How do Type I restriction enzymes work? According to NCBI, type I REases have a specific target sequence but randomly make cuts at sites far from the target sequence.

How does the restriction enzyme travel from the target sequence to the distant site of restriction, and what is the point of having a target sequence if the cuts are random and far away from the target sequence?

To answer your last question first: as long as a restriction enzyme recognises a specific sequence then goes on to cut the DNA it really doesn't matter where the cut takes place, as long as the invading DNA is destroyed.

The WP page on restriction enzymes provides a useful summary of the various classes of restriction enzyme, and led me to a review about Type I enzymes here.

Unlike the familiar Type II enzymes, Type I enzymes require ATP, which they use to power their movement along the DNA, once they have been activated by binding their recognition sequence. The HsdR subunit of the enzyme (R, M and S subunits) contains sequence motifs which mark it out as being related to DNA helicases, which, of course, are able to translocate along a duplex and unwind the duplex.

One particularly striking demonstration of the DNA translocation ability of EcoK1 (a Type I enzyme) is described in

  Davies et al. (1999) The DNA translocation and ATPase activities of restriction-deficient mutants of EcoKI. J. Molec. Biol. 292: 787-796 doi:10.1006/jmbi.1999.3081

The experiments are based upon the mechanism by which phage T7 injects DNA into E. coli cells.  The phage ejects about 850 bp of the 40 kb genome into the host; the entry of the bulk of the DNA is coupled to transcription, first by host  RNA polymerase, and subsequently by the phage-specific RNA polymerase, once the corresponding gene has entered the cell. If the drug rifampin is used to block transcription then the whole process stalls. This block is overcome if the initial leader of 850 bp is engineered to contain a recognition sequence for EcoK1 whereupon the restriction enzyme is able to translocate the entire genome into the cell at 100 - 200 bp per second. Mutations in the helicase motifs of the HsdR subunit abolish this activity.


Do siblings have a bias toward believing they look different from each other? Anecdotally, I have observed (myself included) that siblings tend to think that they look less similar to each other than an unrelated observer would say. Is there any experimental data to back this up, or am I completely wrong?

You are not completely wrong but not completely right either. Some siblings tend to think they are less similar to each other, even twins. It may or may not have scientific reason, but it has sociological reason behind it. Every people in our society want to have their own separate identity and they do not want themselves to be compared with others even with their siblings.It might be also due to the result of fact that, siblings pass times with each other so often that they notice distinct differences in both their characteristics and look while ordinary people, looking at them for the first time, can not notice the differences. This is related to the reason why we can not sometime recognize people from any particular race or ethnicity at first look.


DNA extraction from agarose gel Because DNA is soluble in water, is it possible to extract PCR product by dissolving excised gel containing the DNA band of desired length in water, mashing the gel piece with a pestle, centrifuging it and then pipetting out the supernatant ?

Yes, this is possible (and I have done it uncounted number of times) - the method is called "Freeze and squeeze". What you basically do is to run the gel, cut out the band of interest (be careful with the UV light, it causes damage to your DNA and also sunburns, so wear appropriate shielding for your face), dissolve it in a buffer, then freeze it in liquid nitrogen (or the -70°C, doesn't matter) and centrifuge it at room temperature for 10 minutes. During this time the ice melts and the agarose pellets at the bottom. Take the supernatant, do a ethanol precipitation (with glycogen when you only have little DNA) and you have nice and clean DNA. No need for expensive kits and is done approximately in 2 hours.

You can find a very nice and detailed protocol here: "Elution of DNA from Agarose Gels" (The rest of the handbook is also very useful).


On the effect of polluted air on health. Is it more gradual, or more immediate? I've heard time and again that living in São Paulo (a large city in Brasil) takes 1.5 years from your life expectancy. The allegation is that this happens because of air pollution.

I am just wondering how air pollution harms humans. Is the effect cumulative? Or is it a more immediate effect that makes the elderly die sooner?

The main factors of urban air pollution are nitric oxides, carbon monoxide, and what is called in german "Feinstaub" (very small carbon-rich particles from diesel exhaust). However, do not forget heavy metals: street dust is especially metal-rich and is swept into the soil near the streets where children and farmed plants can take it up. Lead is a heavy metal that can be breathed in with the air. Last not least noise over a certain threshold is proven to be a cause of illness, even loss of life time (10 years near an airport, if I recall correctly, but airport noise is getting better while machines become more fuel-efficient).

To answer your question one would have to look at every single factor. Lead accumulates in bones and destroys your brain. I just see Brazil banned it too in the 80's so this one killer is no more.

http://en.wikipedia.org/wiki/Tetraethyllead

I have found a meta-study that reviews about 80 papers on the subject, especially the Sao Paulo studies, so this should fit exactly your questions:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3093800/


How do you knockout an E. coli gene without disrupting the rest of the gene cluster? I'm familiar with the method to build Keio collection using single-gene deletion with an antibiotic cassette. However, what happens when there are gene clusters or overlapping ORFs and you still only wish to knockout a single gene?

Let's say that we have gene A, followed by gene B so that they overlap with 100 bases. If you want to knock out only gene A, you can do the following:

PCR gene A and clone it into a vector
PCR gene B and clone it into another vector
Insert a antibiotic resistance marker at the overlapping region of gene A and B

now you don't have functional gene A and gene B

Transform your cells only with the vector that contains gene B

Now you have disrupted only gene A but you have a functional gene B.


How is the rate of gluconeogenesis controlled in the cell? As far as I am aware, all steps in glycolysis are readily reversible except the phosphorylation of glucose, the phosphorylation of fructose6 phosphate, and the phosphorylation of phosphoenolpyruvate to pyruvate. I understand how control of the rate of glycolysis can be achieved through allosteric means (for example glucose 6 phosphate inhibiting hexokinase in muscle cells, phosphofructokinase being under allosteric control of the ATP/AMP ratio in muscle or hormonal control via glucagon in liver), however how is the rate of gluconeogenesis controlled compared with glycolysis? When a cell has a high rate of glycolysis, then as the rate of forwards reaction increases the concentration of substrate for each gluconeogenesis reaction also increases. Thus there must be some way to shut off the gluconeogenesis enzymes.

I would be grateful if someone could explain how the relative rates of glycolysis and gluconeogenesis are controlled, and perhaps if this varies according to the cell type (muscle/liver cells etc).

I was also wondering whether every cell is capable of gluconeogenesis. I was considering putting this on a separate post so that there is only one question per post, but I thought that it is quite a short question so it may be better to put it here.

In mammals gluconeogenesis occurs primarily in the liver (together with the kidney to a much smaller extent). When the blood glucose concentration falls, it is the role of the liver to generate glucose for other tissues that are dependent upon it.

Hormones play a key role in this. If one considers the decrease in blood glucose concentration during starvation, this is signalled by a decrease in the concentration of insulin and an increases in the concentration of glucagon. These have differentials effect on the uptake of glucose by different tissues, depending on whether they have receptors for the hormones and the consequences within the tissues, and mass action effects of metabolites will certainly influence whether glycolysis or gluconeogenesis occurs in liver.

However, you are correct in your concern that there must be a way to prevent the futile cycling of intermediates through the different reactions of the three steps that differ between glycolysis and gluconeogenesis. The short answer to how this is accomplished is that the concentrations of various metabolic intermediates change during starvation/feeding, and that these intermediates are allosteric regulators of the reactions, switching one off and the other on. This is described in the section on Regulation of Gluconeogenesis, in Berg et al. (available on-line), from which I reproduce the  diagram below (Fig. 16.30).

Although this diagram illustrates the principle, a few words of caution about the detail are in order. First, the edition of the book this comes from is 15 years old. Second, it is not clear that all the regulatory molecules are effective in liver — some of the work may relate to bacteria. Third, much of the evidence is from studies with purified enzymes. Although it can be shown that an enzyme can be regulated by a particular effector in these conditions, it is different matter to establish that this occurs in a particular physiological condition. Thus, you will need to consult more recent and specialized sources if you are interested in particular details.


Evolution of the haplo-diplontic life cycle From wikipedia > Biological Life Cycle:

haplontic life cycle - the haploid stage is multicellular and the diploid stage is a single cell, meiosis is "zygotic".
diplontic life cycle - the diploid stage is multicellular and haploid gametes are formed, meiosis is "gametic".
haplodiplontic life cycle [..] - multicellular diploid and haploid stages occur, meiosis is "sporic".

To my knowledge, all mammal species are diplontic. It might even be true for all vertebrates (but I am not sure). In plants and in fungi, there is a much greater diversity of life cycle however. In many (all?) bryophytes for example, the sporophyte (the diploid phase) is multicellular and its life is completely dependent on the gametophyte. This diversity of life cycle lead to the following question:

What drives the evolution of the relative time an organism spend in the haploid vs in the diploid phase of the life cycle?

This post comes as a follow up to @JAD's comment here

I just want to report the finding of one paper here. I don't know much about the rest of the literature and can't comment on it.

Otto et al. (2015) investigate this question in sexually reproducing organisms. As I understand it, they assume that the amount of time spent in on phase of the life cycle is proportional to the amount of selection happening in this phase. With a theoretical model Otto et al. (2015) showed that there is a sexual conflict over the length of the haploid phase. Mothers favour a longer haploid phase while fathers favour a shorter haploid phase. The outcome of the model depends upon who is in control of the length of this phase.

For mothers, producing a baby is often costly (see Bateman's principle). As such, the mother might want to ensure that its baby has high fitness. In the haploid phase, deleterious recessive alleles are no masked by their dominant counterpart and hence can be purged out of the population. A long haploid phase, therefore allows purging of deleterious alleles and make the diploid phase more resistant which is in the mothers interest.

Among fathers, the evolutionary pressures are different. Fathers evolve to mask mutations carried by their haploid gametes (e.g., by provisioning with diploid gene products), causing their sperm to be more competitive. As such, a father has interest that the haploid phase is short.


Where can I find the common names for the zoology taxonomy? Forgive me if my question does not belong here or if I'm using incorrect terms, but I'm not educated in biology at all. I'm investigating the workings of the biological classification system.

