How does a neuron know to which one of the next neurons to pass the signal Looking into how neural networks are build in the brain, here are a couple of facts followed by some questions:

The neuron receives the signal through its dendrites and passes it to the terminal at the end of the axon.
A neuron can have as much as 1000 connections to other neurons.

As I understand the dendrites can be connected to multiple neurons, so the neuron we are talking about can receive signals from multiple cells.
Now the questions:

The terminals at the axons can be connected to just one or to multiple neurons?
If the axon terminals can be connected to multiple neurons, how does the neuron transmitting the signal knows to which of the further neurons to pass the signal next? Is it passing to all of them at once?
If the axon's terminal can be connected to only one other neuron (for the single axon neurons), how are the two-axon neurons working? How do they know to which axon to pass the signal next?

The neuron that sends the signal does not know which neuron to send the info to. The job of the neurons getting the signal is to identify whether it is their turn to get activated by the signal.

This is controlled by a protein. Depending on how often the neuron is used, a number of channels are formed on the surface of the dendrites. The activation happens at an optimal level of the protein present in the cell depending on the number of channels on the surface.. Each time the cell receives the signal, this some of this protein is created.

First, the neurons with most channels is activated, but if the organism does not get the memory that is wants, the earlier neuron will continue with sending more signals. Then receiving-neuron-number-1 stops activating (because peak concentration has passed) and the next one starts. This continues for all neurons.

In layman's terms, from info-1 to info-2, info-2 is chosen in the order of thoughts most associated with info-1 to least associated.


Components of the concept of Developmental Noise? Developmental noise is a concept that correspond to the amount of possible phenotypic variance of a given genotype in a given environment.

Intrinsic noise (aka Cellular noise) is a component of developmental noise and it refers to phenotypic variations caused by the stochasticity of biochemical processes.

My question is:

What are the other component(s) of developmental noise?

There are two good papers on this that I like a lot:

Noise in Gene Expression: Origins, Consequences, and Control

Cellular decision making and biological noise: from microbes to mammals.

I think they can tell you better than I can, but the major other source of noise is extrinsic noise. Extrinsic noise typically is taken to means two things (both of which are related):
1. Physical noise from the environment that affects biological processes (thermodynamic fluctuations, for example)
2. Intercellular heterogeneity caused by, for example, unequal division. This is also related to cells not being "well mixed" - essentially, molecules found inside of cells are not evenly distributed throughout it.

There may be other kinds of noise, but I think extrinsic is really the main one you should think about.


Is there in vivo evidence of Amyloid beta toxicity? Amyloid beta is thought to be toxic, however from a brief search, this is based on (1) in vitro (2) measurements of some proxies of toxicity (e.g. Ultrasensitive Measurement of Ca2+ Influx into Lipid Vesicles Induced by Protein Aggregates referenced in Wikipedia).

My impression is that we do not have any high-quality evidence that amyloid beta is toxic in vivo and that there is significant circumstantial evidence against it being toxic (links below). Is this correct?

"30% of elderly people have #Alzheimers pathology (plaques &/or tangles) but no disease"
There's an elderly woman with large amounts of amyloid plaques but no symptoms of Alzheimer's
According to Derek Lowe "all of those amyloid-antibody trials have ended in grievous, expensive failures"

From a quick search, it seems that there is plenty of solid evidence for in vivo toxic effects. A couple of papers here and here.


Time spent in phases of cell cycle I am looking for references to papers containing the time intervals spent in different phases of the cell cycle (ej., G0, G1, S, G2, M for eukaryotes) for different cells. In particular, I am interested in E. coli and CHO (Chinese Hamster Ovary cells), but any reference to studies of this kind for any typical cell will be useful.

I'll accept an answer containing a representative sample of references to the literature on this subject. Preferably recent papers (since 2010).

If you can provide the times spent in each phase but don't have references at hand, that will also be useful.


