: 2984-2993.
Åqvist (2017) Cold Adaptation of Triosephosphate Isomerase. Biochemistry 56: 4169-4176.


How do I effectively visualize data showing change in a lot of samples over two time periods?

Two styles of graph come to mind.

A simple 2 layer histogram showing the distribution of gland counts for each year. This is a kernel density as opposed to a histogram, but it gets the idea across.

Line graph with year on the x-axis and gland count on the y-axis, with a colored line for each plant. This would show a little more detail, and would be better if the mean gland count overall did not change much, but decreased significantly among individuals.


You should understand that it is not the neurotransmitter that is responsible for an effect; it is the neural network that causes an effect and the neurotransmitter is just a mediator.

In CNS, glutamate is generally used in excitatory synapses whereas GABA is chiefly used in inhibitory synapses. Similarly, in peripheral nervous system epinephrine and acetylcholine are used in excitatory synapses whereas glycine is used in inhibitory synapses. Some neurotransmitters always cause excitation in the post-synaptic cell (for example glutamate), however, they can also cause activation of inhibitory neurons and thereby cause inactivation, indirectly. Also, the post-synaptic effect depends on the type of receptor expressed by the post synaptic cell and not the neurotransmitter per-se. For example, α-adrenergic receptors cause smooth muscle contraction whereas the β2- receptors cause smooth muscle relaxation [1]. Similarly, there are both inhibitory and excitatory dopamine receptors [2].

The two divisions of the autonomic nervous system — the sympathetic and parasympathetic systems act in a complementary manner. The former uses epinephrine and norepinephrine whereas the latter uses acetylcholine.


The term complementation refers to the recover of a phenotype or characteristic ("or function of a protein") that was altered due to mutations. The complementation can be a cis, a mutation in the same gene that restores function, or trans mutation on a secondary gene that restore the function.

An example from wikipedia:

  For a simple example of a complementation test, suppose a geneticist is interested in studying two strains of white-eyed flies of the species Drosophila melanogaster, more commonly known as the common fruit fly. In this species, wild type flies have red eyes and eye color is known to be related to two genes, A and B. Each one of these genes has two alleles, a dominant one that codes for a working protein (A and B respectively) and a recessive one that codes for a malfunctioning protein (a and b respectively). Since both proteins are necessary for the synthesis of red pigmentation in the eyes, if a given fly is homozygous for either a or b, it will have white eyes.
  Knowing this, the geneticist may perform a complementation test on two separately obtained strains of pure-breeding white-eyed flies. The test is performed by crossing two flies, one from each strain. If the resulting progeny have red eyes, the two strains are said to complement; if the progeny have white eyes, they do not.
  If the strains complement, we imagine that one strain must have a genotype aa BB and the other AA bb, which when crossed yield the genotype AaBb. In other words, each strain is homozygous for a different deficiency that produces the same phenotype. If the strains do not complement, they both must have genotypes aa BB, AA bb, or aa bb. In other words, they are both homozygous for the same deficiency, which obviously will produce the same phenotype.


It is my understanding that a non-allelic gene is one that affects another's traits, but is not as a typical dominant / recessive manner. If I am correct, this is the same thing as  epistasis - meaning that one gene modifies how another is expressed.
There exists epistatic genes for horse coat color. One gene is the coat color itself (horses may have either brown or red color alleles at this loci), the second gene is for a protein that allows the coat color gene to be expressed.
For example, a horse has two brown alleles at the coat color locus. It also has a wild type gene in the second (modifier) position. This modifier allows the color brown to be expressed and the horse is brown.
B/B, wt/wt --> Brown
If the horse has the two brown alleles, but has a mutant allele at the modifier position, then coat color is not expressed and the horse is white.
B/B, mt/mt --> white

Because the modifier alleles are separate genes from the coat color alleles, the two are non-allelic - yet they both affect the same trait in some way.

I hope this helps.


They are basically conjoined apples which share a common stalk. They are rare but do happen. Here is an article of one discovered in a backyard.

conjoined apple discovered in a store (reference)

It apparently happens because of bad weather conditions, stress and insect damage. Fused fruits are also found in the case of cherries, watermelons, peaches etc.

  Inadequate pollination because of heat and other adverse growing
  conditions causes that section of the fruit in which the seed did not
  develop to not grow and fill out. Also, the fruit primordium
  (embryonic growing point) can be damaged or altered by environmental
  factors and cause strange growth forms. Of course, Siamese twins or
  two fruit growing together is also rather common(reference).

Read more about them on article 1 and article 2.


Could a man be proved positive for a pregnancy test?

Pregnancy test, just like any test, has some non-zero false positive rate. So yes, of course a test could be positive when a man pees on it.

Pregnancy tests work by detecting the presence of a hormone called Beta-HCG. This hormone is produced by both genders but is produced in much higher dose during early pregnancy. Teenagers also produce a relatively high dose of Beta-HCG which can eventually inflate the false positive rate.

It just so happen that tumours from a particular type of testicular cancer also excrete Beta-HCG (see this blog post from the American Cancer Society). If your question arises from a personal experience, then I would strongly recommend that you talk about it with your doctor.


Detrimental effects of fructose in fruit on the liver?

There is insufficient evidence to claim that high consumption of fructose, when part of isocaloric diet (no weight gain), is a risk factor for non-alcoholic fatty liver disease (NAFLD).

Fructose Consumption, Lipogenesis, and Non-Alcoholic Fatty Liver Disease (PubMed, 2017):

  ...the available evidence from human epidemiological and
  interventional studies does not support the hypothesis that
  fructose, when consumed in isocaloric amounts, causes more liver fat
  accumulation than other energy-dense nutrients. The observed
  prosteatotic effect of fructose in hypercaloric trials is likely
  confounded by associated weight gain...

