Genes and Intelligence Assuming that intelligence has a genetic component,

• do we know which genes contribute to it?

and, if so,

• can we predict intelligence from genomic analysis?

A few words on genomic prediction
No complex trait is 100% heritable, hence no prediction based entirely on DNA would ever be perfect. With that said, predictive genomics is progressing at a quite amazing rate right now. So while predictions can be nowhere near perfect, it is getting possible to make DNA predictions that correlate substantially with observed values.
The genes that correlate with phenotypic differences are found using genome-wide association studies (GWAS). The total effects are then aggregated up to what is called a polygenic score.
A success story --  Height
Height is highly heritable, meaning that much of the phenotypic variance (although not 100%) is due to genetic differences. Height is also highly polygenic -- it's a trait influenced by many genes, each of small effect.
Many variants that correlate with height have now been found. Polygenic scores of height correlate higher than ~0.60 with observed height. DNA predictions are generally within a few centimeters of true height (Lello, Avery, Tellier, Vazquez, de los Campos, Hsu, 2018). According to an interview with Stephen Hsu, one of the authors of this paper and co-founder of the company Genomic Prediction, they can correctly predict the height ordering of siblings within the same family 80-90% of the time (source). So based purely on DNA, can we say which of two siblings are going to be taller than the other? Not perfectly, but with decent reliably, yes.
This is about as good as predictions of complex traits can be based on current methods. There are a few principal reasons that correlations are not higher (even though it is quite impressive already in its own right). First, as I said, complex traits are not 100% heritable and therefore predictions are not expected to ever be perfect. Second, current GWAS are typically based on SNPs which are common gene variants. Rarer gene variants are expected to contribute to the variance and their effects are still needed to be uncovered. Third, only additive effects are taken into account, not gene-by-gene interactions.
Genetic IQ Prediction?
IQ, like height, is a heritable trait and is highly polygenic.
There are several approaches to finding gene variants correlated with IQ, however they can broadly be categorized into two. The most obvious approach is to simply give people intelligence tests and get their DNA. The problem with this is that it is difficult to get large samples with good intelligence tests. When this approach is used, usually a very short (say, 2 min) intelligence test is used. The second approach is to use a proxy phenotype. With this approach, the variable years of educational attainment has been used to good success, and has been shown to have a high genetic correlation with intelligence ($r_g \approx 0.7$).
Many variants that are associated with intelligence or educational attainment have been found, see e.g. (Lee et al, 2018; Savage et al, 2018). While many variants are known, IQ is not as well understood as height, and current SNP predictors correlate about ~0.3 with observed IQ (See e.g. Allegrini et al, 2018). This correlation is bound to increase in the coming few years.
Further Information
If you want a simple introduction to what can be read from the genome so far, there is a TED talk on this subject, TED2016: How to read a genome and build a human being. Although, major improvements have already been made in the years since 2016. For anyone that is more interested in the mathematical techniques used for prediction and the underlying theory, I recommend this talk by Stephen Hsu if you're further interested in genomic prediction of complex traits. I also recommend reading this review by Robert Plomin and Sophie von Stumm to get an easily understandable overview of the current state of knowledge on the subject.
References
Lello, Avery, Tellier, Vazquez, de los Campus, Hsu (2018). Accurate Genomic Prediction of Human Height. DOI: https://doi.org/10.1534/genetics.118.301267
Marty Nemko (2018). The Future of In-Vitro Fertilization and Gene Editing. Psychology Today Link.
 Lee, ..., Cesarini (2018). Gene discovery and polygenic prediction from a genome-wide association study of educational attainment in 1.1 million individuals. DOI: https://doi.org/10.1038/s41588-018-0147-3
Savage, ..., Posthuma (2018). Genome-wide association meta-analysis in 269,867 individuals identifies new genetic and functional links to intelligence. DOI: https://doi.org/10.1038/s41588-018-0152-6
Allegrini, Selzam, Rimfeld, von Stumm, Pingault, Plomin (2018). Genomic prediction of cognitive traits in childhood and adolescence. DOI: https://doi.org/10.1101/418210
Sabatini (2016). How to read a genome and build a human being. TED2016 Link to Talk.
Hsu (2018). Genomic Prediction of Complex Traits. Youtube Link to Talk.
Plomin, von Stumm (2018). The new genetics of intelligence. DOI: https://doi.org/10.1038/nrg.2017.104


Possibility of Human cloning Technology has evolved so much as to clone animals. But, what about human cloning?
Is it really possible to create humans in lab? Or is it that technology has not advanced to that level..?

Why cant it be attempted..?

Cloning of animals typically involves:

Taking nucleus from healthy adult cell of animal to clone
Taking a healthy egg and replace the egg's nucleus with nucleus from source animal.
Implanting egg in female, stimulating the pregnancy process.

This same process should work on humans BUT:

"Is it really possible to create humans in lab?" No. Animal cloning doesn't work this way, so human cloning wouldn't either. Animals aren't "created" in lab. The one artificial step is the modifying the nucleus of the egg cell before the pregnancy process initiates. The rest of the egg->embryo->infant pregnancy process is traditional nature and there is no working lab process available to replace natural pregnancies.
Cloning animals is very high risk, it involves lots of trial and error, and involves lots of mistakes, botched pregnancies, abortions, and birth defects. The core concept of replacing the nucleus in an egg cell makes sense, but the practical reality of that procedure involves cell damage and pregnancy risks. With non-human animals, no one cares. With humans, purposefully causing lots of botched pregnancies, miscarriages, and birth defects will make most people squeamish.
Donor Eggs: If the process worked perfectly, a single donor egg would suffice. Since the process doesn't work perfectly, many donor eggs are required. Getting those donor eggs is a very invasive process that I would not want my wife, sisters, or daughters to subject themselves to. With lab animals, who cares, scientists can be as invasive as they want, and harvest all the eggs that they need. Humans have rights which really impedes this type of risky work.

Today, cloning humans is possible, but at prohibitively high cost and risk. It is inevitably going to happen, but the costs and risks will impede its popularity. Process improvements that deliver more safety and reliability will allow human cloning to become more popular.

UPDATE: "Why cant it be attempted..?" It definitely is being attempted. Panayiotis Zavos is one doctor who has been very public about his attempts to clone humans:

"In April 2009, he claimed to have cloned 14 human embryos and transferred 11 of those to wombs."

AFAIK, none of these efforts led to a live birth. I'm sure other doctors have attempted and even more are considering it and waiting until it's a little more practical and realistic.


How do fungi react to being grown in a tissue culture? I know how plant cells and animal cells react to being cultured and grown this way, but what about mushrooms? Would they respond like plants, and result in embryos growing off the mass? Or does the mass just grow indefinitely as in animals? Has anyone done this? How do they react when grown this way?

Generally, fungi are cultured on agar with a food source such as malt extract. One way to do this is to clone a mushroom from the fruitbody of a mushroom or from colonized substrate (e.g. rotting wood). Another approach is to germinate spores.

The fungus will grow as vegetative mycelia until it runs out of food. At that time, some species will grow tiny fruitbodies or sporulate before entering a more dormant phase, dying out. Unless refrigerated, standard agar plates dehydrate. Also, fungi may take on different textures: wispy, bumpy, root-like (rhizomorphic), leathery, powdery, and may darken or change color as they age.

Some cultures start to adapt their metabolism to the media after a large number of transfers (based on observation and discussed in Stamets' "The Mushroom Cultivator".) at this point, cultures may also start to grow more slowly.

The mycelia can be transferred from one plate to another or to another media (substrate) such as a log, 'fortified sawdust' (sawdust with ~30% w/w wheat bran), or pasteurized compost. With the appropriate nutrition and environmental stimuli (CO2 levels, temperature, moisture, light, etc), the mycelia will fruit, creating mushrooms - generally after fully colonizing the substrate.

Here is a figure of 35 agar plates with 16 different fungal cultures that I isolated from the wild (soil, wood, mushrooms, as described in Allison et. al, 2009; LeBauer, 2010), and have transferred from a mature culture (about a 2 months old) to a new plate, which are about two weeks old in this picture. Parent cultures are in the first and third row, with children below (they are genetic clones; instead of counting generations, I count number of transfers.

You can also find cultures of fungi (Yeast) in unfiltered beer.

I have used many techniques to isolate and culture fungi (Isikhuemhen and LeBauer, 2004; LeBauer, 2010) but I would recommend the books "The Mushroom Cultivator" and "Growing Gourmet and Medicinal Mushrooms" by Paul Stamets for more information on sterile culture techniques used in mushroom cultivation.


Why can't we observe haplotypes directly? I am completely a noob to biology and DNAs, but recently I am looking into EM-algorithm used in the case of re-constructing haplotypes from genotype data.

I am just wondering what exactly in the process of DNA data collection prevents us from observing haplotypes directly.

The difficulty of reading haplotypes 'directly' lies in the difficulty of reading any long sequence of DNA, and this is for technical reasons.

Short DNA fragments are sequenced using a variety of methods. Gel electrophoresis can pull these fragments apart by length, but all the fragments have to be relatively close in size to get the accuracy needed to tell fragments that differ by one base pair apart. It's easy to separate a 16-bp segment from a 17bp segment easily, but it's much harder with a 516bp segment and a 517bp segment. Modern sequencing can sequence reads up to about 5kbp in length at a time. The 'reads' are then reassembled.

There are next-generation methods(pyrosequencing, etc) that can read a long dna molecule one base at a time, but for practical reasons sequencing an entire chromosome this way is cost and time prohibitive. As a result, there are always going to be fragments that you need to reassemble computationally, no matter how the sequencing is done.


Are there parts of DNA that do not have genes? A question in my genetics class is "Are the number of genes proportional to the genome size?"
The answer is "no," and is it because the genome is the entirety of all the DNA in an organism, but that there are some segments of DNA that don't have genes on them?  Can someone explain this?  Thank you!

Most the genome is not coding for proteins. Here is a pie chart of what the human genome is made of

As you can see, only 1.5% of the human genome codes for proteins. The term gene is often a bit vaguely defined but if we assume that a gene is all the exons, all the introns and all the regulatory sequences, then 25.5% of the human genome are genes. So, yes many "parts of the genome" do not contain genes.

Now, it is worth highlighting that there is a very high correlation between the genome size and the number of protein-coding genes among lineages. Consider the below graph based on data from NCBI genome reports and styled after Koonin (2011).

There is a high correlation but there are also important outliers. See for example the eukaryotes (green dots) at the bottom right of the graph (probably mainly polyploid plants) that have very big genomes but relatively few protein-coding genes.