Optimal agriculture: maximum yield with minimum environmental impact I read more and more stuff about alternative method of agriculture such as permaculture. Howerver, I'm not an ecologist or biologist so I don't know where to look for really good and serious articles / paper on the subject. I am really interested in food production methods that may be efficient and respectful for both the environment and the health.
The question that interests me the most is the question of crop yield and environment. I wonder if there are studies that compares the crop yield of the different production methods AND if there are scientific researches on the optimisation of the food production under ressources constrains.
Do you have any reading suggestion? I'm mostly interested in scientific papers but I'm open to anything that may be interesting.

Publications by the Food and Agriculture Organization http://www.fao.org/documents/card/en/c/ca9692en of the United Nations would be a good place to start as they are freely accessible. There are plenty of articles looking at crop yield of different production methods and different management techniques. You may consider subscribing to a journal, like Agronomy https://www.agronomy-journal.org/, or CAB Abstracts https://www.cabi.org/publishing-products/cab-abstracts/ as those would contain most of the subject material you're looking for. Those would also contain information on optimizing food production under resource constraints. Happy researching!


Can the third sex be categorized as Male or Female? Hijra are people who have a penis (not sure if sexually active) but look much like a female (perhaps for some feminine biological property). Wikipedia says they are "physiological males who have feminine gender identity"

Also, I just came to know there are some more types of third gender people.

Now, is there really any BIOLOGICAL third gender which cannot be categorized as male or female? Or its always possible to categorize them to male or female?

When dealing with humans, there are only two Biological genders as defined by the presence or absence of the Y-Chromosome. If the Y-Chromosome is not present, or through some process gets totally deactivated, the human will appear and function as a Female.

XX = Female

XY = Male

XXY = Male (Klinefelter's Syndrome)

XYY = Male (Aneuploidy - Normal Functioning Males)

XXX = Female (Aneuploidy - Normal Functioning Females)

X = Female (Turner's Syndrome - Generally infertile, other issues)

Y = Fatal (The Y-Chromosome is drastically smaller than the X-Chromosome, which contains many necessary genes)

XXYY = Male

...

The list goes on, since there have been records of up to XXXXX.

If there is a Y-Chromosome present, the human born will be male.

However, that is not to say that a person cannot psychologically identify as something else. It's also worth noting that the majority of known species are asexual and do not have genders, and that those which do have genders do not always follow the same rules (Fruit Flies, for instance, use the ratio of genes to determine sex).


Where should I go for online information on animals endemic specifically in Mozambique? I've been involved with the citizen science project "Wildcam Gorongosa" for over half a year now (website, forum). As there are lots of unexperienced volunteers, many questions are being asked. Often I'd like to answer, but also not having a biology background I usually have to do some research first to give an accurate answer. For this reason, I'm looking for informative, up-to-date online resources, like e.g. search engines, animal guides etc.

I have come across a few websites that give some information on animals in the whole of Africa (e.g. ultimateungulate.com) - but I wonder if there are more suitable places to go if I'm specifically looking for animals in Mozambique (or even Gorongosa National Park). I'm still relatively new to the topic - where would a scientist involved with research on Mozambican ecology go and look for this kind of "specific" information? As the project deals with pictures taken by wildlife cameras, I am only interested in animals of a certain size (I guess rat-sized and larger). I'd be happy to find e.g. more information on the appearance of each species, its geographic distribution, their respective habitats and their general behavior.

I realize that this question is somewhat broad - please do ask ahead, I'll try to add details if necessary!

Here is a large list of animals (sorted by guilds) that can be found throughout Mozambique.

Each animal in the list is linked to a page with picture and information!

Wikipedia maintains a few lists of animals found in Mozambique.

See here for  a list of mammals (sorted by order).
See here for a list of birds (sorted by order).
They also have 2 lists for mollusks (fresh-water, marine) and 1 for plants.

Gorongosa's own website provides a list of common animals found in Gorongosa:
http://www.gorongosa.org/explore-park/wildlife
As user Sudachi mentioned in a comment below,  iNaturalist and GBIF also have lots of well-managed species lists and observation data.


Protein Conformation Modeling I'm interested in learning about computational modeling in biophysics. I have heard some amount about people modeling proteins as a network of ideal springs to examine things like conformation switching. I was thinking it would be cool to try to make a very simple model of a small motif undergoing denaturation at certain temperatures while being stable at others.