Effect of fructose on markers of non-alcoholic fatty liver disease (NAFLD): a systematic review and meta-analysis of controlled feeding trials (PubMed, 2014):

  Isocaloric exchange of fructose for other carbohydrates does not
  induce NAFLD changes in healthy participants.

Consumption of fruits, if part of isocaloric diet, is also not likely associated with NAFLD.

No association between fruits or vegetables and non-alcoholic fatty liver disease in middle-aged men and women (PubMed, 2019):

  No obesity-independent association was found between fruit or
  vegetable intake and NAFLD.

The main source of dietary fructose are probably soft drinks, not fruits, anyway:

Popular soft drinks can contain 60-70 g fructose per liter (ScienceDirect, Fig. 2).
Four apples (150 g each) contain 36 g fructose, which is more than in most other fruits (USDA.gov).

And finally, even if there is abundant evidence that fructose stimulates lipogenesis in the liver, this does not automatically mean that it stimulates the development of NAFLD (according to the first source above).


"Oblong to Allantoids" .... Is it valid?

Oblong is probably correct in this context, but "allantoids" should probably be "allantoid" to be the adjective form. It's describing translucent (hyaline), oval (oblong) to sausage-shaped (allantoid), undivided (aseptate) spore.


How did the first life form on Earth reproduce without DNA?

So earth is estimated to be around 4.5 billion years old, and life has existed for about 3.4-3.9 billion years of that, around >75% the time. For a little perspective, Homo sapiens have been around for up to ~250,000 years, just 0.00005% of the time earth has existed. In that time the earth has changed massively, early earth was pretty hostile, but that could have made it a good place to develop early life.

What was the pre-cursors to self-replicating DNA like?

Well one popular theory is the RNA world hypothesis, which suggests that precursors to life as we know it were RNA molecules that could self replicate (reproduce). These RNA molecules supposedly evolved in to life in the DNA/RNA/Protein world via an intermediate stage of ribonucleoproteins. The reason why RNA could have preceeded DNA based life is because it has the potential to carry information and to be the catalyst of its own synthesis.

  "The unique potential of RNA molecules to act both as information carrier and as catalyst forms the basis of the RNA world hypothesis.

  "RNA therefore has all the properties required of a molecule that could catalyze its own synthesis (Figure 6-92). Although self-replicating systems of RNA molecules have not been found in nature, scientists are hopeful that they can be constructed in the laboratory." in Molecular Biology of the Cell

However, the RNA world probably wasn't the first step on the road to self-replicating life, but other polymers with characteristics similar to RNA that could have acted as the template and catalyst required for RNA synthesis.

  "Although RNA seems well suited to form the basis for a self-replicating set of biochemical catalysts, it is unlikely that RNA was the first kind of molecule to do so. From a purely chemical standpoint, it is difficult to imagine how long RNA molecules could be formed initially by purely nonenzymatic means. For one thing, the precursors of RNA, the ribonucleotides, are difficult to form nonenzymatically." in Molecular Biology of the Cell

-

  "Shapiro doesn't think it's necessary to invoke multiple universes or life-laden comets crashing into ancient Earth. Instead, he thinks life started with molecules that were smaller and less complex than RNA, which performed simple chemical reactions that eventually led to a self-sustaining system involving the formation of more complex molecules." on LiveScience.com

This means that the first self-replicating RNA molecules were preceded by other molecules that were important in the progression from simple atoms, through non-biotic molecules, to large self replicating polymers which can be considered life. Copley et al suggest a progression in detail, with monomers being an early step in the progression (see figure 4 in the paper, and section 4 for extensive detail) where monomers precede multimers, which precede micro-RNA.

  "Our model describes a continuous path for emergence of this sophisticated system
  from a simpler reaction network fueled by geochemical processes. The processes involved in metabolism and replication were intertwined from the very beginning, a concept that neatly eliminates the chicken/egg problem. Further, this model suggests that many features of the RNA World, and indeed modern life, arose long before the RNA World and were retained as pre-biotic systems became more sophisticated." - Copley et al

An alternative and slightly different theory suggests that viruses were the precursors to modern life, a so called Virus world. Similarly it supposes that early replicators were RNA based, but that viruses evolved in to the earliest forms of self replicating DNA carriers.

  "The Virus World Theory is closely related to the RNA World Theory, which says life first evolved as small pieces of RNA that slowly developed into complex DNA-carrying organisms. The Virus World Theory agrees that life's genetic material began as RNA. But it differs by arguing that the ancestors of viruses evolved before cells." from NationalGeographic.com.

Further good reading here, here, and here. I also recommend the book The Story of Life as an interesting related read.


What is this insect I found in northern Europe?

Definitely not a bedbug. It is a weevil, family Curculionidae. A beetle, and not normally found indoors. It looks a bit like Baris, but I cannot tell from the picture. https://en.wikipedia.org/wiki/Baris_(weevil)


Top speed = 20 mph (32 kmh), according to a-z animals.


Why mutations in genes involved in general processes like DNA repair increase the risk of developing specific types of cancer?

I can't fault @WYSIWYG for mentioning the cited Vogelstein article in providing an answer. You point to what seems like a great explanation for why certain cancers arise in some tissues but not others. However, for those who look closely this paper has some serious errors in its derivation of the model, and for good reason it has come under strong fire in the last couple of months.