So, even though there is a strong correlation, it was quite obvious to me that the answer your teacher was expecting was no, because most of the genome is not coding and despite an existing correlation between genome size and number of genes among lineages there exists species with a very high density of genes and others with a very low density of genes in their genome.


Alternatives to His-tags What are the alternatives to using a histidine-tag in detecting protein-protein interactions? Why would they be more beneficial than his-tags?

This depends on the technology you're using for the interaction detection.  Surface Plasmon Resonance and Isothermal Titration Calorimetry (and others) don't require tagged proteins of any kind.  Though it doesn't hurt either one.

If you're looking purely at chromotography, any tag that will stably capture. I commonly see GST, FLAG, and MBP in order of occurrence.


Is there random assortment in metaphase II? First, a little notation. Call a the first chromosome from my mother and A its homologous partner from my father. b and B would be the second pair, c and C the third, and so on, down to w and W (the 23rd).

The tetrads in interphase would be expressed as aa AA...ww WW (so, for example, AA are sister chromatids). Finally, use the notation a' and A' to express that those two chromatids have crossed over via recombination.

Ok: I understand that in Metaphase I, there's a random assortment of chromosomes at the equator, so that we might end up with a division like so:

aA'    Aa'
bB'    b'B
CC'    c'C
...
wW'    Ww'

Which pair ends up on the right or left is random, and there are therefore $2^{23}$  possible arrangements.

My question is whether an analogous shuffle happens during metaphase II? I visualize metaphase II as taking one of the columns above and turning it on its side, so that for instance taking the right column you have:

a' B  C  ... w'
A  b' c'     W

These "rows" are then split to become 2 of the 4 gametes.

The question is whether at this stage, before this final split, there is an analogous shuffling possible whereby, say, the A and a' could switch sides?

My intuition is yes, of course, but in all the accounts of meiosis I can find online, the "random assortment" and shuffling is all described as happening in metaphase I.

(I think whether the shuffling between this particular A and a' happens in metaphase I or metaphase II is inconsequential in terms of which one ends up in which daughter cell... but I'd still like to have a sense for what's literally physically happening.)

Metaphase I

Your understanding of the metaphase I is not entirely correct. In normal (human) metaphase I homologous chromosomes separate. Therefore, sister chromatides go together. More precisely sister chromatides are kept together at centromere. You have only two possibilities for each chromosome:

<-AA   aa->

or

<-aa   AA->

If we multiply the two possibilities for all 23 chromosome pairs it leads to correct number  223 of possibilities.

There can be one or more crossovers between two or more chromatides but the fate of crossovered chromosome arms is determined by the fate of centromere they get connected to.

Your diagram of random assortment, if I understand it correctly, allows for more than 2 possibilities for chromosome pair:

<-Aa   Aa->
<-aa   AA->
<-AA   aa->
...

And it would lead to incorrect number of possibilities (more than 2)23

Metaphase II

In metaphase II sister chromatides separate as they would in mitose. Yes, there is random asortment of which chromatide goes left and which goes right. With your notation it could look like this:

<- A   A'->
<- b   b'->
<- C'  C ->
<- D   D'->
...
<- w'  w ->

However, as I said earlier, some chromosomes can crossover more than once, so you can have thinks like:

<- g''   g'->

or

<- F'''   F ->

or

<- h'    h'->

Inverse meiosis

For every rule in biology there is an exception. Some species have inverse meiosis. This means they do it in reverse order. In metaphase I they separate chromatides and in metaphase II they separate homologous chromosomes.


Does human eye lens have a magnification of its own? I have always wondered if the lens in our eyes have any sort of magnification by default. And if yes, if we're actually seeing everything around us bigger/smaller than what they actually are!

Has any research been done on this?

The magnification by the lens of the eye is well understood.  This document, written by Dr. Glenn Chapman at Simon Frasier University in British Columbia, Canada, lays out some of the technical details.  The image below is taken from that document. I modified it slightly by enlarging the $s$ and $s'$ variables because they are important for this answer.

For a simple lens like that in our eyes, magnification, $m$, is calculated as

$$m= \frac{s'}{s}$$

where $s'$ is the distance between the lens and the retina at the back of the eye, and $s$ is the distance between the object and the lens. For the human eye, the distance $s'$ is about 24 mm, or just a bit under 1 inch.  For an object to have exactly 1:1 size ratio (no magnification or reduction), it would have to be exactly that same distance from the lens. That is, the object would have to be about 24 mm in front of our eye. The problem is that, unless you are myopic (nearsighted), you cannot focus on objects closer than about 25 cm (about 10 inches)

Most objects are much farther away from the lens than 24 mm. That means $s$ is a much larger value than $s'$, making $m$ a fraction less than 1. A value less than 1 means that our lens is not magnifying the object but instead is reducing or demagnifying the object.

As a simple experiment, hold your finger upright in front of your eyes at arms length.  Bring your finger closer and closer until you feel your eye lashes. Your finger looks smallest when it is farthest away from your eye. As you bring it closer ($s$ is getting smaller) your finger appears larger and larger. When your finger gets to about 24 mm, then $m=1$. When your finger touches your eye lashes, the distance is less than 24 mm, and the finger is magnified to larger than actual size ($s > s'$ and $m > 1$).

This also explains why distant objects appear smaller than closer objects. If you see a stop sign at 500 m and a stop sign at 100 m, the closer sign looks larger than the more distant sign.  But which is the actual size? Neither, because the lens changes the apparent size. The way to see the actual size is to stand with your eye about 24 mm away from the sign. Then, magnification will be exactly 1:1 and you'll know the true size of the sign. You just won't be able to focus on it.


Need for -70 degree temperature for Corona vaccine Recent news of Pfizer vaccine for corona needing -70C temperature, made me thinking why such a low temperature is needed for mRNA based vaccine?
Are there other vaccine around which need such a low temperature?
NewsLink

This is the temperature at which RNA is stored for long term storage without the occurance of degradation. It is also standard lab routine to store RNA at this temperature. Conviniently, this temperature can be reached by dry ice (-78°C), which makes shipping a lot easier.
However, there are indications by Biontech themselves that the vaccine will be stable at refrigerator temperatures between 2-8°C for five days and probably even for prolonged times (see here). This is actually being tested, storing below -70°C is simply the safeguard to ensure nothing bad happens. For injection, it will have to be warmed anyways.


What causes random long white body hairs? I'm sure many of you have experienced this - you scratch your back or brush your hand over your arm and find a ridiculously long thin white hair, sometimes as long as 3 or 4 inches. I know a few people who get these quite frequently, and anecdotal evidence seems to suggest they almost grow almost overnight. A quick Google search for "single long white hair" throws up plenty of references to them, and various beauty advice, but I'd like to know the biology behind them.

What triggers abnormal body hair growth?
What causes these hairs to grow so much longer than other "normal" body hairs in physical proximity?
Why are they so thin and white compared to other body hair?

My primary hypothesis is that the hair cell grows rapidly in an uncontrolled manner, similar to how cancer might, and that the unusual appearance is due to the cells being starved of nutrients. I may be completely wrong, though.

I'm mainly interested in humans here, but if more in-depth research is available on animals that'd be interesting too.

Since it's been so long, I guess a rushed speculative answer might be at least an idea.

DNA gets damaged randomly all the time, and repair mechanisms are in place to fix it. When the damage is too large or of a very complex kind, permanent mutations can develop, and cause disorders such as cells proliferating without control - i.e. tumours.

I could imagine that the same mechanism could result in cells which overproduce keratin (hair) without melanin (pigment), if the associated genes are affected. Considering that trichocytes and melanocytes, the two cell populations at the base of the hair responsible for production, are among the most rapidly proliferating cell types in humans, an increased risk for mutation would not surprise me. I was able to find a few papers on keratin-associated gene clusters by a quick search, but they all seemed to be related to production of fragile hair rather than excessive length.


How does laser surgery correct accommodation problems? When someone undergoes laser surgery to improve eyesight, how does it correct accommodation problems?

Why does it not help presbyopia?

Overview

Laser eye surgery works by altering the shape of the cornea.  The cornea works together with the lens to focus rays of light onto the retina.  The cornea accounts for two-thirds of the optical power of the eye (1) (i.e. the eyes capability to focus light), however unlike the lens is of fixed power. It is the lens that changes is shape by the action of suspensory ligaments and ciliary muscles in order to focus light by the correct amount depending on how far away the light originated from (and consequently the angle of incidence with the cornea).  I'm sure that you are aware of all this, however for the benefit of future readers this is fully explained diagrammatically on this webpage.

Specific Conditions

Three forms of accommodation problems can be treated by laser surgery:

Hypermetropia (long-sight) is where light focusses behind the retina:

Laser treatment is used to make the cornea thicker, resulting in a greater degree of refraction of light and correction of the focus.

Myopia (short-sight) is where light focusses before the retina:

Laser treatment is used to make the cornea thinner, resulting in a reduced degree of refraction of light and correction of the focus.

Astigmatism is where the cornea is not the correct shape - it is closer to a rugby ball rather than the sweeping curve demonstrated in the first diagram.  This results in multiple focal points therefore a blurred image.

Laser eye surgery is used to alter the shape of the cornea until it is more normal.

Presbyopia is an age related condition where the lens becomes more rigid and is less able to change its shape to accommodate the light.

As this is a problem with the lens rather than the cornea, it can not be treated with laser eye surgery.  It must be corrected with glasses, as shown in the above diagram.

(1) Cassin, B. and Solomon, S. Dictionary of Eye Terminology. Gainsville, Florida: Triad Publishing Company, 1990.


Are similar smells usually based on similar chemicals? Building off of this question: Why does freshly cut grass smell like a watermelon?, is it usually the case that things that we perceive as having similar smells are, in fact, the same or a similar chemical hitting our noses (as in the case of cis-3-hexanal in watermelon/cut grass), or is it often a cognitive thing (we're bad at parsing smells, so when confronted with a new smell, we fish around in our experience to find something that seems familiar, even if there's not much chemical similarity)?

With regards to the similar chemicals having similar smells, it does seem that there are trends with smell association and functional group.  This wiki article has a good list of compounds and their smells, and some classes definitely give similar types of smells, amines are rotting/fecal smells (hence the names putrescine and cadaverine), while esters are often fruity.  As you can see its not perfect, but there are definitely patterns.