Does anyone know of a good reference about protein modeling that would be understandable to someone who is decent with math/physics/programming but is in no way a mathematician/physicist/computer scientist?

Also, if you have a better idea of a simple project for me to practice computational modeling in biophysics (or even just any biology) I would appreciate hearing it.

Thanks

Well I sometimes use PDB files from proteins whose structure has been identified and study them. I use swiss PDB viewer software to do this and its pretty neat! I haven't looked at the biophysical data associated with a PDB file but I'm pretty sure they are there since you wouldn't be able to make the calculations and resolve the protein structure and confirmation without that kind of data. All you need is to download the software, go to Uniprot database and use the accession number of a protein you are interested in, see if its structure is resolved and either download the PDB file or use the accession number to download the file inside the software.


What is meant by "the degree to which a gene is expressed" in an individual? Here is an excerpt from a text that I was reading,

  Here is an example of microarray data. The idea is to take a group of
  different individuals and for each of them, you measure how much they
  do or do not express a certain gene. Technically, you measure how much
  certain genes are expressed. The colors in the graph, like red, green,
  grey etc. show the degree to which different individuals do or do not
  have a specific gene.

The data they are talking about is this:

But a gene is either expressed or not expressed right? It's one allele is expressed or another allele is expressed, or yet another one is expressed. It is a discrete thing.

Then what is meant by the extent or the degree to which the gene is expressed? Can a gene be expressed more in certain individuals and less in others? Please explain with example.

It is true that a gene is either being expressed, or not being expressed. However, the degree to which a gene is expressed can vary tremendously. "Degree of expression" basically means the number of times the gene is read by the transcription machinery, which (generally) correlates to the number of copies of mRNA present in the cell, which (generally) correlates with the number of protein molecules being translated. Essentially, the degree of expression of a gene corresponds to how much of the gene's product is being produced. (Of course, this being biology, things aren't always quite as simple as that, but this is the general trend.)

Here's an example. All nucleated cells express housekeeping genes that are required for the normal function of the cells. These are often involved in maintaining metabolism in the cell, sensing and processing nutrients, maintaining the cell's structure and shape, etc. These genes are expressed to a very high degree, meaning they are always "on" and being transcribed. On the other hand, there are many many genes that are not needed in "normal" situations, and are only turned on at certain points in development, during pathology, during a certain point of the cell cycle, or other similar situations. These genes have a very low degree of expression, and in fact may be turned off altogether in some cells.

So, the degree of expression can be described as the rate at which the gene is being transcribed. In a study like the one illustrated in your question, the number of copies of each gene's mRNA in the cell is quantitated, and compared to the expression of a housekeeping gene that should have the same degree of expression regardless of the sample. The relative amounts of each mRNA are then compared among individuals, and scored accordingly. This numerical score is then turned into a color for the purposes of generating the heatmap image.


How do nicks in the DNA strand affect the success of Long Range PCR? Long Range PCR using NEB Master Mix - Hot Start Taq was working fine for me (amplicon sizes of ~10kb) but stopped working all of a sudden. Is it possible that many freeze-thaw cycles on the DNA template introduces nicks into the DNA strand that hamper the polymerase activity ? In certain cases, I am getting no amplification and in some I am getting very weak amplification. Because the integrity of the DNA should be intact over the entire length in case of long range PCR, am I right in thinking nicks in DNA will be especially detrimental if we are trying to amplify large fragments ?

The concentration of the DNA templates I used was 90-140ng/ul in a 10ul PCR reaction, DNA eluted in TE buffer after a magnetic bead method of DNA extraction.

It is not unlikely that nicking is causing trouble. The question is if repeated freezing and thawing is causing the problem, there is an article which has been published in B.R.L. Focus in 1983 which disputes this effect. You can find the PDF with the article here, the article itself starts on page 10 in the PDF. On the other hand there is this paper ("Impact of long-term storage on stability of standard DNA for nucleic acid-based methods."), which shows that sstorage conditions do have an effect on the effciency of qPCR standards. Whatever causes nicking, it is a problem in (long) PCR. The following quote is from Sigma in their long PCR enzyme mix:

  Template High quality and adequate length of the template are
  essential for reliable amplification of larger fragments. Extreme care
  must be taken in the preparation and handling of the DNA target for
  long PCR. Nicked or damaged DNA can serve as a potential priming site
  resulting in high background. Avoid freezing, or, alternatively,
  freeze only once to minimize damage. The condition of the target DNA
  is critical. Depurination during cycling is minimized by use of
  buffers with a pH greater than 9.0 at 25 °C.