See this for a really important rebuttal:
http://ameyer.me/science/2015/01/02/vogel.html

Unfortunately, the paper provides an elegantly specious explanation for, in part, the longstanding paradox of why cancers more readily arise in some tissues like the intestines and from seemingly identical mechanisms, but do not seem to arise in other tissues. My favorite example, though @El Cid you do list some good ones, are inactivating BRCA1 mutations which normally play a role in repairing double stranded DNA breaks. And yet even when mutated in the germline this only seems to increase cancer risk in the breast, and really only in one gender (females).

So the answer is still quite certainly that the field does not understand this paradox, and the cited Vogelstein paper was a total tragedy of a publication. There have been a number of officially submitted critiques of the paper and the Vogelstein lab has been trying to defend it as best they can. This is however a great example of how big name labs can seem to get anything published in Cell/Nature/Science.

Another thing to consider and @El Cid points to a good example, is the pRb mutations (in a very central tumor suppressor pathway for all cells) cause retinoblastoma and not for instance intestinal or blood cancers very readily, and the retina is not a rapidly dividing tissue. So the Vogelstein paper cannot explain this.


Which nucleotide as start point for maximum parsimony?

The "starting point", or ancestral state, is chosen so as to obtain the most parsimonious tree.

Parsimony is used both for choosing the topology and for choosing the ancestral states for a given topology:

1) The parsimony score for a given topology is computed for the set of ancestral states minimizing the number of transformations.

2) Then, the topology minimizing this minimized number of transformations is chosen as the most parsimonious tree.


Can I image Coomassie and GFP in gels at the same time with a fluorescence scanner?

Coomassie blue fluoresces in infrared when bound to protein, so if your reader has the appropriate filter set, it should be possible.


Recombination between DNA segments question

So, apparently the "trick" to this question is in the wording. "between A and B" appears to mean one crossover somewhere in the B segment, which could destroy (delete) a gene in the B sequence if present at the cut.
The answer involving the horseshoe "trick" implies that the chromosome has looped so that the A and C sequences match up, an extremely unlikely condition. Then a crossover occurs while the loop is in place, also an extremely unlikely event.
Another problem is that the horseshoe solution apparently implies that it is a single chromatid that is looping to itself and forming the crossover. That's weird. I could more easily visualize a different solution: One chromatid is aligned tail-to-head with respect to the other chromatid (head-to-tail). This would allow the corresponding A and B segments on the two chromatids to match up, thus allowing a crossover point anywhere (except inside B) to result in an inversion of B. This is also weird.
These two solutions are much weirder and unlikely than a simple crossover inside B: Picture the two chromatids aligned a little off target so that one is cut at the start of B nearest the A segment, and the other chromatid is cut at the other end of B, nearest the C segment. The result is an uncomplicated deletion of the B segment from one of the chromatids and duplication in the other (no inversion). This scenario seems at least as valid as the "correct" choice given in the practice exam.
While I'm glad to have learned the "trick" in this question for when I take the exam, I consider this question "bad".


How to find miRNA binding sites on a specific gene?

There are some tools for predicting the binding:

TargetScan (based on seed match [primary], extra pairing, sequence context 1 — nucleotide composition around the site etc [secondary])
miRanda (based on hybridization stability and seed match[primary] and sequence context [secondary])
PicTar (adds a layer of evolutionary conservation criteria)

1 Context means the position of the target site in the 3'UTR and the surrounding nucleotide composition (which is also considered an indirect metric of secondary structure)

miRanda and TargetScan also have classes called conserved and non-conserved targets. miRanda reports miRSVR scores and TargetScan reports context scores but these measures are based on few experimental results and may not always be meaningful. miRSVR is based on change in target expression upon miRNA overexpression/knockdown. It also uses metrics for target site context. Context+ score of TargetScan includes many metrics which include target abundance and conservation along with the regular context scoring. Some of these metrics may be more useful than the others. But scores based just on miRNA OE/KD experiments can be misleading- especially if target expression is quantified just at the RNA level. Target abundance also varies between different cell types. For more details on these metrics refer to the papers corresponding to these tools.

There are some experimental procedures for target determination which mainly involve Protein-RNA crosslinking followed by immunoprecipitation of Ago and subsequent quantification by RNA sequencing. See HITS-CLIP and PAR-CLIP. These techniques do not really find the targets. All they do is to correlate the levels of miRNA and their predicted targets attached to Ago (you won't exactly know if the ternary mRNA-miRNA-Ago complex really formed or not).

CLASH is a more recent technique which tries to address this issue by ligating mRNA with miRNA. This way you can capture the miRNA-mRNA interaction. However, I am a little skeptical of CLASH; I myself was working on this principle some time back and faced this one challenge. CLASH roughly involves the following steps:

Crosslink protein-RNA
Immunoprecipitate Ago
Use RNAse to digest unbound regions of mRNA (and make it small enough for a short read sequencing experiment)
Ligate miRNA and mRNA bound to Ago using RNA ligase
Degrade Ago using protease
Sequence the miRNA-mRNA ligated pair

My doubt was how would miRNA and mRNA be ligated when the footprint of Ago is bigger than an miRNA (reported ~50-60 nt in HITS-CLIP and PAR-CLIP). When the RNA is nuclease protected then how can it be accessible to ligase. When I was thinking about it then I thought that a partial protein degradation was necessary (after RNAse step and before ligase step) to give some space for ligase to act. Eventually I did not work on it further. Three years later CLASH paper was published and I was happy that someone made it work. But the ligase issue was not addressed (It seems to have worked but I don't know how!!).