There are some weird dose-dependent effects like in the case of indole which is labeled as flowery/fecal, which are two pretty distinct smells.  Apparently its fecal at high doses, and smells like jasmine at low doses.  My guess is that this has to do with different binding affinities of the different olfactory receptors (ORs) that are expressed in the olfactory receptor neurons (ORNs).  Many odorants will bind to multiple ORs, which means they will stimulate a characteristic sub-population of ORNs.  The binding to the different ORs will of course have different affinities.  This probably means that at low concentrations of indoles, you stimulate a certain population of ORNs that your brain recognizes as nice flowers, but as you increase the concentration you get the activation of ORNs with ORs that have a weaker binding to indole, changing the population of activated ORNs to one that your brain recognizes as feces.  Its definitely a strange pairing though..

I'm not familiar enough with the literature to know if the similar smelling things have similar ORN activation patterns, but my guess would be that they do.  If you have a population of different ORs that your odorant is binding to, a slightly different odorant will probably bind to a similar subset of ORs, just off by a few if its missing or has gained a functional group that is in the binding pocket of some of the ORs.  This probably means that if you are presented with a chemical that you have never smelled before, it will probably activate a similar ORN population as other similar chemicals, and your brain will probably say it smells like one of those similar chemicals.


How to predict the effect of a non coding SNP variant on the expressed protein? I am writing a paper for non coding SNPs on patients with metastatic breast cancer. Having used a specific gene panel (NGS) of approximately 60 genes, I'm currently running out of ideas on what to write in the discussion section.

I am looking for suggestions based on somewhat efficient methods like a bioinformatics approach or specific textbooks revolving around RNA biology/biochemistry, in order to predict the outcome of non-coding SNP variants.

Some details:

The majority of the variants are intronic (~2300/3300), so I will mostly focus on splicing.
There are two commonly repeated SNPs in 3'-UTRs in over half of the patients, involving KRAS and CDKN2A.

A) Generate exon & transcript counts for your samples, library size + quantile normalize the data.
B) Group samples into variant/wild-type categories
C) Use wilcoxon's rank sum test to see if there are differences in exon inclusion or overall expression. Remember that 3'UTR variants can also imply differential degradation by miRNA. Tools like TargetScan can help you with miR-analysis.


What is this small black bug found in Turkey? What species is this? It was found in Turkey. It was dead, I did not kill it.

Looks like a scarab beetle (Coleoptera, Scarabaeidae). Species is difficult to tell without better pictures, but perhaps Scarabaeus typhon?

Edit: OP has IDed in comment as Scarabaeus jalof


Role of Calcium and Magnesium in capacitation/acrosome reaction During the acrosome reaction, the activation enzyme present in the sperm dissolves the corona radiata and zona pellucida enabling the sperm to reach the plasma membrane of the egg.
Also calcium and magnesium ions play an important role in acrosome reaction [ref].
What I fail to understand is how exactly do calcium and magnesium ions play a key role in acrosome reaction?

The process is not clearly understood. Calcium helps in capacitation: During capacitation calcium enters the spermatozoa through ion channels; blocking these channels inhibits the acrosome reaction but what calcium does inside the spermatozoa is not very clear. This paper says that calcium activates a certain tyrosine kinase in the spermatozoa which in turn activates a protein called p32. This they say occurs "concomitantly with capacitation". Other papers cited by this article talk about involvement of calcium dependent adenylate cyclase.

This article also says that protein tyrosine phosphorylations are important for capacitation but doesn't describe how.

I could not find a more precise information on this topic. I shall update the answer if I find one.


What is the name of cellular respiration that Prokayotic cells use? Eukaryotic cells use mitochondria using anaerobic or aerobic respiration. Prokayotic cells lack mitochondria but are bacteria. Mitochondria originated from bacteria and can be used in the same way. Bacteria produce ATP the same way that Mitochondria do.

So, what is that kind of cellular respiration called?

Prokayotic cells use anaerobic respiration.

Glycolysis is the only stage of cellular respiration that does not occur in mitochondria.

The glycolysis process does not need oxygen and uses anaerobic respiration. The other stages require oxygen and use aerobic respiration.


What is this worm like creature? Recently while cleaning my garden, I saw this worm like creature which resembles a leech but is humongous in size if I compare that with commonly found leeches in my area, Kolkata, West Bengal, India. I did not see something like this before so, I captured a snap of this creature and posting it here to know more about it if someone can give me a hint.

This is probably a land planarian, a flatworm (Plathyhelminthes) from the Subfamily Bipaliinae, called "hammerhead worm". This Subfamily is native to the Indian subcontinent, which matchs your description.

According to Wikipedia,

  The subfamily Bipaliinae is characterized by having a semilunar head that gives them the common name "hammerhead worms". The head has peripheral sensory pits on the ventral side and small peripheral eyes on the dorsal side.

You can see this semilunar head on the animal's anterior end (right hand side in your photo).

This subfamily contains the largest flatworms known. The larger one is Bipalium kewense, which can grow up to 40 cm.

However, the individual in your photo doesn't seem like B. kewense, which is a quite narrow worm and has a large head, with a different colour and stripes pattern:

Source: https://niceworms.wikispaces.com/Bipalium+kewense?responseToken=05b65f9b09b41aa5da58c3026c7f3ce8e

The one in your photo seems more like B. adventitium, which is a bit wider and has a smaller head:

Source: https://www.inaturalist.org/taxa/82290-Bipalium-adventitium

The problem is that B. adventitious adults are only 10 cm long, and that is hardly humongous.

So, I'd just say "it is a Bipaliinae flatworm", without narrowing it down to the species.

PS: It's not a leech (Annelida) because, among other clues, it clearly lacks metamerism.


Do blood vessel walls have blood vessels in them? If so, do those blood vessels have no walls because they don't need them because they're in the same tissue as that of a blood vessel wall? Are the cells alligned diffently at the edge of the blood vessel than in the rest of the blood vessel wall? Do blood vessels in blood vessels have an outer wall defined a sudden change in orientation of the cells?

Do blood vessel walls have blood vessels in them?

Yes, they do: the vasa vasorum.

When a blood vessel is too large, like the aorta or the cava, it has vessels to supply blood to their outer layers (where the cells are too far away from the lumen), not only to the Tunica adventitia (if by wall in your question you mean only that most external layer), as you can see in this image:

(note: this image is from a quiz in McGraw-Hill site, and the legend is not correct, "intima" and "media" are swapped)

Those vessels inside vessels are thus called vasa vasorum, which in Latin means exactly this: a vessel ("vasa") of a vessel ("vasorum"). You can read more about them in this Wikipedia page.

  If so, do those blood vessels have no walls because they don't need them because they're in the same tissue as that of a blood vessel wall?

No, they do have their own walls. Despite being inside another vessel, the vasa vasorum have the same basic structure of any other vessel with their same width.

Therefore, vasa vasorum vary in size, from vessels with single or multiple smooth muscle layer(s) to simple endothelial channels.

Interestingly, vasa vasorum are normally found next to nerves and lymphatics (see the image above). This close structural relationships "provide evidence that adventitial vasa, nerves, and lymphatics provide arteries and veins with nutrition, neurohumoral input, and an effective pathway to remove waste products from the parent vessel" (Williams and Heistad, 1996).

(source: Williams, J.K. and Heistad, D.D. (1996) "Structure and function of vasa vasorum", Trends in Cardiovascular Medicine, 6(2), pp. 53–57).


What snake is this one? I'm wondering what kind of snake is the one in the attached photo. It looks like Vipera aspis but It seemed a bit too big (lenght of about 1 meter).

This photo was taken near Como, in the north of Italy, in the woods of Parco Spina Verde.

I think it could be Vipera aspis, but that leght what did you descripe is really rare. Anyway it can be Smooth Snake(https://en.wikipedia.org/wiki/Smooth_snake) too. But you know personaly i cant do more from this point of view. The smooth snake is much more common and longer so there is a bigger possibility.


Population dynamics ODE with Allee Effects From reading about Allee effects, it appears that there is a modification of the one-dimensional logistic equation to account for an allee effect given by:

$$\frac{dN(t)}{dt} = rN\left(1-\frac{N}{K} \right)\left(\frac{N}{A}-1\right)$$

Here, $r$ is the species growth rate, $K$ is the carrying capacity, and $A$ is the threshold for the population to not go extinct $(0<A<K)$.

A few questions about this model:

1) What is it in this equation that determines whether or not the allee effect is strong or weak? It seems like the parameter $A$ would determine where the threshold is but not whether or not the effect is strong/weak.

2) I'm interested in an extension to a system of $n$ interacting species. Suppose I have $n$ competing species where each one is subjected to its own allee effect. Is this a suitable modification of the above ODE for $n$ species?

$$\frac{dN_i(t)}{dt} = r_iN_i\left(1-\frac{\sum_{j=1}^n\alpha_{ij}N_j}{K_i} \right)\left(\frac{N_i}{A_i}-1\right)$$

where $1 \leq i \leq n$. In that regard, the first two terms are the usual Competitive Lotka-Volterra model, and the last term accounts for the Allee effect.

First, Allee effects (also positive density dependence) can be modelled in several different ways, and the equation you give is one example. The terms weak and strong Allee effects are in my experience used in a couple of different ways. Most often, strong density dependence is used to denote Allee effects where the per capita population growth rate can become negative, which means that there is a critical point in population size, below which the population will tend towards extinction. Weak Allee effects are then used to describe cases where the population growth rate is negatively affected by low population sizes, but where the per capita population growth rate cannot go below zero (so populations will grow at low population sizes). Remember that in the classic logistic model, per capita population growth rate is maximized when population size is low (limit towards N=0), while it is maximized between N=0 and N=K in models with an Allee effects (in the model includes a concept of carrying capacity).

Using this definition of weak vs strong,  your model has a strong Allee effect, since per capita population growth rate will go below zero at the threshold A (see below). However, sometimes strong/weak is used to denote some sense of relative influence of the Allee effect on population dynamics, for instance if per capita population growth rate at low population sizes is decreased a lot or a little compared to the logistic model, even if both cases would correspond to a weak Allee effect in the first sense.

For comparison, here are two examples of how an Allee effect can be modelled, that shows how the per capita growth rate is affected with an weak Allee effect (see e.g. Boukal & Berec 2002 and Ferreira et al 2012) or a strong Allee effect (your model):

$$\frac{dN(t)}{dt} = \frac{r}{K}N^2\left(1-\frac{N}{K} \right) \tag{weak}\label{}$$

$$\frac{dN(t)}{dt} = rN\left(1-\frac{N}{K} \right)\left(\frac{N}{A}-1\right) \tag{strong}\label{}$$

If per capita population growth rate (dN/dtN) is plotted against population size for these two models, as well as for the standard logistic model, this is what you get:

In these examples, r=0.7, K=100 and A=20. As you can see, there is a big difference between the weak and strong case. The population growth rate (dN/dt) at different N is shown below:

As you can see, if populations using the strong Allee effect are started below A (in this case 20) the populations will decline towards extinction (since dN/dt is negative below A).