This paper ("Effect of Highly Fragmented DNA on PCR") shows that induced nicks affect the efficiency of PCR (although they do a much shorter amplification than you). So to overcome this problem I would make small aliquots of fresh DNA preps and then see, if this helps.


Has the concept of allostasis been adopted in biology, in place of homeostasis? Peter Sterling, among others, has been a prominent critic of the concept of homeostasis.  He instead proposes a process called allostasis.

Homeostasis involves having fixed set points for physiological parameters, and when we deviate from those set points, there are mechanisms that restore them.

However, Sterling argues that this process of homeostasis is inefficient and inflexible.  Instead, he posits that the brain is constantly predicting physiological needs based on environmental and bodily demands, such that the "set point" changes depending on the context.  So your mean blood pressure might be X in one context, but Y in another.  And rather than responding after a deviation from the mean, the brain predicts those deviations and adjusts the body accordingly.  This is allostasis.

Allostasis is much more in line with what we know about the brain (e.g., Clark, 2013), but has this idea been adopted much in biology?  Based on my memory from biology class not long ago, it seems like homeostasis is still considered a central feature of living things.

Thanks!

Allostasis is more than changing set points. The theory of allostasis attempts to unify the theories of stress and homeostasis. And, although Peter Sterling and Joseph Eyer were the first to coin the term "allostasis", the concept is today proposed by a plethora of researchers.

Allostatic responses ensure „stability through change“ in situations of strain and stress. If in allostatic mode a feedback control system is able to change both its set point and its parameters to approach a state vector that is more suitable for survival. An allostatic response involves the activation of actuator variables that is referred to as allostatic state. Although allostasis is basically beneficial for viability it also exposes the organism to some kind of strain, referred to as allostatic load. If ongoing or being excessive, allostatic load may be life-threatening on its own terms. In this situation, it is referred to as allostatic overload.

Figure taken from Chatzitomaris et al. 2017.

The idea of allostasis might have been omitted in your biology class due to didactical reasons. For an introductory course it may be beneficial to begin with the simpler theory of homeostasis.

Today, the concept of allostasis is of increasing importance for psychology and medicine. As of today, a PubMed search for the term "allostasis" results in 730 papers and a search for "allostatic load" delivers 1123 publications (with growing tendency).

The theory of allostasis helped to improve our understanding of a broad range of diseases and non-pathological bio-psycho-social situations. Typical examples include starvation, obesity, exercise, fever, type 2 diabetes, hypertension, thyroid disorders, post-traumatic stress disorder (PTSD) and psychosomatic diseases. Additionally, the recent development of panels for allostatic load facilitates differential diagnosis near the small ridge between health and disease.

References

Sterling P, Eyer J. Biological basis of stress-related mortality. Soc Sci Med E. 1981 Feb;15(1):3-42. PMID 7020084.
Sterling P. Allostasis: a model of predictive regulation. Physiol Behav. 2012 Apr 12;106(1):5-15. doi: 10.1016/j.physbeh.2011.06.004. Epub 2011 Jun 12. PMID 21684297.
Bizik G, Picard M, Nijjar R, Tourjman V, McEwen BS, Lupien SJ, Juster RP. Allostatic load as a tool for monitoring physiological dysregulations and comorbidities in patients with severe mental illnesses. Harv Rev Psychiatry. 2013 Nov-Dec;21(6):296-313. doi: 10.1097/HRP.0000000000000012. PMID 24201821.
Sagner M, McNeil A, Puska P, Auffray C, Price ND, Hood L, Lavie CJ, Han ZG, Chen Z, Brahmachari SK, McEwen BS, Soares MB, Balling R, Epel E, Arena R. The P4 Health Spectrum - A Predictive, Preventive, Personalized and Participatory Continuum for Promoting Healthspan. Prog Cardiovasc Dis. 2017 Mar - Apr;59(5):506-521. doi: 10.1016/j.pcad.2016.08.002. PMID 27546358.
Chatzitomaris A, Hoermann R, Midgley JE, Hering S, Urban A, Dietrich B, Abood A, Klein HH, Dietrich JW. Thyroid Allostasis-Adaptive Responses of Thyrotropic Feedback Control to Conditions of Strain, Stress, and Developmental Programming. Front Endocrinol (Lausanne). 2017 Jul 20;8:163. doi: 10.3389/fendo.2017.00163. PMID 28775711.