To test the predictions you can use a reporter assay (such as GFP or Luciferase) with the 3'UTR cloned downstream of the reporter. These can have artifacts too. Overexpressing the miRNA should be avoided and seed mutations should be done to ascertain the targetability.

Another technique to determine a target mRNA is to mask its predicted miRNA binding site and see the effect on the expression. This has been done in zebrafish using morpholinos complementary to target sites but not on other models AFAIK. This seems to me as an elegant assay- no overexpression and you can precisely determine the target site.


On average, it has been stated to be about five weeks however it differs from person to person based primarily on physical stats.

The process that would occur :

First food that remains in your stomach is digested
Readily available energy is then absorbed (This includes glucose, carbohydrates, anything that generally doesn't mean fat)
Your body then begins to convert fat into a source of energy. Your body would then begin to lose the resources to make protein and you would experience various effects such as night time blindness due to vitamin deficiencies
As you lose salt and other minerals the water you consume begins to build up in your cells via diffusion
You can either die of not enough energy or lack of protein or too many cells disintegrate from too much water

Source(s) : Biology book, Internet, Knowledge.


RNA STRAND v2.0 - The RNA secondary STRucture and statistical ANalysis Database
http://www.rnasoft.ca/strand/

16S rRNA: secondary structure file in ct format

http://www.rnasoft.ca/strand/show_file.php?format=CT&molecule_ID=CRW_00111&check_out_the=View+the+RNA+sequence+and+secondary+structure+for+molecule+CRW_00111

5S rRNA: secondary structure file in ct format

http://www.rnasoft.ca/strand/show_file.php?format=CT&molecule_ID=CRW_00573&check_out_the=View+the+RNA+sequence+and+secondary+structure+for+molecule+CRW_00573


Dahlia cultivars are known to undergo somatic mutations, e.g. mutations that occur during growth that can lead to different flowers. See for example this old paper.

So it would be very possible that your bulbs yield somatic mutations that crop up as you regrow them each year. This could be the case even if your bulb has not undergone the mutation, because the mutation possibly is occurring in the meristem of the plant as it makes new shoots or inflorescences from the bulb.

Other possibilities would include epigenetic changes which do not actually modify DNA but can possibly lead to modifications of the expression of genes. These can occur due to changes in environment, but they are a bit more difficult to demonstrate as such.


The gut microbiome is extremely complicated, and almost anything related to it is only partially known, therefore prone to oversimplification. Trying to explain the phenomenon of gut fermentation syndrome in such a limited fashion (age, gender, ethnicity, quantity of one particular yeast, etc.) will not help us understand it.

  Common yeasts (C. albicans, C. tropicalis and Torulopsis glabrata) and Saccharomyces cerevisiae are able to ferment sugars through the homolactic, heterolactic or mixed acid fermentation pathways, with ethanol as the major end product.

Candida is a very common yeast found in the environment and in and on our bodies wherever it's warm and moist (therefore the GI tract.) Candida species are the most common cause of invasive fungal infections in humans (followed by Cryptococcus and Aspergillus) and can involve any organ. Yet it's omnipresence does not result in clinically recognized cases of ethanol intoxication in even a minute fraction of people who carry it in their gut.

Case reports started appearing in the literature starting in 1972, yet it is still a rare event to see one. In 2001, the case of a 13 year old girl was published. She had short gut syndrome and became intoxicated after ingesting carbohydrates. She had been placed in a rehabilitation facility with no access to alcohol, but still had positive blood alcohols. Aspirates from her small intestines grew Candida glabrata and Saccharomyces cerevisiae. Short-gut syndrome is complicated.

We have no idea how common fermentation into alcohol is in the gut, or what the results are, but it is probably far more common than recognized, can probably result in effects other than intoxication (for example fatty liver disease in non-drinkers), and probably has a role in other illnesses.
It's complicated:

  Carbohydrate metabolism by gut microorganisms is a central process allowing supply of nutrients and energy to the host. This fermentative process is complex and involves several functional groups of bacteria with complementary metabolic activities that interact to ensure the biotransformation of polymers (resistant starch, nonstarch polysaccharides, proteins, mucins…) into end-products (mainly short chain fatty acids and gases). Hydrolytic communities transform complex substrates into smaller fragments that can also be used by other bacterial groups unable to hydrolyse polymers. Other microbial cross-feeding interactions are related to the utilisation of fermentative products such as succinate, lactate or hydrogen and involve specific groups of microorganisms.

All we know is that it happens in some people, and that it can respond to antifungal treatment and some probiotic supplementation. "Why" is still a mystery, and speculation only.

Gut fermentation syndrome
Invasive Fungal Pathogens: Current Epidemiological Trends
IwataK., “A Review of the Literature on Drunken Syndromes Due to Yeasts in the Gastrointestinal Tract,” University of Tokyo Press, Tokyo, 1972, 260-268. Not available online
Functional dysbiosis within the gut microbiota of patients with constipated-irritable bowel syndrome
Obesity and female gender increase breath ethanol concentration: potential implications for the pathogenesis of nonalcoholic steatohepatitis


Yes, ruptured here means that the host cell is destroyed. The virus "hijacks" the cell anyway and uses its protein production machinery to make as much virus particles and its transcription enzymes to makes as many viral genomes as possible. If the ressources of the cell are exhausted, it get destroyed and the viruses are set free.

See this image (from the Wikipedia article on the lytic process). It actually doesn't matter, if the virus infects the cell from the outside or if it comes from the genome.

Adsorption of the virus to the cell.
Injection of its genetic material into the cell.
Production of new viruses (hull and genome).
Rupture of the cell and release of the viruses.


It's a mole cricket (in the family Gryllotalpidae).