The multi-species extension including species interactions that you propose looks ok to me, for that particular formulation of the Allee effect.

Also, for a flexible way to study the Allee effect, you might be interested in this formulation (see Boukal & Berec 2002), which can produce both a strong and a weak behaviour:

$$\frac{dN(t)}{dt} = rN\left(1-\frac{N}{K} \right)\left(\frac{N}{K}-\frac{A}{K} \right)\tag{flex}\label{}$$

This function will produce a weak Allee effect if $A \leq 0$ (very weak if A is far below 0) and a strong effect is $A>0$. The weak model I give above is a special case of this formulation with $A = 0$. Per capita growth of this model is given below, for two values of A (with r = 0.5 for the logistic model and r = 0.38 for the flex models)

As a sidenote, I've also seen cases where negative density dependence at low population sizes is described as an Allee effect (so that Allee effect can be used to denote both positive and negative density dependence at low population sizes), but this is not very common. For a particular species, negative density dependence at low population sizes (in excess of what is found in the standard logistic model) could e.g. be found in situation where predators have a switching behaviour, so that they stop eating the prey when it becomes rare.


Genotypes of gametes produced by an F1 individual? I have an urgent question as I have an exam tomorrow. I was skimming some past exam papers and one question came up which has me completely confused.

A cross was made between a pure breeding diploid pea plant with round, yellow seeds and a pure breeding diploid plant with wrinkled, green seeds.
R and r for round and wrinkled respectively, and Y and y for yellow and green respectively. Assume dominant allele of each gene is upper case, and that the two genes are on different chromosomes and so are independently assorting.
a) Give genotypes of two pure breeding parents
RRYY, rryy
b) Give the genotype of resultant F1 progeny
RrYy
c) Give the genotype and respective frequency of the gametes produced by the F1 individual and indicate whether the gametes are parental or recombinant.
This is the question I am having trouble with and confused about

The reason I am confused is primarily I do not understand what is being asked when referring to the "gametes produced". Is this an F1xF1 cross and the question is asking about the F2 generation? I assumed not as the next question is:

Two of the F1 individuals obtained from the above parental cross were crossed to obtain the F2 generation
d) Give the phenotypes of the F2 progeny and their ratios

If someone could please shed some light on this it would be much appreciated

Gamate is a haploid germ cell produced by either male or female parent. In your question,two homozygous dominant and recessive parants produce RY and ry gamates respectively. F1 would have four types of gamates if we think about their genotype.They should have any one of  RY, Ry, rY, ry as their genotype.
RY and ry are parental gamates. They have the genotype of the gamates that F1's homozygous parents produced. Other two are recombinant genotype. Since they behave independently, you can go with mendelian genetics and draw a punnett squre.write RY Ry rY ry horizontally and vertically then get the F2 cross genotypes. Dominant genotypes will determine the phenotype.


What happens to the complementary base when the other undergoes a base substitution mutation? From what I know only the base pairs A and T/U, or G and C can occur due to hydrogen bonding. So if a base substitution mutation occurs, say an A is replaced by a C on the strand, does it affect only one of the strands on the DNA or does it changes the base pair entirely? Thanks.

Consider a stretch of DNA

A T C C T C
T A G G A G

Let's say that during replication a nucleotide get switched

A G C C T C
T A G G A G

Now, this does not work. The cellular machinery will find this location and try to solve it. It will either resolve it as

A T C C T C
T A G G A G

and no mutation would have happened. Or it will solve it as

A G C C T C
T C G G A G

and a mutation just happened.

You might want to read about DNA repair mechanisms.


Is vision a vestigial sense for deep ocean species? Sunlight doesn't penetrate beyond a couple of hundred feet from the surface of the ocean. Species that exist at greater depth probably live in a state of perpetual night; yet from a quick google image search (i agree it isn't a very authoritative source) for deep ocean species I see that plenty of these have eyes.

So ...

Are the sight organs in deep oceans species merely a remnant from an earlier era?
If they are a remnant, has evolution/mutation modified these organs over time?
Regardless of whether the organs of sight are vestigial organs for deep ocean species, how do the eyeballs withstand the extreme pressure of water in the deeps?

I can't answer your third, but I can answer your first two. With one word, in fact:
Bioluminescence
http://brightnepenthe.blogspot.com/2010/08/palate-cleanser-90.html

That's the deep ocean at night for ya. Unlike underground environments and caves, it's not pitch black pretty much anywhere in the ocean. There are things to see everywhere, and they play an important role in predator/prey relationships and/or mating. The absence of natural light does make things harder to see, but that's why you see the enormous eyes on species which live far down. So, nope! The eyes on deep ocean critters are not vestigial. They're very functional (and, if anything, probably increased in sensitivity).
The basics are summed up here: http://www.lifesci.ucsb.edu/~biolum/functions.html


Heritability in population genetics What is the difference between narrow sense heritability and broad sense heritability?
Does heritability in the broad sense refer to the degree of genetic determination?
Heritability in the narrow sense refers to additive effect of alleles , what does it actually mean?

Heritability in the narrow sense

Heritability in the narrow sense $h_N$ is the genetic variance $V_G$ over the overall phenotypic variance $V_P$

$$h_N = \frac{V_G}{V_P}$$

More information at Why is a heritability coefficient not an index of how “genetic” something is?.

Heritability in the broad sense

The heritability in the broad sense $h_B$ is the additive genetic variance $V_A$ over the overall phenotypic variance $V_P$

$$h_B = \frac{V_A}{V_P}$$

Decomposing of the genetic variance

Adding together the additive genetic variance $V_A$, the dominance genetic variance $V_D$ (and the epistatic genetic variance $V_I$) sums up to the overall genetic variance $V_G$. Here I will ignore the epistatic genetic variance

$$V_G = V_A + V_D$$

, where

$$V_D = x^2(1-x)^2(2\cdot M_{12} - M_{11} - M_{22})^2$$

$$V_A = 2x(1-x)(xM_{11}+(1-2x)M_{12} - (1-x)M_{22})^2$$

, where $M_{00}$, $M_{01}$ and $M_{11}$ are the measurements of the phenotypic trait in genotypes 00, 01 and 11 respectively.

Highly related

Why is a heritability coefficient not an index of how “genetic” something is?
Additive genetic variance with nn alleles
Additive genetic variance with nn loci


When was the purpose of bone marrow discovered? I'm currently reading William Cheselden's book Osteographia or The Anatomy of the Bones, which was published in 1733 (for the pretty pictures, naturally; not up to date anatomy). When he addresses the topic of bone marrow, he says,

  Every cylindrical bone has a large middle cavity, which contains an oily marrow, and a great number of lesser cells towards their extremities, which contain a bloody marrow. [...] The bloody marrow is also found in all spongy cells of the bones. [...] The use of the first kind of marrow I imagine is to soften, and render less brittle, the harder fibres of bones near which it is seated; and that the other marrow is of the same use to the less compact fibres, which the more oily marrow might have made to soft; and that for this reason, there is less of the oily marrow, and more of the bloody in young bones than in old ones.

Which strikes me as completely incorrect -- though correct me if I'm wrong. So, when was the purpose of marrow in hematopoiesis discovered, and by whom?

Answer: In the late 1800s, by a few different guys building on each other.
I personally had no idea, but a little searching around found this little gem, which seems up our alley: The origins of bone marrow as the seedbed of our blood: from antiquity to the time of Osler.  It's only ten pages so definitely worth a read, but a few passages of note:

Neumann and Bizzozero... are credited with making the initial observations leading to the recognition of the marrow as the seat of blood formation... In his report published in October 1868, Neumann described the presence of nucleated red blood cells in the bone marrow sap of humans and rabbits by squeezing bone. He was the first to conclude that during postembryonic life, erythropoiesis was taking place in the marrow.

However, Neumann concluded erroneously that the proliferation of marrow cells occurred inside the blood vessels of the marrow; the concept of marrow sinusoids was not coined until Minot's description in 1901.

It later says that, in the mid-1880s Osler stated

that there can be no doubt that nucleated red cells originate in the bone marrow...

It's actually a pretty interesting read, all in all, and like all of the best discoveries in science, it seems like a few people built on each others' work over the years, with a bunch sort of figuring it out around the same time.


Carbon sink and carbon storage Articles commonly state examples of carbon sinks are plants, soils, and oceans (e.g., link). My understanding is that carbon sinks must directly take up carbon from the atmosphere. Therefore, other organisms such as herbivores and carnivores are not considered carbon sinks (I understand their roles as carbon sources) although they store much carbon. Is this interpretation true?

If so, what is the main mechanism that soils (independent of plants) directly absorb carbon from the atmosphere? It looks as if most articles simply say that soils contain much carbon from plant organic matters, which is a carbon store rather than a carbon sink.

According to Wikipedia:

  A carbon sink is a natural or artificial reservoir that accumulates and stores some carbon-containing chemical compound for an indefinite period.

The key point here is the "indefinite period" part. For example, although my body stores some kg of carbon, I can't qualify as a carbon sink because most of it is likely to be released again in some decades.

On the other hand, soils store large amounts of carbon, and as the soils keep developing that amount tends to grow, making them an effective carbon sink. The mechanism consists mostly on accumulating organic matter, as you say, but as long the amount of that organic matter keeps growing, soil works as a carbon sink.


Difference between facilitated diffusion and secondary active transport in cells Specifically, what is the difference between facilitated diffusion carrier processes (passive transport) and secondary active transport co-transport processes (active transport)?

They seem to be the same thing - doesn't the passive process with the carrier transports substance $x$ against its gradient together with substance $y$ that is moving down its electrochemical gradient?

Similarly, in the active process, substance $x$ is transported against the gradient, and substance $y$ down its electrochemical gradient?

I don't see how energy differentiates the active transport in this case from the passive transport.

Short answer
Facilitated diffusion is a passive process in which membrane channels mediate the transport of polar, or big molecules that are not solvable in the cell membrane. Co-transport, on the other hand, is active transport, as it depends on the electrochemical gradient of ions across the cell's membrane, particularly Na+. Because ATP or other energetic compounds are not directly involved in co-transport, it is referred to as secondary active transport. The electrochemical ion gradient is mainly established by the Na+,K+-ATPase.