I was wondering if there is a list somewhere of all kingdoms, orders, classes, etc., both in Latin and common names?

The Tree of Life project has a browse-able tree of all major taxa, but not necessarily all species. You can start at the root of the tree here. Tree of life uses modern phylogenetic nomenclature rather than more traditional Kingdom-Phylum-Class-etc.

Part of the problem that you will run into is that common names differ across regions/countries/languages. This is the point of species binomials. They are language-invariant.


Can I breed the most productive hen by hatching eggs from the most productive ones? Here is some hypothetical input:

I have a set of eggs.
I hatch these eggs and get chicken from them. Say, 100 hen that can lay eggs.
I have a hypothetical technology to track some parameters of each hen during their life - one of them is the moment a hen lays an egg.
I collect the data and find out which hen laid the largest amount of eggs during her productive period. I mark this one as the most productive.
I collect the eggs from the most productive hen in the generation.
GOTO 1.

Now, if I repeat this loop of death and life, say for 20 generations, hatching only eggs from the most productive hen, will it make next generations more productive and with each iteration or is it an oversimplified picture I have?

By performing this mental experiment I want to figure out if I can use it as a clear predictable factor influencing productivity of future generations.

In theory yes, so long as you maintain genetic variation within your flock of hens (e.g. by bringing in outsider males to prevent inherited diseases spreading), artificial selection will lead to a more productive flock.

However I don't think it would be predictable and not necessarily an improvement every generation, surely productivity would be influenced by lifespan? e.g. is it better to have a hen that lays 100 eggs/month for 24 months, or a hen that lays 120 eggs/month for 12 months? Not necessarily that important, but worth considering.

You would also want to keep more than one hen per generation, maybe 2 chick hens from each of the 3 most productive hens per generation, just in case you selected one that hadn't inherited the productivity traits.

I assume you've read about milk yields. And this looks like it covers the maths of heritability of egg production.


Do any animals other than humans undergo menopause? Do any animals other than humans undergo menopause?

Also, is there any difference between animals in captivity and animals in the wild as regards menopause? For example, even if menopause has been observed in a captive member of a particular ape species, do individuals of that species typically live long enough in the wild to also undergo menopause?

I guess here's what I'm really getting at: is menopause a common thing in the animal kingdom, or is it only a common thing in humans?

Yes. Menopause is common for long-lived mammals. For instance, in the wild, killer whales go in a sort of menopause as reported in 2009 by Ward et al. Front Zool. 2009 Feb 3;6:4. So it is not due to captivity. According to a Nature review, reproductive cessation has also been documented in non-human primates, rodents, whales, dogs, rabbits, elephants and domestic livestock (Packer et al. Nature. 1998; 392(6678):807-11)


Are there differences in cell membrane cholesterol levels between cell types? With different cell types, and cell functions, are there distinct levels of cholesterol in each cell type's cell membrane, or do all cell types have a similar amount of cholesterol?

I am assuming certain cell types require different levels of cell membrane stability, and as such, different levels of cholesterol in that cell membrane.

Yes, there are differences in cell membrane's cholesterol levels among different human cell types.

This table from Alberts (2002) shows the difference in cholesterol composition in a liver cell, a red blood cell and a Schwann cell/oligodendrocyte (myelin):

Table: Approximate Lipid Compositions of Different Cell Membranes

Besides that, the table shows that there is difference in the cholesterol composition among different membranes in the same cell (compare plasma membrane, mitochondrion and ER). Actually, that's a more famous difference, depicted in this figure from Lehninger (2000):

Figure: Lipid composition of the plasma membrane and organelle membranes of a rat hepatocyte. The functional specialization of each membrane type is reflected in its unique lipid composition. Cholesterol is prominent in plasma membranes but barely detectable in mitochondrial membranes.

Sources:

Alberts, B. (2002). Molecular biology of the cell. New York: Garland Science.
Lehninger, A., Nelson, D., Cox, M. (2000). Principles of biochemistry. New York: Worth.


Blood pressure during exercise What happens to blood pressure when we exercise? Does it increase, decrease, or remain the same? If it does increase, why are patients with high blood pressure recommended to exercise?

As pointed out in the answers above, your blood pressure increases transiently as you exercise because more oxygen and nutrients are consumed by your muscles. However, regular exercise increases your "cardiovascular reserve"-this means your body will be able to function well at lower blood pressures. However, caution must be taken in hypertensive patients whose blood pressures are already up the roof. In these patients, gentle exercise and life style modifications (diet, stopping smoking, weight loss etc) may reduce their blood pressures over time. This will also reduce their risk of cardiovascular catastrophes in the future.

So whilst exercise will reduce blood pressure, it is not recommended as a first line of life style modification in hypertensive patients because exercise itself is stressful initially and stress is also bad for a hypertensive patient. Hence, exercise is good but gentle exercise is recommended for hypertensive patients. But again I doubt gentle exercise will do maximum good to your cardiovascular system because the type of exercise that helps lower your blood pressure is one that makes you sweat (e.g tread mill, etc). But once the blood pressure of a hypertensive patient is under control, then they can safely exercise and this should help lower their blood pressure long term. I hope this makes sense.


Comparing BLAST and the Smith-Waterman algorithm I've been asked: how does BLAST improve dynamic programming accuracy?

I do know that BLAST is based on heuristic approach that approximates the Smith-Waterman algorithm and that the Smith-Waterman is too slow for large databases but more accurate.

Can someone settle my conflict?

So I got this answer from my lecturer:

Since Smith-Waterman algorithm is based on DP, we will get the best performance on accuracy, but there is a change that the homologous sequence is not with the highest probability (so better matching sequences will be "hidden" behind worse ones).
Since blast is based on the heuristic approach, it overcomes the disadvantage described above, by adding biological information, and therefore make it more accurate from biologist's perspective.


What is a good introductory book on plant genetics for an outsider? I am interested in plant breeding, but my knowledge about plant genetics itself is unfortunately limited (math major). Would you know of any good introductory '101' books that explain the basic concepts? As elementary as: what exactly is DNA recombination? What is an F1, F2 plant?

Many thanks and kind regards,

David

I am in a PSEO class for plant biology and ecology and I found a book online I believe you would find useful.

Click here

I've used this book to study many times even though it wasn't supplied to me. It does a great job explaining overall concept of plant microbiology. This book will introduce concepts that someone would be new to. I recommend that you give it a read, then after you read it, move to a book specifically on plant breeding.

Hope this helped!

-Sartoaster


Where can I find the genome of the L-strain coronavirus and the S-strain coronavirus? I read an interesting article about two strains of the coronavirus:
https://www.newscientist.com/article/2236544-coronavirus-are-there-two-strains-and-is-one-more-deadly/

I would like to know how the scientists used to classify a coronavirus as l-strain and s-strain.
And more specifically I would like to have the genome(The DNA) for a l-strain and a s-strain.

Article links to this publication which has all the information needed:
https://academic.oup.com/nsr/advance-article/doi/10.1093/nsr/nwaa036/5775463

It is mentioned in the paper that:

  Although we found only 4% variability in genomic nucleotides between
  SARS-CoV-2 and a bat SARS-related coronavirus (SARSr-CoV; RaTG13), the
  difference at neutral sites was 17%, suggesting the divergence between
  the two viruses is much larger than previously estimated.

Their results highlight evolutionary changes in the development of new variations in functional sites in the receptor-binding domain (RBD). These developmental variations have a spike in changes to the RBD of SARS-CoV-2 and viruses from pangolin SARSr-CoVs

How do they define S and L variations?

They did population genetics on 103 available SARS-CoV-2 genomes.
These two major types are well defined by two SNPs which show complete linkage across the viral strains.

It also important to mention that SARS-CoV-2 was found to have 96.2% similairty to a bat SARS-related coronavirus (SARSr-CoV; RaTG13) but not very similar to SARS-CoV (79%) or MERS-CoV (50%).

How do we know that there's two type?

We know there's two types because from the 103 sequenced genomes two SNP locations show significant linkage. These are SNPs at location 8,782 (orf1ab: T8517C, synoniumous) and 28,144 (ORF8: C251T, S84L).

If you have a "CT" (as in base pairs) haplotype SARS-CoV-2 you've got the L-type ("L" type because T28,144 is in the codon of Leucine). Otherwise, if you've got a "TC" haplotype you have the S-type (C28,144 is in the codon of Serine).

They found that S-type is the ancient (less aggressive version) by aligning it with other older viruses. In fact for each variant of the virus the ancestral state was inferred by alignments of SARS-CoV-2 (NC_045512), RaTG13, and GD Pangolin-Cov.

So to be more precise on my answer for finding S and L types. You sequence the genome of an infected individual (you can find these online on NCBI) align it with the current reference sequence (MN908947, NC_045512), look at the SNPs and figure if they have a "CT" or "TC" haplotype to determine S or L type.


Difference between AjuA and ajuA in biosynthesis I cannot for the life of me figure this out. In the following figure, you can find ajuA and AjuA for example.
I do understand that the lower-case ones are the genes. The arrows indicate the direction of transcription. However, what is the difference to the upper-case AjuA? The text speaks of subunits. How are the two related? When do I speak of ajuA and when would I be talking about AjuA?
I would also be happy if you could point me in the direction of some literature about the basics of this kind of notation.
PS: I do understand the mechanisms of the biosynthetic route and am familiar with the different domains in the modules as well as PKS and NRPS modules.

It's just the nomenclature:

  Bacteria: Gene symbols are typically composed of three lower-case, italicized letters that serve as an abbreviation of the process or pathway in which the gene product is involved (e.g., rpo genes encode RNA polymerase). To distinguish among different [but related genes], the abbreviation is followed by an upper-case letter (e.g., the rpoB gene encodes the β subunit of RNA polymerase). Protein symbols are not italicized, and the first letter is upper-case (e.g., RpoB).

[source]

You can check out the Wikipedia article on Gene Nomenclature for more information.