Notice the cricket-like appearance of the posterior/abdominal portion of the insect, but the powerful, broad and flattened fore-legs that are designed for digging (reminiscent of a mole's digging legs). In fact, the family name literally means cricket-mole (from Latin, 'gryllus' = cricket and 'talpa' = mole).

Mole-cricket fore-legs:

Anterior mole legs:

The Gryllotalpidae are a monophyletic group in the order Orthoptera (grasshoppers, locusts and crickets). A 2015 paper by O. J. Cadena-Castañeda clarified/updated the phylogeny of this family using morphological characteristics.

The specific species is dependent on your location and morphological characteristics (and possiblly "song" differences too).
See here for a brief explanation and access to dichotomous keys to use to better ID the specific genus. Other keys exist here (SE USA), here, and likely via a google search. However, I couldn't quickly find a European key.

Here's an additional useful resource on these insects from University of Florida Entomology and Nematology Department.

Based on the OP's location in France, the European mole-cricket Gryllotalpa gryllotalpa (or one of it's closely related European allies in the Gryllotalpa genus) is probably a good initial guess at the OP's specific species. As seen from UC Berkeley's "CalPhotos" collection:


Do any organisms recycle their own waste internally?

All organisms recycle their waste internally. Every cell of every living organisms is constantly breaking things down and re-using the components so produced. But you're presumably wondering about things such as carbon dioxide, urine and faeces? These are not recycled because the benefits of doing so are not worth the costs.

Let's consider carbon dioxide as an example. We know that carbon dioxide can be usefully converted into energy-holding molecules using readily available sources of water, oxygen and sunlight. So why do animals** "wastefully" breathe it out? Because the energetic benefits of respiration are high compared to the energetic benefits of photosynthesis and so photosynthesis is unable to make a useful contribution to the overall energy balance of an animal while the costs of the effectively photosynthesising are quite high (e.g. having leaf-like protrusions, synthesizing chlorophyll and so on).

In fact, it must always be true that there are processes which are not energetically worthwhile because of entropy. An organism that could perpetually recycle its waste would be a perpetual motion machine.

** - and many microbes and, in fact, plants - although their intake of carbon dioxide is typically higher over the solar cycle.


Why do dendritic cells have CD4/CD8 on their surface?

There is no direct connection between CD (cluster of differentiation) receptors and T-cell receptor (TCR).

CD-receptors are used to label and distinguish different cells belonging to immune system: macrophages, T- and B-cells etc. Dendtritic cells play a significant role as antigen presenting cells and belong to vertebrate (and human) immune system and thus bear certain CD receptor.

These cells participate in the process of learning a new antigen by the immune system. During the very first phase the antigen is taken up by these cells, cleaved and processed. Depending upon the antigenic properties of the molecule it can be recognized as a valid antigen. In this case dentritic cells participate in the process of antigen presentation, where this new antigen bound to the MHC receptor is expressed on the cell membrane.

TCR is the protein that binds to this complex (MHC + antigen) and as long as this binding takes place the signal about antigen is propagated further to the immune system (leading to formation or augmentation of immune response depending upon the cell type which connects to this complex).


Mould in buildings can be serious.  It is treated by removing and destroying (fire is good) the things the mould is growing on, and lots of cleaning.

The mould grows on wet cellulosic material like fiber board, gypsum board, paper, or wood.  It can be prevented by fixing the leaks so stuff doesn't get wet, and more cleaning.

You could pour bleach on the contaminated material, kill some of the mould, and what survived would grow back.  Neither chemicals, nor tartigrades are any help here.  Just more cleaning.

Details:  http://www.cdc.gov/mold/stachy.htm


Can you change your gut microbiota by changing your diet? Would that affect calorie uptake?

Firstly, it should be noted that a stable, healthy microbiome is generally thought to be a marker of health; actively disrupting it through diet in an attempt to fight with it over nutrients is therefore not necessarily a good idea, as it can affect the health of not only your gut but also your immune system, etc.
Dysfunctional microbiomes are for example associated with behavioral problems in eating disorders.
Nonetheless, diet shifts have been used as a tool to attempt to control the microbiome and put it in a "healthy state". You can indeed use consumption of some foods to shift microbiome composition. Presumably if you did this in a sufficiently disjointed way, you could throw your microbiome into a sort of ecological chaos.
However, it would be much simpler to just constantly take antibiotics to ensure that your gut load of microbes was generally low. This still isn't a good idea, as it can lead to Clostridium difficile or E. coli infections or other bad things, but it would be a much more straightforward way of getting to the desired end state.


The basic steps of ChIP-Seq are:

Crosslinking proteins to DNA - this fixes the proteins in their natural positions
Nuclease digestion - this removes regions that are unbound to protein; nucleases are sterically hindered from digesting protein-bound DNA
Immunoprecipitation - this allows isolation of the target protein by binding it to a selective antibody
Sequencing to determine the bound DNA sequence
Mapping the reads to the reference genome

Why so many reads? They are taking many reads from different cells. Why are the reads so short? Many modern next-gen sequencing methods are limited to ~30 bp reads. Thus, the reads you see are not actually the entire protected sequence but rather just a shorter fragment from the 5' end (where sequencing starts from). The why behind this is explained by Jiang and Pugh, 2009 (Nucleosome positioning and gene regulation: advances through genomics):

  Three DNA sequencing technologies have been used to map nucleosomes. Pyrosequencing using the Roche 454 GS20/FLX
  sequences nucleosomel DNA end-to-end, allowing both nucleosome
  borders to be linked in a single sequence. This method provides the
  greatest mapping accuracy, particularly in genomic regions of low
  complexity. By contrast, other platforms, such as those provided by
  the Illumina-Solexa Genome Analyzer and Applied Biosystems SOLiD,
  generate only 25-35 by sequence tags, requiring both nucleosome
  borders to be inferred. Nonetheless, these short-read technologies
  produce >100 times the number of sequence tags at a similar cost as
  the long-read technologies, and so the short-read technology is
  currently the only practical technology for mapping nucleosomes in
  large genomes. The higher tag count of the short-read technology
  enhances mapping accuracy and thus provides a practical way of
  mapping nucleosomes.