Background
As commented upon by others, your question is not entirely clear and the best way to approach this question is by defining the various terminologies and physiological mechanisms used in your question:

Active transport needs an energy source such as ATP. For example, the Na+,K+-ATPase is an enzyme that pumps Na+ and K+ ions against their concentration gradients into the cytosol (K+) or out of the cell (Na+). Note that both Na+ and K+ are transported against their chemical gradients (and Na+ also against its electrical gradient as the cell is negative). Therefore your statement that [...] in the active process, substance x is transported against the gradient, and substance y down its electrochemical gradient is untrue, and likely the cause of your confusion.
Passive transport is mediated by diffusion, which typically occurs through a concentration gradient. Only small, relatively hydrophobic molecules are able to diffuse across a phospholipid bilayer at significant rates. Examples are gases (such as O2 and CO2) in the lungs, and small polar but uncharged molecules (such as H2O and ethanol) (Cooper, 2000).
Facilitated diffusion is an example of passive diffusion, but aided by membrane-spanning channel proteins that span the lipid bilayer. Therefore the particles (molecules or ions) do not have to dissolve in the cell membrane's hydrophobic lipid bilayer, allowing hydrophylic and larger molecules (carbohydrates, ions) to be transported into the cell. No external source of energy is needed and  travel across the membrane in the direction determined by their concentration gradients and, in the case of charged molecules, by the electric potential across the membrane (Cooper, 2000).
Co-transport is active transport, where the energetically unfavorable transport of a particle against its electrochemical gradient is facilitated by the co-transport of a favorable one down its gradient. In other words, multiple particles are transported so as to neutralize the sum of the transport. For example, sodium-dependent glucose tranporters transport glucose into the cell against the concentration gradient (unfavorable) and Na+ is transported along with it into the cell which is a favorable transport (Haraki & Inagaki, 2012). This is an example of a symporter. An example of an antiporter is the Na+/Ca2+ antiporter found in the heart to transport Ca2+ out of the cell against a steep concentration gradient and electrical gradient, while 3 Na+ is imported into the cell to balance the unfavorable Ca2+ transport. Note that all these mentioned co-transporters and many others are dependent on the Na,K-ATPase that ultimately generates the Na+ and K+ gradients by pumping Na+ out of the cell and K+ into the cell using ATP (Freeman, 2000). This generated membrane potential works like a battery being charged, and co-transporters discharge it by using the energy stored by importing Na+. Hence, it is referred to as secondary active transport, as no direct energy input from ATP is needed, but instead it utilizes the electrochemical gradient created by the Na+,K+-ATPase.

These considerations should clarify your issues and answer your question on what co-transport exactly is. Specifically, the glucose transporter mentioned, GLUT1 as you refer to, is a symporter that mediates secondary active transport.

References
- Cooper, The Cell, 2000
- Haraki & Inagaki, J Diabetes Invest 2012; 3: 352-3
- Molecular Cell Biology, 2000


Why did eukaryotic cells develop? If eukaryotic cells can survive in extreme conditions, then why are their still prokaryotic organisms?

As far as I understand your question, the "development" of eukaryotic cells can be linked to the endosymbiotic theory Symbiogenesis.

This diagram only depicts a possible trajectory of evolution which is still unknown.

A cell that respired anaerobically took in a bacterium that respired aerobically, supplying both itself and the larger cell with energy in the form ATP. This created a competitive advantage for the larger cell because aerobic respiration is known to be more efficient than anaerobic respiration. Unhurriedly, the aerobic bacteria evolved into mitochondria and the larger cell into a heterotrophic eukaryote.
A heterotrophic cell took in a smaller photosynthetic bacterium, which supplied it with organic compounds, thus making it an autotroph. The photosynthetic prokaryote evolved into chloroplasts and the larger cell into photosynthetic eukaryotes.


CRISPR/Cas9 edited E.coli on AFM? I am doing CRISPR/Cas9 experiment on E. coli. I am introducing recombinant plasmid  BPK764 (which carries Cas9 + sgRNA designed and added later in that plasmid) into compentent E.coli cells which already carries another plasmid with GFP gene. sgRNA will be designed so that it corresponds to that GFP gene becouse my main point is to cut out GFP gene. The main result of this experiment will be E.coli cells that do/don't express GFP gene (depending on CRISPR/Cas9 efficacy), therefore, the resultant cells will or hoply won't light green. I will see that under UV lamp, and by fluorescent microscopy.

Now I'm getting to my question.
Is there something on those resultant cells (some trait, like membrane structure, youngs modulus, that differs from CRISPR untreated cells) that can be visualized on AFM (atomic force microscopy)? Something that changes on cells after inserting plasmid that can confirm efficacy of this experiment?

Or maybe some other idea on this experiment using AFM?

Unless you're specifically targeting genes involved in the physical morphology of the cell, I doubt you would find any differences with CRISPRed vs non-CRISPRed cells that is measurable via AFM.

Perhaps you should instead target genes known to contribute to the structure of the cell wall, which I would expect to be the dominant material contributing to the Young's modulus. Since you mentioned GFP as a tool for selecting for "successful" cuts, it might be worthwhile looking into generating a multiplex plasmid that allows you to target several loci with a single construct. Such kits are available on Addgene and contain associated publications and manuals on how they can be used.

So to summarize, no, I don't think there is anything physically different about cells that have been CRISPR treated compared to a control group. If you did want to use CRISPR to effect a knockout of the fluorescence in the competent cells you described and alter the cell mechanics, you would likely have to generate a multiplex CRISPR plasmid with multiple gRNA cassettes for both GFP and perhaps some gene involved in cell wall formation. Keep in mind that your efficiency percentage is compounded with each new target in the same multiplex – instead of a single cut being deemed successful, you will have raised the bar to 2 cuts being deemed successful without doing anything to improve the efficiency of a single cutting event.

Hope this helps, and I'd be happy to discuss this more.


Why do only two sexes exist for animals? Why, from the natural selection point of view, do only two sexes exist for animals?

To get a non-circular answer to why humans and other mammals have only two sexes, it's helpful to take a look at our evolutionary history.  While mammals possess several adaptations to a terrestrial life cycle, including internal fertilization and gestation, which require substantial anatomic specialization between males and females, these are all secondary features that evolved long after our aquatic ancestors had acquired two distinct sexes.

Indeed, if we look at animals like fish, which reproduce via external fertilization, it's not at all obvious why they might not have more than two sexes.  After all, for many aquatic animals, mating involves little more than the female and the male releasing their respective gametes into the water, where they meet and fuse to a form new zygote, which can then divide and grow into a new adult.  Seen that way, there seems to be no reason why there could not be more than two "mating types", as in many fungi, such that gametes of any two distinct types could fuse into zygote.

The answer lies in the fact that the male and female gametes aren't actually that similar: the female gametes, or eggs, are typically large cells that contain all the nutrients necessary for the new zygote to develop into a viable individual, whereas the male gametes, or sperm, are tiny and produced in huge numbers.  This asymmetry is known as anisogamy, and modeling its origin has been an important topic in the theoretical study of evolution.

Without going into details on the evolution of anisogamy, once it exists, it clearly forces the mating types to also split into two groups: there's no advantage in two microgametes (sperm) fusing, since the resulting zygote would lack the nutrients it needs to be viable, whereas the fusion of two macrogametes (eggs) would simply be inefficient — eggs, being large, are comparatively rare and expensive, and wasting two of them to produce only one offspring would be suboptimal even if the resulting zygote was viable.  Nor is there really room in such a scheme for gametes of intermediate size: they'd be too small to fuse into a viable zygote with sperm, but too large to be produced in sufficient amounts to be effective in fertilizing eggs.

Of course, there's nothing that would stop a single adult from producing both micro- and macrogametes, but such an adult would not really be a third sex — it would just be male and female at the same time, a mating strategy known as (simultaneous) hermaphroditism, which indeed occurs relatively often in nature.

So, if pretty much all animals are anisogamous, why do fungi remain isogamous (and often have multiple mating types), then?  Well, one explanation is that the main drivers for the evolution of anisogamy — sperm competition and transportation risk — don't really apply to fungi, which mate when two sessile haploid mycelia grow and come into contact with each other.  Since the gametes are not motile, there's no advantage for either/any sex to produce more of them (at the cost of smaller size) in order to increase the chance of successful mating.  Thus, isogamous mating works fine for the lifestyle of fungi, and having multiple mating types is then a useful adaptation to make successful mating between neighboring mycelia more likely.


Assembly of metagenomic data I'm trying to assemble metagenomic data that comes from termite guts. The sequences comes from SOLiD and no paired, so the reads are extremely short (25bp).

I have tried multiple assemblers (CLC, velvet, metavelvet, Meta-IDBA) but all produce few contigs (15 contigs, 1000bp average). The contig output is scarce considering the amount of raw data (5 Gpb).

Has anybody has any success in a task such as this?.

Thanks.

This depends on your coverage and the number and relative proportion of species in the mixture.  this seems unlikely to produce results unless the protocol biases the library (rRNA universal primers for instance.)  I think at 25 bp sequences, even 30x coverage would not give full assembly sequences. Typically I believe 25 bp reads are only used to resequence close variants from similar or reference genomes.


Why is secretin sensitive to acid? My textbook says, secretin secretion is triggered by the presence of acidic chyme in intestine.

But why is secretin sensitive to acidic environment? I checked the wikipedia page of secretin and found no related information.
Is there some mechanism for secretin to secrete in presence of acidic chyme?

The exact mechanism by which secretin is released is still not known.

  The mechanism by which acid brings about secretin release is not fully understood but probably involves acid sensing ion channels of the Trp family present in the brush border of S-cells.

Physiological reason for susceptibility to acid: It is because this hormone acts on pancreas and increases the secretion of bicarbonates to increase the pH. It also reduces gastric motility thereby allowing longer digestion within the stomach. So, it effectively prevents deterioration of duodenal mucosa and helps in efficient absorption of lipids by increasing ph in duodenum which is required for better action of lipases. So, its secretion is induced by increased acidity from chyme (so that it can increase pH).

Thus, we can conclude that secretin is acid sensitive.

Source: https://www.pancreapedia.org/molecules/secretin


What kind of flying insect is this? What kind of flying insect is this? It kinda resembles a dragonfly but it had what looked like a stinger on the end of it's tail. It was found in Franklin, Ohio.