What does microglia process length tell us? I'm reading a study investigating traumatic brain injury and alcohol consumption and the researchers measured microglia process length as an indicator of brain damage. I was wondering what that would indicate and how does it an imply brain damage?

Part of this question is due to the function of microglia in the healthy brain (as we currently understand it).  The general idea is that microglia in a healthy brain are in "surveillance mode," and have long, thin processes that extend of the cell body to monitor the environment.  It would be like beat cops splitting up and walking the streets when no crime is reported, they're just monitoring one large area by spreading everyone out.  However, when some insult occurs and microglia are activated (which just means they get into a mode responsive to some insult or injury), which results in them having shorter processes and enlarged cell bodies to focus on the damage done in their immediate vicinity.  This would be like one of the beat cops seeing a crime, then calling for back-up.  Now the focus is on the scene of the crime or site of damage.  Therefore, if your microglia have long, thin processes, everything is pretty much normal because these microglia are not activated.  However, having a lot of microglia with short, thick processes indicates that they are activated in response to some injury or insult.  This is why a common practice is to use microglial process length as an indicator of microglial activation and, in turn, some form of damage to the brain.

In shorter terms:

Long, thin processes = lack of microglial activation and little to no brain injury
Short, thick processes = microglial activation, indicative of brain injury

My source is just my experience in neuroscience and reading these types of papers, but there's more information on microglial activation here: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5431479/ which includes some discussion of process length and morphology.


What is the difference between osmotic potential and osmotic pressure? Which term is used to calculate water potential? Does osmotic potential mean the same as solute potential?

Osmotic pressure: pressure applied by a solution to prevent the inward flow of water across a semi-permeable membrane.

Osmotic potential: the potential of water molecules to move from a hypotonic solution to a hypertonic solution across a semi-permeable membrane.

Osmotic pressure can be calculated using the following formula:

$$Π = iMRT$$

where
$Π$ is the osmotic pressure in atm

$i$ = van 't Hoff factor of the solute.

$M$ = molar concentration in mol/L

$R$ = universal gas constant = 0.08206 L·atm/mol·K

$T$ = absolute temperature in K

The following page has a worked out example.

As for your question on solute potential vs osmotic potential, the answer is that they are indeed the same. You can compare the formula for $\Psi_{\pi}$ on the wikipedia page and the page of this pearson textbook. These formulas are the same:

$\Psi_{\pi} = -Π =-iMRT$

So there's a simple relationship between osmotic pressure and osmotic potential.


Mice that have been reconstituted with geneX-transduced cells I read this article in the following:

  ... Mice that have been reconstituted with geneX-transduced cells

Now, someone who is not familiar with animal sciences, what does this exactly mean? It is in the context of hematopoietic stem cells. I have two possible interpretations as a result:

An Hematapoetic stem cell with geneX was successfully transplanted into the mouse
The mouse cells (from the embryo) were engineered to contain geneX, and hence the mouse has been reconstituted with geneX transduced cells

Are any of these correct? If I am wrong please let me know!

Your second interpretation is correct.  The mice have been reconstituted from stem cells that were "transduced" (using a viral vector) with a construct containing the appropriate geneX. The link gives comparison of transduction vs. transfection.

https://www.vectalys.com/blog/what-are-the-differences-between-transfection-and-transduction-222


Why can't this be 1st meiotic division non-disjunction as well? The child has gotten 2 "sick" chromosomes from his dad and 1 healthy from his mom, leaving it with trisomy 13.
I can see how this can happen in the second meiotic division of the father but I can ALSO see how this can happen in the FIRST meiotic division by non-disjunction.
Let me illustrate both ways which I see it and you can tell me where I go wrong as my book only illustrates that is the second division:

The black is the healthy chromosome and the red is the "sick" one. As you can see, we should end up with a double sick chromosome in both cases??

Non-disjunction and trisomy 13.

Why can't this be 1st meiotic division non-disjunction as well?

It absolutely can be 1st meiotic division non-disjunction as well. Patau syndrome can occur as a result of either meiotic non-disjunction event, and furthermore a mosaic form of the disorder can occur after mitotic non-disjunction.
Non-disjunction generally.
Non-disjunction can occur in meiosis I, but it's not necessarily the same result as non-disjunction event in meiosis II. This image helps describe the formation of the gametes from non-disjunction events.

(source: bioninja.com.au)
The most obvious point is that there are more aneuploidy cells born from a meiosis I non-disjunction event than a meiosis II non-disjunction event.
Furthermore non-disjunction occurs between homologous chromosomes in meiosis I or between sister chromatids in meiosis II. Was this subtlety perhaps what your lecturers/teachers were trying to describe?
Confusion somewhere in the question perhaps.
I think the problem comes from your first diagram, which appears to be an inaccurate sketch of what trisomy 13 looks like in a karyotype. This is what trisomy 13 actually looks like:

(source: iupui.edu)
How non-disjunction leads to a disease karyotype.
Lets pretend that the 'long' chromosomes in the first diagram of this answer are chromatids of chromosome 13. Thinking about the fusion event between gametes - the aneuploidy (n+1) gamete formed from either meiotic non-disjunction event and a normal (n) gamete could fuse to make the trisomy 13 result shown in the karyotype above; there would be three 'long' chromatids rather than two.


Is Richard Dawkins's interpretation of the theory of evolution circularly? I think we are all familiar with the basics of Dawkins's theory of evolution. In a nutshell: All creatures are nothing but vehicles of genes with the sole purpose of passing through these genes, and in the case of human beings besides genes also memes are involved.

Isn't this interpretation of evolution circularly:
"Why do all organisms exist? Because the purpose of organisms is to pass on genes which have the ability to develop new organisms, thereby creating new organisms under all kinds of environmental pressures". In short: "Life exists to produce new life", which is a circular expression because, in the reason we search for life, the term "life" (for which we try to find a reason) is used.

I think there are more "friendly" interpretations of evolution, of which I have no doubt that it took place.You can interpret evolution for example from a less egoistic perspective, and say evolution takes place to give new organisms a chance to live. Ande, in the case of human beings, create memes to let other people enjoy them (and not just to let your memes live further in other human beings).

If we follow Dawkins's interpretation then the scientific meme is self-undermining because the way we use science is damaging the earth to such an extent that it's the question if the earth will face a long-term future.

The following is more an extended comment than an answer...

Why the question is off-topic

Your question has actually nothing to do with biology. You are looking for a purpose behind the existence of organisms. Science does not care about purpose, nothing has a purpose, everything just happen mechanically. If the theory of evolution gives you a bad feeling, then I am sorry for you that it does but that point is not to be discussed on a science forum. I am voting to close for this reason.

Tautology

Please note that evolution is the science that has for goal to explain the change in allele frequency through time. The process studied is a continuous succession of reproduction and therefore in some respect a repetitive process but it does not make the explanation of how change in allele frequency occur a tautologic explanation. You will note by the way, that evolution does not explain the origin of life, this is the role of another of field of biology that we call abiogenesis.

Did you say Dawkins's theory of evolution?!

I often get a little mad when people write Darwin's theory of evolution thinking this is a modern concept. But writing Dawkins's theory of evolution is even worst. Dawkins is foremost a popular science communicator, so there is really no such thing as Dawkins's theory of evolution. Dawkins was also a researcher before and he brought some knowledge that allowed to grow our theory of evolution which we call the modern evolutionary synthesis (some argue that we should rename it Extended evolutionary synthesis in the light of recent discoveries).


Were Telomeres the Master Key to Abiogenesis Knowing as we do now that all manner of complex organic molecules and viscelles/micelles form spontaneously in various environments, from hot vents perfect for basic hydrophobic H-C fatty acids and stable charged H-C-O-P hydrophobics - to volcanic glass micro-chambers, clay-layer geometry and water ice fractal symetry,  that all combine to create ideal nanoscale everywhere rapid self assembly scenarios for various amino acids etc that in turn can form RNA like segments and combinations... I can't help but wonder what scenario is best situation pre-biotic that can form Telomeric sequences.

It seems to me, an instinctive feeling after viewing so many bioscience and life origin videos, that in all the random prebiotic assembly and disassembly of molecules, the perfection of replication lies in repetition that first needed a master start and stop sequence control, as master of other sub gene start stop codons.

Of course a myriad of biophysics factors come into play in origin theory and I am far from expert but I wonder if anyone can provide solid
references about abiogenisis and telomeres?

Tough question to word here, and too vast a topic when I try and narrow the web searches.  However, the amino squences for telomeres are finite I believe and so before life kept repeating itself what molecules in what environment crates the combination best?

No, they weren't. Interesting hypothesis though!

However, that hypothesis is missing a very important piece of information: prokaryotes don't typically have telomeres.

Because their DNA is typically circular, rather than linear, telomeres aren't necessary, and there is no shortening problem.

See the Wikipedia page on telomeres for more information. There are various theories on the origins of telomerases and telomere evolution, check out Google Scholar.


Are sensory mechanoreceptors and mechanical nociceptors the same type of neurons or are they different? I always supposed the neurons / receptors which transmitted touch and pain were the same, since they react to stimulus which are the same but with different intensity, and they just sent a stronger signal in the case of something that has to be interpreted as pain. Though recently I've read some articles that imply they aren't, even so they don't say it directly. Reading more information I found this,

A nociceptor ("pain receptor") is a sensory neuron that responds to
damaging or potentially damaging stimuli by sending “possible threat”
signals.
Types and functions
Mechanical nociceptors respond to excess pressure or
mechanical deformation.

Nociceptor
Then,

Are sensory receptors neurons?
Receptor cells are specialized neurons

Are sensory receptors neurons?
And finally,

Sensory receptors are primarily classified as chemoreceptors,
thermoreceptors, mechanoreceptors, or photoreceptors.
Mechanoreceptors detect mechanical forces.

Sensory receptors
This doesnt give me a definitive answer, but it tells me both "sensory mechanoreceptors" and "mechanical nocireceptors" are neurons which responds to pressure/ mechanical forces. Are they supposed to be the same types of neurons named differently by different authors, or are they different types of neurons?