Why are the reads overlapped? I can think of a few explanation for that. For starters, Protein-DNA binding is variable in its specificity. In other words, a given protein might bind at the exact same site every time or it may bind 'around' a site or it may bind randomly. A protein that binds an exact sequence would be expected to produce reads that are more in phase that one that binds more variably. Next, the nuclease digestion process is random (or at least expected to be). Thus the DNA cleavage point relative to the protein is variable and your reads start from different points. Again, from Jiang and Pugh:

  At any given genomic locus, the preferential positioning of nucleosomes--called phasing--can be described. At most loci, there is an approximately Gaussian (normal) distribution of nucleosome positions around particular genomic coordinates, ranging from ~30 by for highly phased nucleosomes to a random continuous distribution throughout an array. How much of this variation is due to genuine positional heterogeneity and how much is an artefact that is caused by overtrimming or undertrimming of the DNA at nucleosome borders by micrococcal nuclease during sample preparation remains to be determined.

Does that answer your question? Basically the reads are overlapped because there are many of them and they may differ either because of actual variance in the DNA binding site (which is biologically significant) or because of variance in the DNA digestion site (which is a methodological flaw). As with any biological experiment, you must perform many replicates to statistically determine the source of the variance and this is done by taking many reads. I recommend you read the article I quoted from, it is a good overview of histone mapping with ChIP and is likely also applicable to what you're studying.

Also, do you know why there are two sets of reads (red and blue)? I would venture a guess that they are taken from opposite strands. In other words, they are reads of the same DNA region taken from different directions. That might help clarify what's going on.

To conclude:

DNA is not extracted from a single cell. In usual procedures it is
always from a collection of cells or from tissues.
The overlap in TF associated reads arises because of the TF bound
sequence coming from different cells in this collection.
Each DNA piece is amplified and clusters are formed in the NGS
sequencers (for the ease of detection);
In a homogeneous cell collection i.e. all cells are of same type, the
variability in the read position usually arises because of
flexibility of binding sites (i.e TF wont exactly bind to at a
certain locus). Also, as previously mentioned the variability can
arise during the technical procedures.
In case of heterogeneous tissues the variability arises because of
different biochemical status of different cells. Strictly speaking
there is always some heterogeneity even in an apparently homogeneous
tissue but tissues such as brain are highly heterogeneous
In the case of nucleosomes the positioning is not exact because the
sequence contribution to the position is very minimal. Certain
nucleosome positions are tightly maintained for e.g. around the TSS
(transcription start sites) whereas in other regions the positioning
is fuzzy because of the dynamic nature of the chromatin.


What you are asking about is the precipitation of DNA (or any other nucleic acid) by isopropanol (or ethanol, which is more common). To do so, you add salt (usually slightly acidic sodium acetate) which makes sure that the phosphate backbone of the DNA is saturated with sodium ions to make it less soluble. Then you add the organic solvent, which precipitates the DNA from the solution by changing the polarity of the solution. This makes the ions form salts and the DNA precipites. The principle is explained in the Wikipedia article on ethanol precipitation. Finally the solution is centrifuged to collect the DNA at the bottom of your reaction tube and to be able to take off the supernatant.


How are viruses weakened to be suitable for vaccination?

There is a Wikipedia page on the topic of attenuated vaccines.

Basically the idea is that the virus is grown on some sort of foreign host such as cells in culture, eggs or an animal. This selects for mutant viruses, present in the original population, which are pre-adapted to the new host (so that they grow better). By repeating this process several times it is possible to develop a new variant of the virus which grows poorly in the original host (i.e. humans) but is still able to stimulate an immune response. The resulting antibodies, will recognise a subsequent infection by the original disease-causing virus as long as the viral component responsible for the immune response is still present in the attenuated virus that is used for vaccination.


Producing a genetically modified animal with cell walls

Mammalian cells have a semi permeable membrane not a true cell wall like a plant cell. I could imagine that if the semi permeable membrane were replaced with a plant like cell wall then osmosis and other biochemical processes necessary to the organisms growth and survival could not occur correctly.


To measure frequencies of eosinophils and neutrophils in airways

The original tests where done with blood and then:

  An eosinophillc index was calculated by multiplying the percentage of
  eosinophiles found in the routine white blood count by the total white
  blood count. An index of greater than 250 was considered positive.

See table 8 in this paper: "Field evaluation of a respiratory syncytial virus vaccine and a trivalent parainfluenza virus vaccine in a pediatric population." So they measure the eosinophils in the periphery not in the airways.

This article used histologic techniques: "Respiratory syncytial virus disease in infants despite prior administration of antigenic inactivated vaccine." Both articles are from 1969.

Newer studies used micropical techniques and FACS analysis, but these experiments were done with mice: "Respiratory synctial virus infection in BALB/c mice previously immunized with formalin-inactivated virus induces enhanced pulmonary inflammatory response with a predominant Th2-like cytokine pattern."