... it kinda resembles a dragonfly ...

That's because it is a dragonfly! This is a female Tramea onusta, most commonly known as a "Red Saddlebag", which comes from the red coloration found at the lower regions of the dragonfly's hindwings.

  ... it had what looked like a stinger on the end of it's tail.

That's exactly correct! Female dragonflies have what look to be a stinger, however, they're used for laying eggs instead (and not as a weapon). (source, p.5)


Can someone identify this creature? I discovered a few of these while cleaning an outdoor fish pond north of Sacramemto California. What is this?

This is a Burrowing Mayfly nymph (order Ephemeroptera), more than likely of the family Ephemeridae.  The Bugguide site has very few photos of nymphs, but you'll find a near miss here (the species shown is not Californian, but the related Ephemera simulans Walker, 1853 is; see here for other possibilities [you'll want to look for nymph photos of the species listed from "USA: SW"]).


Is this an Emperor Penguin or a King Penguin? I have a book from Dorling Kindersley called Animal Encyclopedia (the German version that I have is called Das große Tierlexikon) with images from animals.
One is titled Emperor Penguin (Kaiserpinguin) which is in my opinion clearly recognizable as a King Penguin (Königspinguin).
This is the image:

I wrote to Dorling Kindersley and they told my that their investigation revealed that it really is an Emperor Penguin.
I am not a biologist nor a penguin expert, but from all the descriptions and images I could find (even in the same book on other pages!) I think the publishing company is wrong and just too lazy or arrogant to admit this error and too miserly to release a revised version of the book.
Who is wrong? Me or Dorling Kindersley? Emperor or King?
Update 2020
They seem to inherently admit it themselves, that the book was wrong (and that they lied to me), as they used the same picture on one of their websites and with king penguin in the caption of the picture:

Found this image here. I've also seen references to the "closed orange ear patch" of the King Penguin, which fits with the image. So my vote is for the DK image being a King Penguin.


Its there a gene or genes for intelligence? I don't know almost nothing of genetics but I felt a little interested in the subject of genetics and its role in intelligence and i found to reports that talk about certain genes that contribute to intelligence

https://www.nature.com/news/smart-genes-prove-elusive-1.15858 https://www.newsweek.com/how-be-smart-intelligence-linked-500-genes-large-new-study-842454

What I don't understand is if only some people have this 500 genes or all human population has this genes?

Is IQ heritable?

Let me start by saying that there is no commonly agreed upon method to measure IQ (thank you @mdperry). Keeping this in mind...

Yes, studies have shown that IQ is heritable. Or rather, IQ has a heritability that differs from both 0 and 1, meaning that both environment variation and genetic variation plays a role in determining an individual's IQ. Studies show IQ heritability varying between 0.5 (ref) and 0.8 (ref). For more information, please have a look at this post.

To understand the concept of heritability, please have a look at Why is a heritability coefficient not an index of how “genetic” something is?.

  What are the genes that contribute to it?

IQ is a polygenic trait, meaning that many loci (locus = position in the genome) are affecting the variation in IQ. For more information about those loci, please have a look at this post.

  What I don't understand is if only some people have this 500 genes or all human population has this genes?

Your misunderstanding comes from a misunderstanding about the concepts of gene and allele. You should start by having a look at the definition of the three following terms

gene
allele
locus

Below, I will not comment about the 500 genes claimed in this popular article and will just consider them as valid without considering the complication behind the methodology used for such estimation and about what original articles this popular article is citing.

With the exception of eventual copy number variation, the entire human population share these 500 genes but not everyone has the same allele at these 500 loci.


Nutrient limitation in terrestrial and freshwater ecosystems In terms of primary production, it is often described in textbooks that nitrogen is the most limiting nutrient in terrestrial ecosystems, while phosphorus is the most limiting nutrient in freshwater ecosystems. What creates this difference?

The traditional explanation for this is that nitrogen compounds are more mobile than phosphorus compounds. As a result, nitrogen is more likely to flow through terrestrial ecosystems and accumulate in freshwater ecosystems, making P relatively more limiting than N in freshwater.
Phosphorus compounds (e.g., phosphate) are more "sticky" and tend to bind/sorb to compounds in the soil and aquatic sediments, e.g., ferric compounds. Thus, most phosphorus gets bound up in terrestrial ecosystems because it's less mobile than nitrogen, or gets bound up in aquatic sediments. As a result, nitrogen becomes relatively more limiting than phosphorus in terrestrial ecosystems, and the phosphorus that does enter freshwater ecosystems often becomes inaccessible to biological organisms like primary producers.
Note that this paradigm is a generalization, and is dependent on many other factors. Lake pH and concentration ferric compounds can regulate whether the sediments are sources or sinks of P; anoxic conditions can lead to denitrification, a loss of N that could offset N inputs. Anthropogenic additions of N and P (either to the freshwater system directly or to the terrestrial ecosystem that drains into it) could dramatically perturb the natural balance between N and P limitation in terrestrial and aquatic ecosystems in a way that does not conform to the paradigm.
Some references you might find useful:
Elser, J. J., Bracken, M. E.S., Cleland, E. E., Gruner, D. S., Harpole, W. S., Hillebrand, H., Ngai, J. T., Seabloom, E. W., Shurin, J. B. and Smith, J. E. (2007), Global analysis of nitrogen and phosphorus limitation of primary producers in freshwater, marine and terrestrial ecosystems. Ecology Letters, 10: 1135–1142.
Vitousek, P.M. & Howarth, R.W. Biogeochemistry (1991) 13: 87.


Are all action potentials the same shape and amplitude when graphed with respect to time? The most common visualization of an action potential is a graph of the difference in membrane potential (y axis) at a particular time (x axis).

According to my textbook Cognitive Psychology by E. Bruce Goldstein, an action potential sent from neuron down the axon remains the same. That is, if we plot the action potential as described above, then at each as it is propagated down it will have the same shape on the graph (within some range of error obviously, but he is saying the error is trivial).
But he then says on page 34

  One way to answer the question of how action potentials determine different qualities [(e.g. taste of something sweet)] is to propose that the action potentials for each quality might look different. However, [Edgar] Adrian rules out that possibility by determining that all action potentials have basically the same height and shape.

My Question

Can someone confirm these two facts:

Once an action potential is sent from a given neuron down the axon, does the shape and amplitude remain constant as it is propagated?
Do all action potentials have the same amplitude and shape?

Short answer
Action potentials differ in shape between neuronal cell types, and action potentials may even change shapes during action potential propagation within one and the same axon.

Background

  Once an action potential is sent from a given neuron down the axon, does the shape and amplitude remain constant as it is propagated?

Although the textbooks will typically say action potentials are transmitted without their amplitude being changed this claim is theoretically virtually impossible due to the many variables encountered in and around the axon. For example, axons in the sciatic nerve may extend to a meter and it is virtually impossible to keep the exact conditions along that length exactly identical. The amplitude of the action potential is mainly dependent on the influx of Na+. Slight variations in membrane potential, concentration of sodium, or channel (subtype) densities may therefore change the amplitude. In addition, temperature affects action potential amplitude (Hodgkin & Katz, 1949) and slight temperature differences along long axons may therefore be expected to alter amplitude. Likewise, shape may alter as well. For example, glutamate released alongside axons of hippocampal pyramidal neurons results in widening of action potentials (Sasaki et al., 2011).

  Do all action potentials have the same amplitude and shape?

Therefore, given the answer under question 1 no, they do not have to. Even a propagated action potential in a given axon may change amplitude and shape, as said. Most notably, different neuronal types may in fact be classified according to their action potential morphology, such as the various neuronal types in the dorsal root ganglia of the spine that can be differentiated based on their duration (Villiere & McLachlan, 1996).

References
 - Hodgkin & Katz, J Physiol; 109: 240–9
 - Sasaki et al., Science 2011; 331: 599-601
 - Villiere & McLachlan, J Physiol 1996; 76: 1924-41


Is the cell cycle applicable to meiosis as well, or just mitosis? All the diagrams I can find, show the cell cycle as having G1 phase (growth 1), S phase (DNA replication), G2 (growth 2) before the Mitotic phase (mitosis + cytokinesis).
Is there an equivalent "cell cycle" for meiosis, since the chromosomes in parent cell in meiosis also having "double" the genetic material prior to cell division (presumably from DNA replication too)?
Is it simply the same cell cycle as mitosis but with a Meiotic phase instead of Mitotic?
If so, would appreciate if anyone had a diagram :) Thanks!

The cell cycle is only associated with mitosis. The cell cycle is the normal process of cell division with which cells can indefinitely increase their number by cyclically repeating the process.  When a cell goes through the cycle, the result is two cells that are genetically identical.
Meiosis is a special type of cell division (which can occur only in eukaryotes) that produces cells that are not genetically identical to the initiating cell.  The number of chromosomes in each of the resulting cells is half the number that were in the initial cell.  (These haploid cells can later participate in fertilization, producing a cell with the original number of chromosomes.)  Many of the steps of meiosis are similar to the steps involved in mitosis, but overall the process is more complex. Since meiosis reduces the number of chromosomes, it cannot be repeated and so does not take part in a cell division cycle.


How do mutations and protein synthesis link to cancer? How do mutations and protein synthesis link to cancer?

I know that a mutation in DNA can cause the triplet code on the mRNA to change so different amini acids are made and a different order means a different protein is made but how does it link to cancer when cancer is caused by uncontrollable mitosis.

Thank You

This question is at GCSE level so freshman/sophomore level.

Mutation in DNA can be beneficial, harmful, or may have no effect. This is dependent on the gene location where this mutation has occurred.

Various genes linked to cancer are:

Tumor suppressor genes: These genes regulate cell growth by keeping check on cell division, repairing mismatched DNA  and regulating cell death.  Mutation in this type of gene leads to unregulated cell growth and lead to formation of tumor.

Examples:

TP53 is most commonly mutated tumor suppresor gene. More than 50% of
cancers are caused due to mutation in this gene.
Mutation  in BRCA1 or BRCA2 genes is responsible for breast and
ovarian cancers. It  may also increase the risk of pancreatic cancer
and melanoma.

Proto-oncogenes: These genes help cells to grow normally. Mutation in this gene cause its permanent activation and unregulated cell growth takes place and lead to cancer. This abnormal gene is called oncogene.

Examples:

HER2 is responsible for breast and ovarian cancer.
RAS family of genes, responsible for cell communication, cell growth,
and cell death.