Short answer
Nociceptors are different from mechanoreceptors.
Background
Mechanoreceptors in the skin have specialized dendritic regions that facilitate their specific role in sensing different types of mechanical force, e.g., pressure receptors (Merkel’s disks) versus vibration receptors (Pacinian corpuscles and Meissner's corpuscles). See Fig. 1 for schematic representations of these types of receptors (Iheanacho et al). By contrast, pain receptors (or nociceptors) do not have specialized dendritic regions and consist of free nerve endings that respond to harmful mechanical forces (Purves et al., 2001).

Fig. 1. Skin receptors. source: Teach Me Phsyiology
References
- Iheanacho et al., Mechanoreceptors. In: StatPearls. Treasure Island (FL): StatPearls Publishing (2020)
- Purves et al., eds. In: Neuroscience 2nd ed. Sunderland (MA): Sinauer Associates; 2001. Nociceptors


When happens when pollen grains land on the a part other than the stigma of a flower of the same species? When happens when pollen grains land on the a part other than the stigma of a flower of the same species? Would the pollen be transported to the stigma or would it just sit where it landed and nothing would happen?

Sometimes, the morphology and the topology of the flower structure is such that the pollen grains falling on certain parts are gravitationally (or hydrostatically) drawn towards the stigma.
I remember having read that the waxy streamlined stigma of submerged hydrophytes (Vallisneria, Hydrilla)  creates mini vortices around it during steady water flow. These vortices then pull nearby pollen, (which may be sitting on nearby flower parts) towards itself. Certain hydrophyte morphologies also maximise the water flow towards stigma, which in turn gathers pollen incident elsewhere on the plant and bringing in towards the stigma.(For example, the streamlined and bladder shaped hydrophyte flowers have stigmas at their centre)

Another way to do this is via the common sloping surface of the petals or the perianth, which on gathering pollen, gravitationally push them to the centre of the flower where the stigma usually resides. The entire inflorescence stalk might be modified into specific shapes to do this. The common pyramidal arrangement of the inflorescence (broad at the base, tapering towards the apex) helps in gathering the pollen incident on non-stigma parts of the apex region at the bottom.

Apart from this, pollen falling elsewhere, may again be taken up by the agents of pollination. But I believe the formation of pollen tube never occurs at any place other than stigma. Nor does any re-absorption take place.

It is also worth mentioning that just because pollen falls on the correct stigma does not ensure fertilization. Absence of stigma maturity/receptivity, synergid abnormality, inviable pollen etc could still hinder fertilization.

[I am not perfectly aware about studies on whether any chemical reaction occurs if pollen lands on places other than stigma. But I doubt it, since the chemical specificity required to begin the pollen tube formation is very high in most species.]


Gene density percentage What do we mean when we say that: Haemophilus influenza genome is 85% genic.
How do we measure gene density in percentage, especially for the above-mentioned case?

It means that 85% of its genome is coded for proteins (ORFs). The other 15% not, so these can be regulatory elements, repeats, or other.

You can measure that by measuring the total length of all ORFs, and compare it with the total length of the genome.


Why is it important to study chromatin to understand cancer? Many labs and many projects in biology institutes and university departments have been starting to study chromatin. Chromatin states, chromatin interactions, chromatin loopings, chromatin behaviours, etc. seem to have become the new priority of cancer scientists.

I'm new to this field so there are many things that I still have to understand about chromatin and its relationship to cancer. These questions just flowed into my mind:

What is the relationship between chromatin and cancer?

In cancer research, why is it so important to study chromatin and how chromatin loopings form?

What do scientists would like to find out about chromatin when they investigate it?

Most cancers involve, in addition to genetic changes, a whole suite of epigenetic changes that orchestrate changes in transcriptional profiles. Additionally, multiple epigenetic modifiers (Eg - EZH2) are associated with worse prognoses.
There is also the fact that chromatin modification machinery is very highly mutated in cancers; examples include EP300 - a histone acetyltransferase, and members of the SWI/SNF nucleosome remodelling complex. The study of epigenetic factors needed for the continued transcription of oncogenes like Myc has also led to the formulation of potential therapeutic strategies (Check out some of the literature on inhibiting Brd4 to silence Myc in certain settings).


Could cyanobacteria thrive with very high CO2 concentrations and almost no oxygen to start with? Has there been research to see if cyanobacteria could live in high levels of CO2, like in the atmosphere of Venus ?

Because cyanobacteria caused the Great Oxygenation Event one might expect that they could !

I like this exobacteria theory question because they implement a strategy for answers that may go against or for the idea of out of space terraforming. Simply providing detail won't be enough in this case. Cyanobacteria are not very durable in Venus atmosphere. The temperature of Venus is of much higher average and they will be feeding of the atmospheric pollution as well causing an oxidative affect on the cell when too much co2 gives off oxides. But more importantly hydrogen buildup in the protein folds could cause inhibitory stress (prevents binary fission). So no I would not use Cyanobacteria as a space project. But please go against me if I'm false.


What are some effective strategies for testing whether a trait is an adaptation? Although signs of evolution are to be found everywhere across taxa, it sometimes seems difficult to discern whether a trait is a retained accident or an adaptation. It also seems like there is a temptation in people to come up with just-so stories to explain traits as adaptations. What is an effective strategy for coming up with tests to determine whether a trait is an adaptation or not?

See if the trait gives any significant advantages as compared to absences of trait. Also if the trait is present in almost all organisms and no variation is found, then see if it has any use. Like appendix is found in almost every human; although it can be surgically removed, normally it is present, but is useless in humans.


Find the concentration of free receptors in a solution of 90% free ligand and 10% receptor-ligand complex, knowing only the value of kD I could use some guidance on how to utilise the equation for the disassociation constant kD to find the concentration of free receptors [R] in a solution containing 90% free ligand [L], and 10% bound [RL] complex.

The Kd of the receptor-ligand interaction = 10^-8 mol l-1

Where Kd =  ([R][L])/([RL])

I assume as a percentage I could state, [L] = 0.9 and [RL] = 0.1, but am not sure if I'm taking the right approach.

Any clarification on this would be appreciated.

One big thing you're missing is units: Concentrations here must have concentration units - they can't be dimensionless numbers or percentages.

So one of the things you need to figure out is how to convert the percentages into concentration units. In this case, it's difficult to do directly, but we can apply a bit of algebra to figure it out. We're talking about 90% and 10% of the ligand in different forms, but we don't know anything about the total amount of ligand - that's alright, we'll just represent the total concentration of the ligand as $\ce{x mol \cdot l^{-1}}$. Therefore, we can now state that:

$$ \ce{ [L] = (0.9x) mol \cdot l^{-1}}$$
$$ \ce{ [RL] = (0.1x) mol \cdot l^{-1}}$$

Now the other bit of information we have is the equation for Kd:

$$\ce{ K_d = \frac{[R][L]}{[RL]} }$$

So we're looking for $\ce{[R]}$ (with associated concentration units!), and we know $\ce{ K_d }$, $\ce{[L]}$ and $\ce{[RL]}$ - or at least up to the unknown of $\ce{x}$. But, if you substitute the values you do know (including the factor of $\ce{x}$) into the equation and do some algebraic manipulation, I believe you'll find it doesn't actually matter what the value of $\ce{x}$ is - it should cancel out.

Note: If the value of $\ce{x}$ doesn't matter, why did I bother with the whole rigmarole of including it? Why didn't I just substitute 0.9 and 0.1 directly?

Well, the answer to that is my lead sentence - the concentrations in the equation should have (compatible) concentration units. If you don't have concentrations, you're using the equations incorrectly. (Look into the concept of dimensional analysis for a valuable way to help make sure you're doing many (but not all) calculations like this correctly.)

While for this specific problem things worked out nicely if you substitute the fractions/percentages directly, that's not a general solution. Depending on the exact setup of the problem, the $\ce{x}$s may or may not cancel cleanly. You may have to use some other equation/knowledge to put additional constraints on the value of $\ce{x}$. The only way to know that is to properly account for them from the start.


For how long can a person drink sea water? How long could a person of lets say 18 years be able to drink sea water without getting too much into trouble ? Or can a person drink it without noticing that it is a very bad idea ? I don't mean in just 1 drink session but like can one manage a day or two ? Can one drink it and go to sleep and be still healthy (although very thirsty) in the morning ?

(this is just a hypothetical question, I'm not a scientist at all, I'm not sure what tags to use actually)

Additional brainstorming:

kidney failure
any other organ failure
dying of thirst
...

(source: free.fr)

Alain Bombard

He is a french biologist who voluntarily tested how many days a man can survive drinking seawater and how?

Biologist point of view

Sea contains ~3.5% of salt$^1$. Our kidney separates the waste from water and excrete them in urine provided the salt content is less than ~2%.$^2$
So, it will take the water already present in the body. Causing excessive thirst and dehydration, eventually cause death.

Alain's Experiment

  Just one spoon of seawater at 20 minute intervals, drinking very
  slowly and letting the saliva in your mouth reduce the saline in the
  water you have swallowed.

Though he survived 65 days (From and including: Sunday, 19 October 1952
to Tuesday, 23 December 1952, ~4,400km) of his journey and lost 25 kg of weight, this result is never successfully reproduced.

Source:

http://oceanservice.noaa.gov/facts/whysalty.html
http://paradise.docastaway.com/drinking-sea-water


IgA-s in an immune system vaccined intramuscularly against Hepatisis A As IgA are immunoglobulins associated with secretion and mucosis membranes, I am interested whether after intramuscular vaccination with Hepatitis A vaccine IgA antibodies will be produced by the immune system before an actual infection?

Also, would they be secreted into breast milk, intestine lumen etc. before the infection coming in a traditional (gestational) way?

Or does it take to have the antigen presented at the mucosis mambrane to start IgA production or secretion?

Antibodies are produced after exposure to cognate antigen.