Genes controlled by bidirectionl promoters are in head-to-head configurations, meaning that their 5' ends are facing one-another.  Remember that DNA is double stranded, so this means one gene is on the 'top' strand and one gene is on the 'bottom' strand.  Check out the diagram below, genes are in capitals, bidirectional promoter in parenthesis.  Both genes are transcribed 5'->3'

                                         --> Gene 1
 5'-atgcagtcatga(ctgactaagt...tcagtcatga)CTGACTGACTAGTCAT-3'
    |||||||||||| ||||||||||||||||||||||| ||||||||||||||||
 3'-TACGTCAGTACT(gactgattca...agtcagtact)gactgactgatcagta-5'
      Gene 2 <--

As for why they are more commonly found in eukaryotes, those questions are definitely hard to answer.  It has been shown that genes on bidirectional promoters are expressed together more often than two genes that are next to each other on different promoters.  That means this might be a eukaryotic strategy similar to prokaryote's usage of polycistronic mRNA, an easy way to have similar expression patterns of genes that should often be expressed in similar amounts.


First step is the calculation of efficiency, denoted by lets say $E_{gene}$. See this post for calculation of primer efficiency.

So the fold change for that gene will be calculated by $E_{gene}^{-\Delta Ct_{gene}}$

Where:

$\Delta Ct  = Ct^{treated} -Ct^{control}$

But these Ct values are not normalized. For normalization, you take some reference gene which need not be a housekeeping gene. Reference gene should chosen such that it is not affected by the treatment. In some cases usual housekeeping genes can also get affected for e.g. in treatments affecting cell cycle or differentiation. In such cases you should use a spike-in (an artificial RNA bearing low resemblance with any known gene).

You can either normalize the fold change (Case A) or find fold change of the normalized expression (Case B).

Means the same mathematically.

Case A:

$E_{gene}^{-\Delta Ct_{gene}} / E_{ref}^{-\Delta Ct_{ref}}$

Case B:

$\large\frac{[E_{gene}^{-Ct^{treated}_{gene}}]/[E_{ref}^{-Ct^{treated}_{ref}}]} {[E_{gene}^{-Ct^{control}_{gene}}]/[E_{ref}^{-Ct^{control}_{ref}}]}$

You can rearrange the numerator and denominator to get Case A from Case B. I'm not sure how you are ending up getting different values. Recheck once. It may be because of numerical approximation errors.

Case A looks much neater; so it is best to calculate that way :)


Are identical twins clones?

A clone is an individual that is genetically identical to another (see wikipedia > cloning). As you said, identical twins (better called monozygotic twins) are genetically identical to one another and therefore an identical twin is a clone indeed.

The role of the environment

Be careful, to not think of clone (incl. monozygotic twin) as individuals that look exactly alike or behave exactly alike. Even for traits that are highly heritable, environmental variation is causing a lot of phenotypic variation and two monozygotic twins do not encounter the exact same environment and can eventually grow up to be very different people. Note that the two blastulas will differ a little bit in concentration of proteins, fats, developmental factors and other things. Such small differences can have important impact on the development of the fetus.

See this post on heritability to have a better understanding of the underlying environmental variation explaining phenotypic variation in populations.

But they are clone for life, right?

Well, it depends on the exact definition of clone but it is important to understand that the expression of genes varies a lot in response to the environment. See for example wikipedia > epigenetics. Also genes may change slightly as we age (see Can genes change as we age?).


The matter in plants is mostly carbon, hydrogen, oxygen, and nitrogen, with various metal ions and some sulfur and phosphorus. The carbon, hydrogen, and oxygen are taken from carbon dioxide in the air and water from the soil through photosynthesis. Nitrogen is taken up from the soil as ammonia or nitrates, or fixed from nitrogen gas, but this only happens in legumes. Phosphorus is also part of a nutrient cycle. Metal ions such as sodium, potassium, magnesium, and calcium are taken up through the roots with water.

If you're asking about how this material is replenished, fertilizer is an important answer. For centuries, nitrogen was a limiting nutrient in farms because it would get removed faster than it was replaced, especially if crop rotation was not used or legumes weren't grown. Thanks to the Haber Process we can produce humongous amounts of ammonia from nitrogen gas, this has greatly increased the amount of nitrogen available for plants, but has also resulted in nitrate pollution in waterways and algal blooms and eutrophication. Phosphate and potassium are also used in fertilizer and are usually mined, however phosphorus reserves are limited.


Exactly which amino acids are phosphorylated in higher plants during state transitions?

The protein in question from Arabidopsis has this UniProt entry. In the comments you read: The N-terminus of the protein extends into the stroma where it is involved with adhesion of granal membranes and post-translational modifications; both are believed to mediate the distribution of excitation energy between photosystems I and II. As known PTMs we have (see Sequence Annotations) Threonine-38 and Arginine-36; below you can see known mutations. My guess, though, is that they are a few years behind and so it's better to look at recent work.

Let us then take the PMID 11113141 referred to in the above entry and see the citing papers, e.g., via CiteXplore where I see at least a few relevant references on the topic of LHC phosphorylation. If there were a review, it would be listed there. Apparently, there is also a plant phosphorylation site database PhosPhAt which might help, see PMID 22723801.

In summary, not much is known, lacking even a single review on the subject.


How often can you reuse coomassie stain?

Since there's a lot of methanol in Coomassie stain, a significant amount would probably evaporate off each time you microwave it. Therefore, it'd be probably a good idea not to reuse it because (1) you're losing methanol, and (2) the concentration of everything else is thrown off.

Why do you boil the stain? I just pour mine at RT right on the gel and it works fine.


What do the text annotations in an electron micrograph mean?