DNA repair genes:  These genes play role in repair of DNA, which is mismatched during replication.   Defect in DNA repair gene, leads to synthesis of incorrectly formed DNA and eventually incorrect protein synthesis.


Epistasis: Why should a recessive allele be a hypostatic gene? Let us take the example of Recessive epistatsis, an epistasis in which a double recessive gene mask the phenotypic expression of alleles  of another locus.
 (adapted from: An Introduction to Genetic Analysis)

An example from the same book:

  In  plant blue-eyed Mary (Collinsia parviflora), the biochemical pathway is as follows:

  The w and m genes are not linked. If homozygous white and magenta plants are crossed, the F1 and F2 are as follows:

  Complemention results in a wild-type F1. However, in the F2, a 9:3:4 phenotypic ratio is produced.

  This kind of interaction is called epistasis, which literally means “standing on”; in other words, an allele of one gene masks the expression of the alleles of another gene. In this example, the w allele is epistatic on m+ and m$^1$. Conversely, m+ and m can be expressed only in the presence of w+.

Interpretation & Question:

The gene product of m$^+$ is needed to form blue pigment from magenta. On the other hand, in the absence of w$^+$ allele (i.e. w w genotype), no magenta (precursor of blue) is formed so the phenotypic expression of m$^+$ allele(s) is masked. Now, what has m got to do here? $^1$ It is not encoding anything.

Note:

On referring other books I found they do not suggest a hypostatic gene to be recessive (as $m$ has been considered here).

My idea of recessive allele is that one that due to loss-of-function mutation either produces a non-functional variant of the protein or the same protein at a lower quantity.

Has recessive allele been considered an hypostatic allele here considering that it might be able to code normal functional protein at a lower rate?

Scope of answer:

Which concept should be followed? Why (ideally with citation)?

In the context of this textbook, m is simply an allele that codes for a non-functional protein product. The protein product of m is incapable of converting magenta pigment into blue pigment.


Which animal that lives in the forest makes this noise? Which animal makes this noise? Link to audio file

The file was recorded next to a forest in Germany.

It is a bird sound and most probaby a young bird of prey. It might be a young buzzard. Or, if it's in the eveving or night it might be the sound of a young owl.


How to know if a woman is fertile without actually making her pregnant? How to know if a human female is fertile (can give birth to child in future) without making her pregnant? Any signs, tests?

Of course. There's several fertility tests available to determine the quality and quantity of egg reserve, and whether or not the there are abnormalities in the uterus.

However, some of them are invasive procedures, and all of them should be performed by a professional. I doubt the layperson would know what they're looking at on an Ovarian Ultrasound.

If you're asking whether there's an "easy" way that doesn't involve a trip to a doctor - then I would say 'no.' Casual inspection would only reveal any abnormalities in the vagina and the opening of the cervix, and hormone tests are only partial indicators.

Then again, if a woman has reached physical adulthood and is under the age of 38 then the chances of being infertile (or have difficulty conceiving) are quite low - about 3% to 10%. Infertility is usually much more of a concern to women who wait until after the age of 35 to have children, as there is a definite biological window (the number of eggs the woman was born with) to consider that starts to close as a woman nears her 40's.

It's also important to note that trouble conceiving can stem from either partner, and there's about a 40%-50% chance in a couple trying to conceive the male has an 'issue' and the woman is perfectly healthy.


same SNP rs# referenced to be found in two different genes Two GWAS papers have referenced the same SNP (rs7442295), but one states it's found in the gene GLUT9 and the other states it's found in SCL2A9. The ncbi dbSNP says it's in SCL2A9, and I thought that the rs number was unique to each SNP, so how can it be in two different genes? I'm really new to GWAS, so it might be a really stupid question, but any advice would be great!

The NCBI dbSNP entry shows rs7442295 to be in the gene SLC2A9, not SCL2A9 stated in the original question.

As the Wikipedia article for SLC2A9 says, synonymous names for SLC2A9 include:

  solute carrier family 2 (facilitated glucose transporter), member 9, GLUT9, GLUTX, UAQTL2, URATv1, solute carrier family 2 member 9

So GLUT9 and SLC2A9 refer to the same gene, and the two papers are not in conflict about the location of the rs7442295 SNP.


What are the units of Q10 (temperature sensitivity)? $Q_{10}$ is the increase in a rate (e.g. activity of an enzyme) observed with a 10° temperature increase.

According to Wikipedia:

$$Q_{10}=\left(\frac{R_2}{R_1}\right)^{{10}/\left({T_2-T_1}\right)}$$

It is apparent that the units of $R$ (e.g. $mol/g/s$) cancel out, but what about the units of temperature? Does $Q_{10}$ have units? It seems the units would be "per 10 °C", but it is not clear how this comes from the referenced equation

Figure. A schematic diagram showing the effect of the temperature on the stability of an enzyme catalysed reaction. The curves show the percentage activity remaining as the incubation period increases. From the top they represent equal increases in the incubation temperature (50 °C, 55 °C, 60 °C, 65 °C and 70 °C).

The $Q_{10}$ is a unitless number, that summarizes the effect of raising temperature 10°C on the rate of a chemical reaction. A $Q_{10}$ of 2.0 suggests that raising the temperature of a system by 10 °C will effectively double the rate of the reaction. This value would be expected for most chemical reactions occurring within normal physiological temperatures.

Mathematically, $Q_{10}$ can be represented by the following expression:

$$Q_{10}=\left(\frac{k_2}{k_1}\right)^{\frac{10}{t_2-t_1}}$$

$t_2$ = higher temperature
$k_2$ = rate at $t_2$
$t_1$ = lower temperature
$k_1$ = rate at $t_1$

Usually the temperature difference is about 10 °C, then you can simplify the equation

$$Q_{10}=\left(\frac{k_1}{k_2}\right)^{\frac{10}{10}}=\frac{k_1}{k_2}$$

Edit: You can easily calculate $k$ form Arrhenius equation

$$k=Ae^{\frac{-\Delta G^*}{RT}}$$

where $k$ is the kinetic rate constant for the reaction, $A$ is the Arrhenius constant, also known as the frequency factor, $-\Delta G^*$ is the standard free energy of activation ($kJ/mol$) which depends on entropic and enthalpic factors, $R$ is the gas law constant and $T$ is the absolute temperature.


Why doesn't Diabetes cause death by starvation? The main cause for diabetes is lack of insulin in the body. Insulin is the hormone that allows body cells to absorb glucose from the blood. With out insulin, the body cells can't get glucose from the blood. So, why doesn't diabetes cause death by starvation?

Not all cells depend on insulin to take in glucose from blood (e.g. vascular endothelial cells). But the majority do (muscle tissue and fat tissue).

The lack of insulin causes the cell to use auxiliary metabolic pathways to generate its energy [1]:

in muscle, the protein breakdown is stimulated
liver gluconeogenesis is stimulated by low insulin levels and high amino acid levels in blood and using substrate from muscle and fat tissue
glucocorticoids stimulate lipolysis
liver starts ketone body synthesis, which along with medium chain fatty acids prove to be quite a good alternative energy source for the brain

Energy from nutritional principles is as follows:

Lipids = 9 kcal/g
Proteins = 4 kcal/g
Carbohydrates = 4 kcal/g - the most important because they are used as is. Lipids and proteins require energy from other sources to start chemical reactions which yield energy.

References:

Mark Brandt, Ph.D. Endocrine Notes Supplement from Rose Hulman Institute of Technology, pages 78-80
Wikipedia (links)


Small mottled beetle identification I live in Chapel Hill, North Carolina, and recently started seeing a bunch of these little guys in my house. They're about 1/8" long (estimate), with brown/black zigzag stripes; it's possible they're babies, but over the last two weeks their size has remained consistent so this seems unlikely.

It's probably an adult varied carpet beetle (Anthrenus verbasci). They are quite small and commonly found in homes. Here's one of a number of images available on Wikimedia:


How are hereditary neural circuits created in the brain during early development? Whilst our experiences shape the specifics of our brains throughout life, we know that there are a lot of shared properties between us. We all share the same basic layout as, for example, the V1 cortex is always in the same place. Thus it is evident that whilst some of the neural development is experience-dependent, some of it is hereditary/genetic or "hard wired".

It would seem to me that the extent to which the brain is "hard wired" depends on the species. Humans seem to have a lot more room for specialisation in life, whereas some animals don't exhibit much individuality, tending to follow very regular behavioural patterns that have no doubt evolved over time, subject to natural selection.

I have read up to some degree on how experience-dependent development works, but have been largely unable to find any detailed research into how experience-independent development works. That is, how does DNA encode these "hard wired" neural circuits?

Furthermore, the human brain contains some 100 billion neurons. If I assume that maybe 1% of them are "hard wired" into circuits from birth, that's still a billion neurons, each with several connections to other neurons that need to be somehow coded into a DNA sequence which only amounts to a couple of gigabytes worth of data. So how is the complex structure of these "hard wired" (experience-independent) neural circuits encoded in such a limited amount of DNA? How much of the brain is actually hard wired in this way and how much is open to experience-based development? Am I right in associating this process with the phenomenon of "instinct", that is, "hard coded" behavioural patterns in animals which appear to be hereditary?

Is there a name for this field of study? Specifically the study of how neural circuits are generated in the earliest stages, to lay down the high level structure of the brain before experience-based development can take over?

This is one of the most important question in neurosciences and we are far from understanding it. This is also the topic of the entire subfield of neurodevelopment (to answer your last question).

First, you are right that the exquisite degree and physiological correspondence between individuals of a species, and even between species, indicate a strong genetic component. But you are also right that we have good evidence for a developmental component to brains physiology. Here are a few random examples (at the top of my head, so maybe not the most important/influential papers):

Cells selectivity in the primary visual cortex depends on visual experience. Animals housed in an environment with only horizontal or vertical stripes will have cells selective only to horizontal or vertical orientations (Blakemore & Cooper, 1970).
At birth the primary visual cortex doesn't have cortical maps. They develop over time (e.g. Chapman, Stryker & Bonhoeffer, 1993).
Due to synaptic pruning, newborn have actually more connections than later in life. These connections will be progressively eliminated during youth.
Inserting a third eye in the forehead region of frogs makes connections to their optic tectum and creates columns of ocular dominance just as their normal 2 eyes (Constantine-Paton & Law, 1978). Even though having a 3rd eye is clearly not genetically encoded.
Similarly, rewiring the retinal projections of ferrets to their auditory cortex will form orientation columns just as in the primary visual cortex (Sharma, Angelucci & Sur, 2000), even though this area usually processes a completely different modality.
Putting amblyopic (a developmental visual disorder) rodents in complete darkness for some time seems to "reboot" their visual system and cure them from amblyopia (He, Ray, Dennis & Quinlan, 2007).
Efficient encoding of natural statistics mimics the response properties of cells in the nervous system (e.g. Olshausen & Field, 1996).