Electroporation vs gene guns What are the pros and cons of using electroporators (left) and gene guns (right) for transformation in terms of:

Price
Target organism
Efficacy
Ease of use
Maintenance

I am not an expert on gene guns but I will try to give my answer on this question anyway.

Price-wise they are both relatively cheap. The electroporators consumables are only the cuvettes, they cost 5-10 dollar/each. The gene guns use microbeads as bullets and depending on the material they cost between 200 and 300 dollars per microgram, 10-50 dollars per shot, a bit more expensive than electroporation.

About the organisms, guns are used mostly for plant-cells and few other "hard to electroporate" organisms. I don'd have a proper list of them but roughly, if you work with bacteria, yeasts and mammalian cells, then go for an electroporator.
If you need to work with tissues or entire organisms like worm/insects/plants then go for a gun, you definitely cannot electroporate a leaf. But in general, check the literature on what is currently the best method to transfect your system of choice.

Efficacy, also in this case it depends form the cells you are working with. Electroporation reach 10^9/10^10 transform ants per microgram of DNA in case of E.coli and this is the best efficiency you can get nowadays. All other cells will be transfected at lower efficiency, how much lower? It depends from the cells!

Easy of use. They are both very easy to use, it is matter of pressing a button. For the electroporation you need to prepare electrocompetent cells, but the procedure is very easy. For the gene guns you need to coat the beads with DNA, also very easy.

Maintenance. The electroporator do not need any maintenance at all while the gun may need some care in the long run since it has pumps and pressurised chambers, this stuff usually need some attention but nothing special.

Some references:

bio-rad.com/LifeScience/pdf/Bulletin_9541.pdf

bio-rad.com/webroot/web/pdf/lsr/literature/4006174B.pdf

bio-rad.com/webroot/web/pdf/lsr/literature/4006217A.pdf


Why do men have a greater chance of suffering from hair loss? If we look around we'll find that men are more likely to suffer from hair loss when compared to women. Is there is any specific reason for this?

As per my comment above, some types of hair loss is androgenic, and therefore related to testosterone levels. This is why eunuchs can be resistant to some forms of hair loss.


What factors should I consider when selecting a reference genome for mapping? I am under the impression that the most recent reference genome is typically the best case. What other things should I consider when selecting a reference genome? For example, is there any particular reason not to go with the most recent reference genome when aligning short reads from RNAseq?

There are many reasons!

Let's assume you are using the Human reference genome. The latest version is hg38 or GrCh38. This came out roughly three years ago (Dec 2013). Although now these same reasons do not really apply to this particular assembly, but no other assembly comes to mind where these reasons are demonstrable. When dealing with RNA-Seq data you carry out a few common tasks.