Remember that B cells start off expressing membrane IgM and/or IgD. IgA requires class switching recombination at the B-cell receptor locus to the IgA isotype. Further differentiation of the B cells to antibody-secreting plasma cells results in soluble IgA production and immunologic memory to the antigen. Whether you'll get IgA, IgE or IgG antibodies against the vaccine will largely depend on the signals they get in the muscle, however (Figure 1). I think IgG is largely a result, since the tissue antiviral response is often interferon gamma (Figure 2).

The importance of intramuscular vaccination is outlined here, just in case it wasn't apparent.

Figure 1. Activated helper T cells that can recognize the same antigen mediate the class switch by providing co-stimulatory signals and cytokines. Source

Figure 2. Class-switching continued. Source: Parham, The Immune System, 4th Ed.


Dynamic mutation and huntington's I read that Huntington's is a disorder caused by dynamic mutations in the DNA, which means that a triplet sequence of DNA changes from generation to generation. Say we have the sequence ATGATGATGATG. The child of this person with have ATTATGATGATG and the grandchild will have ATTATTATGATG etc.
This means that Huntington's will be worse (debut earlier) the longer the generation lasts.

My questions are: Is my understanding of dynamic mutation correct? Is there no MINIMUM age where Huntington's will debut? In other words, if a generation is very long and has Huntington's, can a baby have symptoms at birth?

At the moment, the youngest diagnosed Huntington's case was 2 years of age. This paper appears to discuss not only this boy's onset, but also the diagnosis of symptoms in the early-onset disease.

Here they research a link between age-of-onset and the length at which the repeats are.

The thing is that these repeats won't just constantly get longer. There is "slippage" during replication which causes the repeats to get longer, but it also causes the repeats to get shorter. It's possible that mom's bad chromosome may have been inherited but because of the slippage, it no longer produces Huntington's symptoms.

This image doesn't show actual mechanics of it happening, but it shows how the repeats can be added and subtracted.

As it turns out Kayser et. al decided to look at chimps and humans to discover which of two proposed mechanisms are more likely. Their findings suggest the slippage is closest to the "heterozygote instability model".

The model suggests:

  heterozygous loci might have a higher mutation rate due to mismatch repair events that occur during synapsis

To answer your question in short:

It appears that the "minimum age" so far is 2, however, that does not mean that it hasn't occurred earlier. Huntington's is characterised by a change in motor skills, and if the change occurs before birth it might not be noticed. In theory, it is possible that Huntington's symptoms can start pre-birth.


Are coronaviruses gaining an evolutionary advantage? So there are 7 known strains of coronavirus that are known to infect humans: 4 that cause the common cold (229E, NL63, OC43 and HKU1), and 3 that have been known to cause acute respiratory infection (SARS, MERS and now COVID-19). They're all beta-coronaviruses except for 229E and NL63.
I can't help but notice the latter 3, which also happen to be the most serious, have all emerged very recently and within less than a decade apart from one another. I tried to find out how long the common cold strains have been around for, but can't find too much information on that (I found one article from science daily that says the common cold could have originated in birds around 200 years ago, but that's about it).
Does anyone have more information on this? Is the fact that SARS, MERS and COVID-19 emerged so close to one another a trend or just a coincidence? Are there any notable scientists who've noticed this and have an explanation as to why?

It is not a coincidence, but it doesn't have to do with sudden evolutionary changes, rather with human behavior.
The three viruses you mention are zoonotic — they can infect different species, including humans.
Increased development of formerly untouched lands is bringing people into contact with animals (and existing, but formerly unknown zoonotic pathogens) in greater numbers.
Humans bring the virus back to concentrated human populations — cities, say — either being infected themselves, or bringing back infected animals for consumption. This increases the opportunities for further spread.
With the help of global leadership that is corrupt, incompetent, or antiscience, the multiplier effect of repeated infections in cities turns a small pool of cases into a pandemic. Rinse and repeat.

The risk of emerging infectious diseases such as COVID-19 from animals is on the rise, in large part because of our environmental footprint and the blurring between the natural and the built environments. Increasingly, humans, livestock and wildlife are interacting in new and unexpected ways, bringing new species – and their resident infections – together with unpredictable results.
Climate change is accelerating the loss of animal habitats and the ways humans change the land. Cutting down old-growth and rain forests, which harbour a rich biodiversity of life, to create agricultural or pastoral land potentially brings people and livestock in closer contact with previously isolated populations of bats, and other animals harbouring previously unencountered disease. In turn, biodiversity loss threatens natural food sources which means animals seek other sources of food found where people live. As climate change causes large disasters like floods and drought, human food sources are also lost, and growing food insecurity pushes people to further encroach on animal habitats, increasing animal contact and contributing to the trade in wildlife.
The speed and magnitude of environmental change has implications for future epidemics and pandemics. The first few cases of COVID-19 have been traced back to a ‘wet market’ that contained wild animals sold for food or medicines. Such markets can be ideal environments for zoonotic spread as the unusual mixing of animals (which is not common in the wild) can provide opportunities for viruses to jump between species, and potentially then to people.

Development isn't just loosing coronavirus — there are other pathogens that have been loosed by encroaching on their natural reservoirs:

We invade tropical forests and other wild landscapes, which harbor so many species of animals and plants — and within those creatures, so many unknown viruses. We cut the trees; we kill the animals or cage them and send them to markets. We disrupt ecosystems, and we shake viruses loose from their natural hosts. When that happens, they need a new host. Often, we are it.
The list of such viruses emerging into humans sounds like a grim drumbeat: Machupo, Bolivia, 1961; Marburg, Germany, 1967; Ebola, Zaire and Sudan, 1976; H.I.V., recognized in New York and California, 1981; a form of Hanta (now known as Sin Nombre), southwestern United States, 1993; Hendra, Australia, 1994; bird flu, Hong Kong, 1997; Nipah, Malaysia, 1998; West Nile, New York, 1999; SARS, China, 2002-3; MERS, Saudi Arabia, 2012; Ebola again, West Africa, 2014. And that’s just a selection. Now we have nCoV-2019, the latest thump on the drum.

The three viruses you mention are serious. MERS and SARS have high fatality rates. The third (SARS-CoV-2) is highly contagious. These attributes disrupt everyday life.
But the aforementioned and other viruses are also serious for similar reasons. Zika, for instance, can cause life-altering birth defects, has been known about for decades, and human-caused climate change has been enabling it to spread to more densely-populated areas.
Evolution — natural selection — takes place over thousands to millions of years. Human behavior has changed the earth only within a few hundred years, much of it in the last century or so.


Why does this oxygen duration chart have increased times above 30,000 FT MSL? This oxygen duration chart from an airplane shows the amount of time a pilot can be on oxygen at a specified altitude (in 1000s of feet).  For example, the chart shows two pilots able to cruise at a cabin altitude of 35,000 FT MSL for 182 minutes using a diluter demand system or 192 minutes using 100% oxygen.
I have one question.

Why does the oxygen duration chart show increasing times above 30,000 FT MSL?

This is related to the diluter demand system, O2 present in the cabin, and tracheal pressure.

The diluter demand system is designed to compensate for the
short-comings of the continuous flow system. It   gives the user oxygen
on-demand (during inhalation) and stops the flow when the demand
ceases (during exhalation). This helps conserve oxygen. Additionally,
the incoming oxygen is diluted with cabin air and provides the proper percentage of oxygen, depending on the altitude. This system
is typically used at altitudes up to 40,000 feet.

Source: Oxygen Equipment: Use in General Aviation Operations - Federal Aviation Administration
When you get at altitudes higher than 35,000 feet you're more or less totally reliant on the oxygen provided by the diluter, that's why the diluter demand is very close to the cruise time. If there's low air pressure in the cabin above 35,000 feet there won't be enough oxygen for normal body function, and you run the risk of becoming hypoxic within half a minute.

Toe of Useful Consciousnees (TUC) per Effective Performance Time (EPT)

Look at the chart below:

Tracheal oxygen partial pressure starts at 149mm. Hg for sea level and can drop to 20 at 40,000 feet. If oxygen is given according to the % supplement O2 required for inspired air, the tracheal pressure stabilizes back to what it is at sea level. Above 30,000 feet, tracheal oxygen partial pressure cannot be maintained at 149mm. Hg. Therefore you need to use the diluter longer to at least maintain it close to 149mm. Hg. Or at level where the mm. Hg. isn't extremely low.
The required mean tracheal oxygen partial pressure can be different at the same altitude depending on the liters of O2 per minute BTPS (Body Temperature and Pressure Saturated) being inspired.
Source: Introduction to Aviation Physiology
Fore example, according to 14CFR 23.1443:

(ii) At cabin pressure altitudes above 18,500 feet up to and including
40,000 feet, a mean tracheal oxygen partial pressure of 83.8 mm. Hg
when breathing 30 liters per minute, BTPS, and with a tidal volume of
1,100 cc. with a constant time interval between respirations.
(2) For each flight crew member, the minimum mass flow may not be less
than the flow required to maintain, during inspiration, a mean
tracheal oxygen partial pressure of 149 mm. Hg when breathing 15
liters per minute, BTPS, and with a maximum tidal volume of 700 cc.
with a constant time interval between respirations.

So, at above 30,00 feet you will use most of the diluter demand oxygen to preserve tracheal pressure until the plane has stabilized. At lower altitudes the diluter demand is lower because you can reach safer altitudes faster.


Was there ever a very first Homo sapiens? My friend keeps saying that there was a first Homo sapiens. Meaning, there was a very first human being that was ever born.

I can't really understand what she means to say from a selection/gene mutation perspective. I can't understand how there would be anything that could be considered the very first human being.

Was there ever a very first, singular human being that could be discerned as such?

No. It is important to distinguish "species" as a human system of classification, and "speciation" as a biological process. Except in cases like chromosomal speciation (changes in ploidy), speciation takes a long time. Probably thousands of years between some initial restriction of gene-flow, and fixation of a specific identifiable trait, present in all individuals of a species, and not present in any others. As a human system of classification, the taxonomists who define species would all understand that speciation is a process that occurs over time, although they may make some arbitrary distinction for convenience. For example, a node on a cladogram symbolizes an instantaneous process of species bifurcation, but this is understood to be an unrealistic simplification.