What these different experiments suggest is that the overall structure of the brain is genetically determined, but development is truly what shapes the function and selectivity of cells.

Blakemore, C., & Cooper, G. F. (1970). Development of the brain depends on the visual environment. Nature, 228(5270), 477-478.

Chapman, B., Stryker, M. P., & Bonhoeffer, T. (1996). Development of orientation preference maps in ferret primary visual cortex. Journal of Neuroscience, 16(20), 6443-6453.

He, H. Y., Ray, B., Dennis, K., & Quinlan, E. M. (2007). Experience-dependent recovery of vision following chronic deprivation amblyopia. Nature neuroscience, 10(9), 1134-1137.

Constantine-Paton, M., & Law, M. I. (1978). Eye-specific termination bands in tecta of three-eyed frogs. Science, 202(4368), 639-641.

Sharma, J., Angelucci, A., & Sur, M. (2000). Induction of visual orientation modules in auditory cortex. Nature, 404(6780), 841-847.

He, H. Y., Ray, B., Dennis, K., & Quinlan, E. M. (2007). Experience-dependent recovery of vision following chronic deprivation amblyopia. Nature neuroscience, 10(9), 1134-1137.

Olshausen, B. A. (1996). Emergence of simple-cell receptive field properties by learning a sparse code for natural images. Nature, 381(6583), 607-609.


Why is oxygen needed for the electron transfer phosphorylation? I understand that oxygen is the acceptor of electrons and hydrogen ions during the electron transfer phosphorylation, the last step off the ATP-producing aerobic respiration.

But why?

Aren't there any other alternatives for this acceptor? Oxygen is already recognized to have several harmful effects to cells - wouldn't another molecule be a better choice?

Why does it even require an "acceptor" to accept the electrons and hydrogen ions? What would happen if they were left alone?

I apologize if my question was due to my ignorance in basic chemistry or biology, but do please point it out and explain it to me. Thanks!

Aren't there any other alternatives for this acceptor?

Not that we're aware of. Every other alternative requires an anaerobic environment - which means small, and often less efficient.

  Oxygen is already recognized to have several harmful effects to cells - wouldn't another molecule be a better choice?

When we're talking about a molecule's fit there are many things to consider. Primarily its electronegativity, as that determines its stability, ability to accept and donate electrons, protons, and its ease of acquisition given plentiful amounts in the environment.

Molecular Oxygen is comparatively stable to a lot of di-atomic molecules, and comparatively reactive to others. It's in the butter zone for the act of being the terminal acceptor.

Let's think about Fluoride: Almost all of it is bound up in rocks with other elements. It's not available everywhere. It might be an alright candidate if we could eat rocks, but it also replaces minerals in our bones and teeth. Yes, you're familiar with this - but too much leads to fluorosis - where too much of the calcium compound is replaced, and it ends up making the bones and teeth much weaker.

Alright, let's think about Nitrogen - Very stable, pretty good electronegativity, abundant... but a little too stable. Yup, it's a gas, it's everywhere, and we can't use a lick of it. It's so stable that it's basically inert. The only reason rhizomes and other beneficial bacteria can use it is because they're in a controlled environment away from oxygen with significantly different biochemical processes which produce much less energy (and probably wouldn't be able to support large multicellular organisms that are as active as we are). So, Nitrogen is out.

Carbon? Nope, as an ion it's dangerously reactive, and as anything else it's too stable. Plus, we're carbon-based! If we used carbon as the terminal acceptor then the proteins handling the electrons would have to be even more exotic and filled with other elements to prevent them accidentally gobbling up the electron and becoming useless.

Sulfur? Not electronegative enough for human purposes, unfortunately. It wouldn't act as a terminal acceptor unless our bodies seriously oxidized it; and any oxidized molecules floating around would be more dangerous than molecular oxygen floating around. Plus most sulfur is bound to minerals as well - not abundant unless you're in the ocean.

Oxygen is both incredibly abundant and easy to perform the chemistry with. More reactive molecules are usually not abundant and tied up in the Earth's crust and could be more dangerous.

Less reactive molecules tend to be so non-reactive that we can't do anything with them, and if we could force them into a state where they would be reactive they tend to be violently reactive or require very specific environments that we can't reproduce on a scale necessary to be as mobile as we are.

Oxygen is not perfect, but it's a good fit.

  Why does it even require an "acceptor" to accept the electrons and hydrogen ions? What would happen if they were left alone?

Same thing that would happen if you clogged a pipe or hose. Once all of the electron acceptors on the transport chain are full, movement stops. The electrons won't be magically absorbed by other parts of the proteins making up the chains, and while there might be errant reactions with other molecules, you'd be lucky to get a whole ATP molecule out in a day - assuming you could magically stay alive.

In reality, Cyanide poisoning is precisely what you're asking, and will kill you very quickly.


Possible genotypes for blood types? If I am blood type B, what are all the possible genotypes that could be expressed by my parents?

I think it might be 16 but I was reading online and saw this:

  Similarly, someone who is blood type B could have a genotype of either
  BB or BO.

So if someone can help me answer this, that would be great.

Parent 1 and 2 have each 5 possible genotypes (OO, AO, BB, BO and AB).

Here a Punnett square with each possibilities. I highlighted the possible parent genotypes.

The total number of possible crosses is exactly 21. Note that here A = Ia, B = Ib and O = i.

OOxBB,OOxBO,OOxAB
AOxBB,AOxBO,AOxAB
BBxOO,BBxAO,BBxBB,BBxBO,BBxAB
BOxOO,BOxBB,BOxAO,BOxBO,BOxAB
ABxOO,ABxAO,ABxBB,ABxBO,ABxAB

This is starting from the information based on your blood type only (i.e. no information about your genotype).

Some background information. Antigen expressing alleles (here referred as Ia or A and Ib or B) are dominant. Not expressing an allele is notated i or O. Being of blood type O is when you don't express both alleles so it is a recessive trait (only possible genotype is ii or OO genotype).


MOL2 to PDBQT conversion via OpenBabel and MGLTools removes hydrogen atoms I am trying to convert a MOL2 file (includes partial charges and hydrogen atoms) into a PDBQT file for re-scoring in AutoDock Vina. However, both approaches that I tried don't keep the hydrogen atoms from the MOL2 file (the PDBQT file doesn't contain hydrogen atoms).

The command I used for OpenBabel is

babel -i mol2 my.mol2 -o my.pdbqt

When I look at the documentation, they babel has a dedicated "-d" flag for removing hydrogens. So I assume that this shouldn't happen by default?

The same thing happens if I use MGLTools

prepare_ligand4.py -l  my.mol2

Any ideas of what might be going on here?

Thanks for your help!

will append the MOL2 file if someone wants to try it:

@<TRIPOS>MOLECULE
mymol2
   25    25     0     0     0
SMALL
USER_CHARGES
@<TRIPOS>ATOM
      1 C1         -1.0341   29.2934  -14.5590 C.ar      1 <0>       -0.1745
      2 C2         -0.1917   29.9513  -13.6630 C.ar      1 <0>       -0.1483
      3 C3         -2.3919   29.1585  -14.2689 C.ar      1 <0>       -0.1608
      4 C4         -0.7068   30.4744  -12.4770 C.ar      1 <0>       -0.0956
      5 C5         -2.9070   29.6816  -13.0828 C.ar      1 <0>       -0.1543
      6 C6         -2.0573   30.3323  -12.2033 C.ar      1 <0>       -0.0209
      7 C7         -5.0136   30.3602   -8.9792 C.2       1 <0>        0.9092
      8 C8         -1.1556   29.8264   -9.1470 C.2       1 <0>        0.9071
      9 C9         -2.6151   30.8987  -10.9189 C.3       1 <0>       -0.0262
     10 C10        -3.5221   30.2951   -8.6255 C.3       1 <0>       -0.1568
     11 C11        -2.5717   29.8912   -9.7583 C.3       1 <0>       -0.1554
     12 O1         -5.7013   31.2223   -8.3667 O.co2     1 <0>       -0.8817
     13 O2         -0.7003   30.9084   -8.6799 O.co2     1 <0>       -0.8929
     14 O3         -5.3714   29.5329   -9.8669 O.co2     1 <0>       -0.8807
     15 O4         -0.6188   28.6818   -9.1887 O.co2     1 <0>       -0.8571
     16 H1         -0.6331   28.8861  -15.4824 H         1 <0>        0.0899
     17 H2          0.8655   30.0564  -13.8891 H         1 <0>        0.1079
     18 H3         -3.0478   28.6460  -14.9665 H         1 <0>        0.0917
     19 H4         -0.0427   30.9855  -11.7849 H         1 <0>        0.2049
     20 H5         -3.9661   29.5717  -12.8653 H         1 <0>        0.1145
     21 H6         -2.0757   31.8190  -10.6595 H         1 <0>        0.0142
     22 H7         -3.6485   31.2140  -11.1119 H         1 <0>        0.0547
     23 H8         -3.4370   29.5769   -7.7988 H         1 <0>       -0.0109
     24 H9         -3.2268   31.2722   -8.2199 H         1 <0>        0.0482
     25 H10        -2.8394   28.8903  -10.1212 H         1 <0>        0.0739
@<TRIPOS>BOND
    1     1     2 ar
    2     1     3 ar
    3     2     4 ar
    4     3     5 ar
    5     4     6 ar
    6     5     6 ar
    7     6     9 1
    8     7    10 1
    9     7    12 1
   10     7    14 2
   11     8    11 1
   12     8    13 1
   13     8    15 2
   14     9    11 1
   15    10    11 1
   16     1    16 1
   17     2    17 1
   18     3    18 1
   19     4    19 1
   20     5    20 1
   21     9    21 1
   22     9    22 1
   23    10    23 1
   24    10    24 1
   25    11    25 1
@<TRIPOS>SUBSTRUCTURE

EDIT:

The solution to the problem with prepare_ligand4.py would be

prepare_ligand4.py -l  my.mol2  -U \""" -C

to keep the partial charges and hydrogen atoms (oddly, -U "" didn't work for me: prepare_ligand4.py: option -U requires argument)

You saw my last answer of your question? you can do that easily, just use

prepare_ligand4.py -l  my.mol2 -A "hydrogens"