The 1.40kX is the zoom (1400x), WD is the working distance (distance between the final lens and the object), 20kV is the voltage used to accelerate the electrons, 20μm is the scale.

I'm not aware of the other two.


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

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

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

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


What kind of big bird is this seen walking around Taipei?

I am fairly certain that this is a Malayan Night Heron (Gorsachius melanolophus).

Taiwan is listed as one of the countries where the Malayan night heron can be found. Its diet consists of small reptiles, snails, chilopods, arachnids, crabs and insects. This would explain why you have observed it bend down a lot to look for food.

Needless to say you can find more information in the corresponding Wikipedia article.

Here a photo with better resolution:

Photo by: Pete Morris/Birdquest

In addition, here is a link to a video taken in Taiwan. Does this remind you of the bird that you saw?


Why the length of UTR in the genomic sequence of gene X is too much longer than the same region in the corresponding Refseq mRNA sequences?

UTRs are involved in post-transcriptional regulation. See the wikipedia articles on the 5' and 3' UTRs. Alternative splicing of UTRs allows for exposing/hiding these regulation sites, which may then be useful for differential regulation in differing tissues.


For a PCR preparation, swing bucket or fixed angle does not make any differences. The only thing you want is that everything is soluble, in the same volume, and homogeneously mixed.

The main difference between swing bucket and fixed angle is how the pellet will be formed in the tube. Depending on the type of extraction or purification you are doing it would be advantageous to have a large pellet on the side (fixed angle) or at the bottom (swing bucket).

This article explains it in much more details if you are interested: https://handling-solutions.eppendorf.com/sample-handling/centrifugation/this-and-that/detailview/news/when-to-use-a-fixed-angle-rotor-or-a-swing-bucket-rotor/


The Journey of Man is a great book that really dives into the archaeology but also the genetic history of evolution.


What are these little leaves growing on these other leaves? (plant growing near the ocean)

These are really cool, and I am absolutely not certain of this, but I would hazard that they might be some kind of bulbil? Ferns (if I have started my ID correctly) can use them to asexually reproduce. For example the New Zealand endemic Asplenium bulbiferum grows little bulbils on the adaxial surface of its frond.


I have only used NEURON and the DIY approach for small scale simulations.

You can have a look at this comparative table:

  https://grey.colorado.edu/emergent/index.php/Comparison_of_Neural_Network_Simulators

which was last updated in 2014.
Except NEURON, GENESIS, and NEST, I have also heard positive comments about Brian.


What percentage of a Neanderthal's DNA could be in a Denisovan?

You should be very careful trying to conclude something from what is known about Neandertal genetics.

To answer question 1: NO! This is probably not what he meant. To date, we have only two high-quality full genomes of archaich humans, one being the (Neandertal from Denisova cave, called Altai Neandertal (Prüfer et al., 2014)) and one being the (Denisovan from Denisova cave (Meyer et. al., 2012)). From this sample (which is exactly one Neandertal) you cannot draw conclusion for the whole population. It seems, however, that this Neandertal individual from the Altai Mountains was indeed inbreed (high runs of homozygosity in the genome) - it does, however, not even tell us in what way her parents were related. Prüfer et al. (2014) write

  We conclude that the parents of this Neandertal individual were either half-siblings who had a mother in common, double first cousins, an uncle and a niece, an aunt and a nephew, a grandfather and a granddaughter, or a grandmother and a grandson.

You cannot say more. You also cannot say if this was due to preference in mate choice, or caused by the fact that this group was very isolated, or  that this population had an extreme small effective population size (note that it is debated whether the last two effects are actually equivalent).
To make a long story short: based on the available data it is not wise to draw general conlcusions about Neandertal mating behaviour. Altai is the only example where direct inbreeding could be shown, all other genetic data from Neandertals suggest that genetic diversity was just low.

To answer question 2: I do not really know what this means, 70% Neandertal DNA in Densiovans. I can just generally tell you something about Densiovan-Neandertal differences. The Densiovan might be the only (at least mammal) species that was defined based on genetic information alone. Alle that was found were a few teeth and a pinky bone. People thought this was another Neandertal. After sequencing the DNA from that bones to high coverage (vaguely, a measure of qualtiy), one found that the DNA falls both outside the variation of modern humans - showing that this was not a Homo sapiens, but interestingly it also clearly falls outside the variation of known Neandertal sequences - showing that this was not a Neandertal. It also became clear that Densiovans are more closely related to Neandertals than to modern humans (you might now ask yourself how this is possible with just one genome. In fact, there are more genetic data availabe: low coverage genomes, exome sequences, mtDNA and all of them show the same thing: Neandertals and Densiovans are different but more closely related to each other than to modern humans). Overall, Denisovans also seem to have had rather low genetic diversity (which by the way is also a characteristic of modern humans).
Long story short: There seem to have been admixture events between Denisovans and Neandertals but I do not know how to relate this to the 70%. Prüfer et al. (2014) detected about 0.5% contribution from Neandertals in Denisovans.

One last comment about this mysterious species (nobody says it but most people think of Homo erectus): again, Prüfer et al. (2014) found some interesting patterns of derived allele sharing between present-day Africans, Denisovans and Neandertals (this should be equal for African-Denisovan and African-Neandertal comparisons, but present-day Africans share about 7% more derived alleles with Neandertals than with Densiovans - even 13-16% in alleles fixed in present-day Africans). This is either ancient population structure (however, with very deep lineages) or, as suggested in the paper, due to gene flow from a (genetically) unknown archaic hominin into Denisovans.

I hope this clears things up a bit. Feel free to ask in the comment and I will edit the post as it might be a bit unstructured.