Independent contrasts with non-homologous traits I have morphometric measurements for a trait across various animal taxa, and would like to study the relationship between the size of this trait, and the animals' body size. In theory, I can account for the non-independence of the data with phylogenetic methods, such as independent contrasts. However, I have very different groups in my tree (for example insects and lizards), and even within more closely related groups, the structures are often not homologous. Does this present a problem for independent contrasts/phylogenetic least squares? For example, the structure is not homologous between ants and flies, yet every (sensible?) tree would treat a fly as more similar to an ant than to any lizard. Is this justified if structures are analogous? If not, are there any ways to deal with this problem?

When you calculate the PICs of a trait, you are making a statement about how that trait evolved. The purpose of PICs is to account for phylogenetic non-independence. However, when you are comparing two analogous traits, those two traits are in fact phylogenetically independent of each other; they do not share a common origin. Thus, I think it would be an error to perform PICs on analogous traits because those traits do not share an evolutionary origin.

How to deal with this problem would depend on the specific question you are asking. One thing to do would be to perform PICs on each trait independently on just the portion of the tree that that trait occurs so you are not comparing analogous traits.

You've probably already read this, but I recommend that anyone who hasn't check out Felsenstein's 1985 paper describing the PIC method.


Local storage of NCBI database in MongoDB My short term goal in a project is to build a local database of the NCBI dbSNP database. The data and schema are available on the FTP site(). I was going to implement the database using MySQL, but I just learnt about MongoDB. Is it possible to somehow convert the sql schema code to mongoDB architecture? Also, are there any real advantages to implementing the dbSNP database as MongoDB?

I've played with mongoDb.  It is a nearly schemaless data store - each record (analogous to a row) can have nearly any entry name set except for a unique ID that mongoDb uses.  In practice most of your records will have the same labels and names

Leaving SQL for noSQL is turning out not to be a great win.  MongoDB will excel in retrieving records quickly and processing records by their content.  It has some constraints too compared to SQL.  It requires that the main index be stored in RAM, which might or not be an issue.   For very large datasets mongoDB can be configured to shard the data automatically - splitting it up over a cluster of machines for high throughput fast processing applications.

If you need flexibility in your data record and you have a good machine (or a good cluster) to put it up on it could offer some advantages. We have a reasonable store of dbSNP on a recent MySQL machine and it performs okay.  Not thousands of transactions a second, but we can do reasonable throughput of record processing.


When gene editing are both chromosomes in a pair changed? Sorry for the possibly confused question, my knowledge of genetics is limited to medical training only but I have a question.

Are gene editing techniques such as CRISPR used on both of the chromosomes in a pair or just on one of them?

Some of the general searching I have done suggests that it can hit one or both. Is there a preferred outcome?

Gene editing using CRISPR-Cas9 can result in both heterozygous and homozygous conditions. It is just the event of probability. But even if u get heterozygous line, making it homozygous is not very difficult. You just have to cross two heterozygous line and screen for homozygous line through markers.


How does mutation cause natural selection? and is it common in protists or prokaryotes? Why is it inevitable that evolution by mutations alone should be a common cause of evolutionary change in most natural populations? And do you expect mutation-driven evolution to be more common in typical protists or typical prokaryotes? Why?

Your question, as I understand it, concerns the relative role (compare to natural selection and drift probably) of mutation in evolution. But evolution is not one process. Mutation and natural selection are processes that influence populations in very a different manners. At first sight, it seems to me that it does not make sense to weight the important of mutation versus other processes such as selection. But again, in what term would weight these processes?


Why does flu vaccination only work against specific strains? I was wondering why the flu vaccination doesn't protect us from all different types of flu. I know there are 3 major groups A, B and C and they mutate really fast. For example Influenza A virus has 2 different proteins on the surface hemagglutinin (H) and the neuraminidase (N). There are 18 different hemagglutinin subtypes and 11 different neuraminidase subtypes. So if they produce a vaccination which covers 187 of the virus (from H1N1 to H18N11) wouldn't it mean that the Influenza Type A could be eradicated from the world ? And wouldn't it work the same way for Type B and C?

I'm going to try and focus on the latter part of your question; if you want to know why the tri- or quadrivalent flu vaccine doesn't provide protection like many other vaccines, that's already been answered.

Anyway, the main reason we can't is because there are simply too many.  You say 187 (not sure why, 18*11=198) but the truth is that not all H1s are the same.  The different subtypes constantly mutate, so one H1N1 may not be the same as another H1N1.  There are hundreds upon hundreds of flu types, constantly changing.  And that's not even accounting for type B viruses.

When you make a vaccine, you need a certain amount of protein.  The major quadrivalent vaccine study used 15µg of protein of each strain.  The more protein you put in, the bigger the vaccine, the more it hurts, and the more likely the body is to have a significant negative reaction.  You'd have to test all of them as well - the FDA doesn't usually work on a "three is safe, four is safe, so hundreds is safe" principle.

Plus, you have to MAKE all that protein.  We're not very good at making enough for the tri- or quadrivalent vaccines now, much less hundreds or thousands of times more.  We simply don't have the capacity for that level of production.  Even if we could, it's not likely that immunity to all strains would take.  Besides, erradication is unlikely because there are large animal flu reservoirs (avian and swine, most famously) that can and will jump over to humans.  That's the piece everyone forgets about smallpox - with no animal reservoir, it was easy to eradicate.

That's not to say the cause is lost.  Intense research has begun on universal flu antibodies, and it looks somewhat promising.


What determines sex in birds? Is there production of TDF in birds? If so which gene produces it?

Sex Determination System

Birds have a ZW sex determination system meaning that males are the homogametic sex. Or yet, in other words, males have two Z chromosomes while females have one Z and one W chromosome. You might want to have a look at Do males of all sexual species have Y chromosomes? for a short review of the diversity of sex determination system.

Dosage compensation

In birds dosage compensation exist but appear quite different than in mammals (Mank and Ellegren, 2009; Mank et al., 2011; Uebening et al., 2015; Naurin et al. 2009)

Sex determining locus

The DMRT1 gene on the Z chromosome appears to be important for male sex determination by affecting the testicular marker, SOX9 however it might not be the whole story (Smith et al. 2009). It is possible that several loci are involved in determining sex in birds.


What do Illumina HiSeq/MiSeq paired end reads look like? My understanding is that paired end reads from the Illumina HiSeq/MiSeq platforms looks something like this:

R1:
    AAAAAACCCCCC
R2:
    GGGGGGTTTTTT

Where the reads found in R2 are the reverse complement of those found in R1. This does not appear to be the case however, for my sequencing data. If it helps I have a read pair from one of my MiSeq runs below.

R1:
@M01814:86:000000000-A6MU9:1:1101:15397:1339 1:N:0:2
TACTCGCACCTATCCGGCACAGCAACACCATCTGGGGCTGAATCGCAATAGCATCTCTCACTTCCTCCATATCAGATTGCTCAAGGCAAGCACTACGCTGCAGTGCCCTCCACTCCCAATTCCCTGATGCTGGTCGTAACTTGCCACACCA
+
>>AA?BBBBBFFGGG2EEEGFBGHHHGA2FGHBGHF2EE?GHGHHFFEEHDGHEFGF5FEEFBGHGBCB5FHHH5F553@434FF31G11??233B1/1/?333B?3FB?/B24B2/2B2?44?3?23333B223<>@0CB22@2@F0/?/

R2:
@M01814:86:000000000-A6MU9:1:1101:15397:1339 2:N:0:2
TAAGGGGCCTAGAACAGGCACCATACATTCAATTGGCTGTGGCAAGTAACAACCAGCATCAGGGAATGTGGAGTGGAGGGCACTGCAGCGAATTGCTTGCCTTGAACAATCTTATATGGGGGAAGTAGACGAACCAATGTGGAGTCAGCCC
+
>AA>>>ADDAFFGGGGG4FGGGFHFHFHHHFHHHB3B32EFBGGE25FGHHHHACEGG533BAGFFF355331BG1@1>EF1E23F333/>//134B43?F34B3334B334444?443B?/<C/23333////<0/<11111/?01?G0?

For reference, this is the reverse complement of R2:

GGGCTGACTCCACATTGGTTCGTCTACTTCCCCCATATAAGATTGTTCAAGGCAAGCAATTCGCTGCAGTGCCCTCCACTCCACATTCCCTGATGCTGGTTGTTACTTGCCACAGCCAATTGAATGTATGGTGCCTGTTCTAGGCCCCTTA

This is the alignment (with BLAST; alignment shown only for the HSP):

                                                           60                                                                                148
                                                           |                                                                                |
TACTCGCACCTATCCGGCACAGCAACACCATCTGGGGCTGAATCGCAATAGCATCTCTCACTTCCTCCATATCAGATTGCTCAAGGCAAGCACTACGCTGCAGTGCCCTCCACTCCCAATTCCCTGATGCTGGTCGTAACTTGCCACACCA
                                                           |||||| |||||| |||||| |||||||||||| | |||||||||||||||||||||  |||||||||||||||| || ||||||||||
                                  GGGCTGACTCCACATTGGTTCGTCTACTTCCCCCATATAAGATTGTTCAAGGCAAGCAATTCGCTGCAGTGCCCTCCACTCCACATTCCCTGATGCTGGTTGTTACTTGCCACAGCCAATTGAATGTATGGTGCCTGTTCTAGGCCCCTTA
                                                           |                                                                                |
                                                           126                                                                                38

Where the reads found in R2 are the reverse complement of those found
  in R1.

This statement seems incorrect.

Paired-end reads comes from opposite ends of a fragment (you could learn the reason it happens from Illumina's video). If insert size is 150bp, read length usually is ~60bp as quality score after 60th bp is unacceptably low. In this case, R1 length is ~60bp, and it is 5'3', R2 length is ~60bp, and it is 3'5'. When a number of reads are enough to cover the gap, they form a contig.

Here's an illustration from Illumina's website:


Trying To Identify this Fish My 4 year old fell in love with this fish at the aquarium.

I'm trying to find out what species it is so we can learn more about it.

It looks like a unicornfish (genus Naso), maybe Naso vlamingii, the Bignose Unicornfish. They're Acanthurids, related to surgeonfishes and tangs.

These are mainly found in Indo-Pacific ocean around the depth of 50 mts from surface. Coral reefs are their main habitat and destruction of coral reefs is their current biggest threat alongside trading by fisheries. A good source of information for this species is available here.

A copy of this fish.

Picture credits: UM Rosenstiel School


What happened to ProteomeCommons.org? ProteomeCommons.org seems to once have been a resource for raw proteomics data. Thought, the website now offers gardening tools. It seems to be hacked. Does anyone know whether the data is still available somewhere?

According to Lars Juhl Jensen on a Biostars forum,

  The Proteome Commons Tranche sadly shut down around 2013 due to lack of funding. It is a good example why important bioinformatics infrastructure needs dedicated funding and should not have to operate out of research grants for individual groups.


Model for fluctuating selection Is there any mathematical model to predict the behaviour and long-term consequence of counter-acting selection at different time scale?

For example, let's consider the bi-allelic gene A, with alleles A1 and A2. During a long period of n1 generations A1 is slightly beneficial (differential of selection: s1). After this period, follows a short period of n2 generations when A2 is highly beneficial (differential of selection: s2).

What mathematical model describes the frequency fluctuations of alleles and which allele will get fixed at the long term given the initial frequency ( f0 ), assuming infinite population size and random mating.

The frequency fluctuations will be determined by a standard model of selection as found in any basic population genetics text. In this scenario they take a very basic form: during each long period $i$ the frequency of $A_1$ increases from $f_i$ to $f_i\cdot (1+s_1)^{n_1}$ and during each short period $j$ the frequency of $A_1$ decreases from $f_j$ to $f_j\cdot (1/(1+s_2))^{n_2}.$ Thus over each pair of periods the frequency of $A_1$ changes by $(1+s_1)^{n_1}/(1+s_2)^{n_2}$. If this quantity exceeds 1, $A_1$ goes to fixation; if it is less than one $A_2$ goes to fixation.

More generally, for an infinite population in a fluctuating environment, the allele with the higher geometric mean fitness will go to fixation. Early discussions of these results are due to Dempster (1955; Cold Spring Harbor Symp. Quant. Biol.), Haldane and Jayakar (1963; J. Genetics), and Lewontin and Cohen (1969; PNAS).


What is the mechanism through which fractals arise in plants and animals? Many biological organisms -- such as trees, broccoli, and the blood vessels in animals -- can be approximately described using fractals.
What is the reason behind such fractals? Specifically, do we know of the way certain cells split that lead to fractals? Do we know if there are specific genes that tend to generate fractals?

because fractals are emergent structures created by simple rules, as are many biological structures. The same kind of simple recursive signals that lead to fractals are simple enough to be stumbled on by biological evolution and are effective ways to deal with the scaling problems created by the square cube law.
https://www.complexityexplorer.org/system/explore/model_series/pdf_files/000/000/008/original/Biological_Scaling_Series_.pdf?1554498961
https://www.jstor.org/stable/2898653?seq=1


Is fluoride toxic, and how worried should I be about it? A recent flurry of "fluoride is bad!" posts are appearing on my social network news feeds.  Usually I can simply ignore them after a brief look, but this one, stemming from a recent article in The Lancet, isn't easy enough for me to understand and apply or ignore.

The posts link to a March, 2014 article, Neurobehavioural effects of developmental toxicity, from The Lancet Neurology, Volume 13, Issue 3, which has the summary (emphasis added):

  Neurodevelopmental disabilities, including autism, attention-deficit hyperactivity disorder, dyslexia, and other cognitive impairments, affect millions of children worldwide, and some diagnoses seem to be increasing in frequency. Industrial chemicals that injure the developing brain are among the known causes for this rise in prevalence. In 2006, we did a systematic review and identified five industrial chemicals as developmental neurotoxicants: lead, methylmercury, polychlorinated biphenyls, arsenic, and toluene. Since 2006, epidemiological studies have documented six additional developmental neurotoxicants—manganese, fluoride, chlorpyrifos, dichlorodiphenyltrichloroethane, tetrachloroethylene, and the polybrominated diphenyl ethers. We postulate that even more neurotoxicants remain undiscovered. To control the pandemic of developmental neurotoxicity, we propose a global prevention strategy. Untested chemicals should not be presumed to be safe to brain development, and chemicals in existing use and all new chemicals must therefore be tested for developmental neurotoxicity. To coordinate these efforts and to accelerate translation of science into prevention, we propose the urgent formation of a new international clearinghouse.

I don't have full access to the article, so I can't refer to the epidemiological study it says shows fluoride to be a developmental neurotoxicant.

What is a developmental neurotoxicant?
How strong is the research that claims fluoride is a developmental neurotoxicant?
What relationship, if any, does this report or research have with typical fluoride compounds used in US water treatment at the levels typically present in US water (sodium fluoride, fluorosilicic acid, or sodium fluorosilicate at 0.7 mg/L)?

First of all: Yes, fluoride is toxic, but the toxicity depends largely on the form (soluble vs. unsoluble, which fluoride salt etc.) occurs. It also depends on the environment since insoluble salts which are subjected to strong acids can release fluorine ions.
The certain toxic dose for adults is 32-64mg/kg body weight, a 75kg adult needs to take up between 2,4 and 4,8 grams of fluoride ions (for sodium fluoride this would be between 5,3 and 10,6 gr of the salt). For children this is about 5mg/kg body weight.
For the water the added dose of fluorine is much lower, somewhere between 0,7 and 1.2 mg/l. Other sources of fluroride are food (especially sea food) and also black tea.

The toxicity of fluoride is mediated by different ways: First it forms an insoluble salt with calcium in the cells, effectively causing hypocalcemia. Calcium is an important second messenger in different signal transduction pathways as well as highly important for the functioning of nerve cells (which also explains why it is neurotoxic in the development of nerve and brain cells). It also causes the inhibition of a number of different enzymes as enolase (disturbs the glycolysis) but also phosphatases and katalase. For all of this have a look into the Wikipedia if you want to know more details.

About the paper: It is a review of published research articles which sums up the situation in this field. The paper mentions fluoride only twice: Once on the abstract and once in a table about newly identified developmental neurotoxins (table 2 to be precise). It references only one meta-analysis on this topic.

The cited meta-analysis ("Developmental fluoride neurotoxicity: a systematic review and meta-analysis") which did a statistical meta-analysis of published papers and their data. They find a significant relation between the fluoride content of the drinking water and the IQ of the children.
However this is not undisputed (to say it mildly), since while a finding can be statistically significant, it doesn't necessarily mean that there is clinical importance. The other important point which @Doctor Whom mentioned is that a correlation doesn't imply a causation. So even if there seems to be a correlation between two things, they are not necessarily connected (see the famous example of storchs and birth rates).

This paper ("Developmental fluoride neurotoxicity: clinical importance versus statistical significance.") is published as a comment on the original paper and claims exactly this. They say the the mean difference in IQ is about 7 points, which is not of clinical importance. Another paper critizes the relatively low quality of the original papers used for the study ("Fluoride and children's IQ.").

They also mention a low consensus about what is a high concentration of fluoride in the drinking water and also show the very wide variation of the fluoride concentration in the original studies. The highest concentrations mentioned are around 10mg/l which is about 10x the concentration used for adding fluoride to the water. Even if we take in account that children are more sensitive to fluoride and also need lower fluoride concentrations to cuse some developmental damages (below the fatal concentration) this would still add up to quite absurd amounts of water they have to drink.

Regarding your questions:

A developmental neurotoxin is a substance which interferes with developing neurons or nerve cells. It either inhibits their growth completely or at least impairs the cells.
Given on the articles I found (and cited above) I would say that fluoride is a developmental neurotoxin. Nevertheless it seems to me that it is not very strong in this context as the current studies are contradictory. Thinking about the amounts of fluoride present in water (even if the concentration is much higher than recommended) makes me doubt if this is really the causative agent.


How can I find the mRNA sequence for a specific prokaryotic gene? What I want to find out is the start of the transcription for a specific gene, how long the UTR is before the actual coding sequence starts.

I've looked at various databases like NCBI Gene, Refseq or a specialized one like PRODORIC. But none of them actually contain the mRNA sequence or any information about the untranslated parts of the mRNA. Just the coding sequence itself.

Is that kind of information simply not annotated for many bacteria? I'm not looking at model organisms like E. Coli or B. subtilis, but I would have expected some information to be available.

Is there a database where I can find the actual transcript sequences for prokaryotic genes?

mRNA specific queries

Add this to your NCBI query: AND mrna[filter]

If it's not available in major databases it may not be known.

However mRNA data can be obscure to find even in those major databases but it should be there. I would be surprised if that is the case, however since you're not working with model organisms there may well be nothing available.

When looking for a transcript gene, NCBI have some tips that you can see here for searching their database. #8 might be relevant to you as it's a way of filtering exclusively mRNA records.

  If there is no UniGene cluster for this gene and organism, perform a
  search in the Nucleotide database with the gene name, product name, or
  symbol. Include the organism in the search to find the most relevant
  results and filter for transcript sequences, for example: Cytochrome c
  AND bullfrog[orgn] AND mrna[filter].

Predicting mRNA

Basic: ExPasy DNA translation tool

Advanced: regrna 2

Assuming that advanced querying doesn't reveal what you need you might be able to make some useful predictions before taking it to the lab. There are a handful of other predictive tools that can maybe help you out if that's the only option available. I can't get my head around exactly what information you have as an input. Assuming you have the DNA sequence, I would start with the obvious choice: the ExPasy DNA translation tool.

I would then say that regrna 2 might be able to steer you in the right direction regarding more subtle translational elements.


Difference between inbreeding and interbreeding Is inbreeding the same as interbreeding?

On this site interbreeding is defined as (http://www.thefreedictionary.com/interbreeding):

  To breed with another kind or species; hybridize.
  To breed within a narrow range or with closely related types or individuals; inbreed.

But I am sure that interbreeding is not the same as inbreeding. Inbreeding would be between genetically related members of a species and interbreeding would be between genetically un-related members of the same or different species.

after looking at wikepedia pages for both terms as well as searching the english oxford dictionar I am certain they are different

You are basically correct. Most common usage in my experience:

Inbreeding refers to sexual reproduction between genetically closely related individuals, within a species. Inbreeding will increase the relatedness between individuals in a population.

Interbreeding refers to reproduction with another species (or race), and is often used as a synonym to crossbreeding or hybridization (when referring to hybrid offspring from two different species/races/breeds, not DNA hybridization). This is also how 'Interbreeding' is defined in the Oxford English Dictionary. However, 'Interbreeding' is sometimes used just to signify that two individuals can breed and have viable offspring ("...these two individuals can interbreed..."), and under this usage this can also include/overlap with inbreeding.

The latter usage can be seen in the Species article in Encyclopædia Britannica, online:

  Species, in biology, classification comprising related organisms that share common characteristics and are capable of interbreeding.
  ...
  Interbreeding only within the species is of great importance for evolution in that individuals of one species share a common gene pool that members of other species do not.


Atmospheric gas changes, and their effects life I was curious how life on Earth, or an Earth-like planet, would be effected by changes in the gases which make up our atmosphere.

Assuming there is a similar level of oxygen in an atmosphere, could other gases be reduced or even replaced and still be able to maintain life as we know it?

Not really biology, but if the following could be kept in mind too that would be amazing:

[To give some context, I would like to ask how a sky could be light blue with a purplish hue, which supports some life larger than what we see on Earth, but still capable of supporting life which we find on Earth.

I am assuming a slightly higher percentage of oxygen is needed, but what other gases which are none lethal, but give a purplish hue?]

Thank you to all who take the time to give an answer, very much appreciated!

The Earth is blue (at least the non-land mass) because of the light our atmosphere refracts from the sun. A planets color is primarily determined by distance from sun, not from gas components.

Most gas does not refract light. Therefore a planet's gaseous composition can not be identified based on color.

To elaborate on your primary question, gas composition balance is essential to most life on Earth. Carbon dioxide, for instance, is responsible for photosynthesis occurring in plants. Different concentrations will affects photosynthetic rates. Another example is that CO2 levels, CO levels, and hexa-fluoro-carbons affect the amount of heat trapped in this planet.

Gas composition is highly delicate and must stay in balance to preserve life on Earth.


What is the name of this plant with small, 5-leaved divided pink blooms? I found this in a forest in Karlsruhe (Germany).

The blooms are pink and have 5 leaves. Each leave is divided into two parts. It is pink and has a diameter of about 1-2cm.

It looks like a Red Campion, which is native to northern and central Europe.

It would be nice to see a close-up of the calyx (which is usually striped) and the leaves to be sure; it may be a cross between a White and Red Campion.

There are many members of the genus, and many look alike. Your close-up is of a male flower (anthers only). The plants are male or female.


Salvaging a plasmid from a cell culture stored at the incorrect temperature I have E. coli with transformed plasmid on agar in a vial.  It has been stored at -20 degree C without glycerol stock for 18 hours.

This is a continuation of: Survival of E. coli on agar plate at -20 degree C without glycerol stock

I have transfered this vial from -20 degrees to 4 degrees after 18 hours when I determined that I had made a mistake. Since this is a very important vial and I don't have another one, what should I do in this stage?

What is the procedure for saving the plasmid if I am unable to save the whole cell?

I would rinse the cells off the agar using a small volume of LB or similar rich medium. Then use a small aliquot (10 μl) to inoculate a 5 ml culture under selection to see if anything will grow. Meanwhile the remainder of the cell suspension from the vial can be used as input for your favourite miniprep procedure.

If necessary, the DNA that you recover should then be used to transform a suitable E. coli strain. Don't bother trying to analyse the rescued DNA first since polysaccharide contaminants from the agar will probably inhibit any restriction enzyme that you might use.

Good luck!


How Anopheles crop doesn't digest gametocytes of P. vivax? Background

According to my A-level textbook: When Anopheles mosquitoes inject their proboscises and suck up blood from human host of malaria agent, they suck all stages of malaria parasite present in the blood like merozoites, cryptozoites, gametocytes etc.
But, Anopheles mosquito's crop digests all other stages of malaria schizogony except the gametocytes.

Question

Well, how does the digestive system of Anopheles distinguish the gametocytes from other stages of malaria parasite?
Or, is there any protective mechanism for gametocytes to stay untouched in face of digestion in Anopheles crop?

Disclaimer: I am trying to answer the question without finding any academic research on the topic. So, appreciate hypotheses and feel free to point out mistakes.

Short Answer : Co- Evolution

Broad Answer: 2 hypotheses

The gamete stage of Malaria parasite simply co-evolved with Anopheles sp. to develop a protective mechanism to survive digestion in crop. Whereas, the other stages of Malaria parasite didn't co-evolve,  so they get digested.
Parasites had already the protective mechanism for surviving digestive enzymes in Anopheles crop. They entered mammals later and evolved a life cycle with a new protective mechanism for new host's immune system.

Why is that?

The answer to this question is not so clear according to known biology, as I haven't found much research in this phenomenon.
But, we have to remember that biology sometimes (or always?) doesn't explain why rather explain how.

The following words are corresponding to what I think about the mechanism of this co-evolution

Hypothesis 1:
It could have simply happened that some point in ancient times, the gamete entered the Anopheles crop from a mammal, but not only that; it tried to continue its life cycle on this new host. But, the environment of crop was unsuitable for the gamete to survive due tto digestive enzymes. So, the first few million or billion tries went into vain. But, the parasite slowly started to evolve to adopt in the Anopheles crop.

After 'some' time, the parasite developed a working protective mechanism from digestive enzymes and continued it's life cycle in Anopheles.

As @Another Home sapien points out, there should be some benefits for this evolution. While it's hard to tell exactly what the benefits could have been; I think it's simply to adopt to new potential host's physiological environment.

But why didn't other stages evolve of Malaria parasite in a same way?

This is another hard question to answer. However, it's not so that only the Anopheles and the parasite co-evolve; the mammal host co-evolved too in this period. And the whole system evolved gradually to get to the present life-cycle of malaria.

Hypothesis 2:

It might have happened that the original host to malaria parasite was indeed Anopheles. So, it had developed a protective mechanism long before entering any mammal host. Then, after entering the mammal host it developed another protective mechanism to survive host's immune system and continued  it's life cycle.

I think hypothesis 2 is more probable as insects pre-existed mammals. Another hypothesis can be drawn the life cycle of parasite is shaped up simultaneously in mammal host and Anopheles host. But, it's hard to hypothesize what could have happened in this scenario.

Reference : 1. Wiki: Co-Evolution

2.Article on this co-evolution


How far do 2 ant colonies of same heritage have to be in space (and generation) in order to fight? (Kinda follow-up to this.…)

I've heard before that if you put 2 ant colonies side by side they're going to attack each other.

But then from the previous question, there could be "sister" ant colonies which (assumingly) don't harm one another.

I can probably see that generation-by-generation colonies would just naturally be either too far apart in space, (or too close in "generation"), to have any fights.

But what actually makes ants decide whether to fight or to not?

And whatever it is, is it a spectrum or a limit..? (i.e would there be a case in which some ants of a colony will fight and some wont?)

Space and generation don't directly affect whether ants fight, that's all regulated with pheromones. Some ant species are more tolerant of different smells than others (see the argentine supercolonies mentioned above) while some species of ant have 'rival' nests that they are particularly aggressive to.

So I guess the answer is 'it depends'. On pheromones produced by the queen, and species. And probably diet/weather/local food availability/ some other things I haven't thought of.

I don't think it's possible for some ants of a colony to fight and others not to, but I don't have any evidence to back that up specifically.


Valve-like layers example in nature? I am searching for an example in the nature, where a layer of something (skin, coat, film etc) can allow fluid to flow trough (not absorb) from one direction and prevent/repel from other direction. I am not talking about vein valves, prefer more like a nano-structure of valves as a layer on/around something.

Update:
I found something similar what i am searching for, but its not clear:

  Gap Junctions (animals)

  Directly connects the cytoplasm of two cells, allowing various ions
  and molecules to pass freely between the cells.

And there is a reason why this channel is hydrophilic, someone can explain this?

About me I have no deep knowledge about biology, please be patient and help me to understand things on basic level. Thank You!

I don't know any-such continuous-membrane-material that can do so. But yes certain membrane-transport-proteins can do so.

Carrier proteins are normally highly specific about in which-direction to transport which molecule; and in general,  they are classified as uniporters, symporters and antiporters.  *

So an uniporter would be an accurate example of situation you are asking about.

Carrier proteins those utilize ATP for pumping (those shows "primary active transport"), are also normally highly specific to direction. For example the Na+-K+pump and the H+ pump.

Channel proteins too, sometimes show directionality, for example certain K+ channels ** such as inward-rectifying potassium channel

A potassium channel diagram showing the selectivity filter (diagram from The cell/ Cooper **, slightly edited: Na+ filter-out not shown, and the term 'selectivity filter' is labelled in image ).

KcsA potassium channel diagram from wikipedia. In its open-conformation out of the following;

i.e. the third one, can conduct the K+ ion in a specific direction, because the pore-region is very specific- it allows K+ ion only to enter in the cell.

  Reference:

  * Plant biochemistry by Hans Walter Heldt, 3rd edition, Academic Press-Elsevier, Paperback edition.
  ** The Cell, a molecular approach/ Cooper/ Sinauer and ASM press.
  Harper's illustrated Biochemistry/ Murray, Bender, Botham, Rodwell, Well/ Lange and McGraw Hill.
  Wikipedia.