Annotations: When a new assembly comes out, all existing annotations are standardised on the previous assembly. Take for example GENCODE, that particular links to the current version of gencode, which is now based on hg38. But, more importantly notice that they still maintain the same release for hg19/GrCh37. From my experience, it takes about 1-3 months for annotation databases to migrate to a new genome assembly after the assembly is released.
Conservation tracks: These are the tracks which take the longest to get updated. I will not post a link to the tracks here. But, here's the UCSC table browser, you can go to the comparative genomics tracks and view the conservation tracks (Phylop, Phastcons) which are available for each assembly. Again from experience, it took more than a year for these tracks to be generated for hg38. So it is just better to work on the previous assembly if you want to this particular information, because generating these tracks by self is a very tedious and computationally intensive task.
Risks associated with unfinished genomes: This does not really deal so much with the human genome as the gain is ever smaller with each consecutive assembly. But considering a assembly which consists of 70% scaffolds, the variation between assemblies tend to be huge. For functional studies as opposed to insilico studies, it makes no sense to redo the entire analysis every time a new assembly comes out, since the insilico part of the study is the predictive pillar on which functional validations are based. Although the same does not apply to insilico studies where the results presented to the public are solely predictive.
Incoherence with existing studies: This is a major obstacle for using a newer assembly, especially applicable towards unfinished genomes, wherein the results may be widely variable and do not align with pre-existing knowledge. Of course, you may be the one who is correct but it is also possible that the variability in your results is the result of human error. Therefore, it is just better to wait for a "landmark" study to introduce the assembly to the public, allowing your study to undergo less stricter perusal and also allowing you to validate the expected variability in your results.
Pitfalls during functional analysis: For RNA-Seq analysis it is common practice to use RT-PCR for a particular gene to establish the expected expression level for that gene, which in turn will validate a successful RNA-Seq experiment bereft of shady PCR duplications and artefacts. For this particular part you would first create a primer, which validates the expected expression level of that gene. But this particular primer originates from a particular assembly. It is also possible that the region which is amplified may have shifted or changed between assemblies. So when you align your data on a different assembly from the one which was used to create the primer, you may get an unexpected expression level for that gene, as the original primer amplified an incorrect region, which got fixed in the newer assembly.

I know there are many more. But, these are the only ones which comes to mind at the moment.


What is the pH of the mitochondrial intermembrane space? The proton gradient is stored between the mitochondrial double membrane. More protons mean more hydronium ions and lower pH, but how much exactly?

According to the authorities Roos and Boron the difference of pH across the inner-membrane of mitochondrion is  0.5 with pH outside the membrane equal 7.0 and inside the pH is 7.5 (pH-mit = 7.5, pH-out = 7.0) according to Intracellular pH


General Enhancer Questions (Methylation Patterns, ect.) I have a biological question(s) for ya'll involving enhancers.

1.) Enhancers work by being the binding sites for TFs. But how does this increase transcription? (Especially when enhancers can be extremely far away from the gene they control.)

2.) Enhancers can become methylated. When they do, does this usually prevent transcription factor binding? And if it does prevent the binding, how does this affect the role of the TF and gene expression.

EDIT:  Here's what I found.

It seems that enhancers can be far away from the gene they act upon, but the binding of TF via their DNA-binding domain can cause looping of DNA to help them reach the promoter region of the gene of interest. Thus, increasing the rate of gene expression.

On the reverse, methylation can sometimes be seen to act as silencing of gene expression. So, if our enhancer region is methylated, this may prevent TF binding and the enhancer from increasing gene expression.

BONUS:  Methylation in promoters can also cause silencing by preventing RNA polymerase II, and the required proteins (ect) from carrying transcription.

If anybody wants to add (or correct anything, let me know!)

This subject is actually both complicated and incompletely understood. For example, there is evidence that some enhancers don't result in loops at all — instead their influence travels along the chromatin to a nearby promoter.

You can think of enhancers as being staging areas where protein complexes that promote transcription are assembled. In some cases enhancers are where the RNA polymerase complex is first bound.

When loops do form, this allows the proteins at an enhancer to interact directly with the transcriptional start site.

I think you will find this 2015 review to be a helpful introduction.1

As for methylation (which maybe would be better as a separate question), it is generally true that methylation acts to reduce transcription factor binding and thus decreases transcription.2

However, that overall trend disguises some more complex dynamics.3

References:
1: Pennacchio, L. A., Bickmore, W., Dean, A., Nobrega, M. A., & Bejerano, G. (2013). Enhancers: five essential questions. Nature Reviews Genetics, 14(4), 288.
2: Lea, A. J., Vockley, C. M., Johnston, R. A., Del Carpio, C. A., Barreiro, L. B., Reddy, T. E., & Tung, J. (2018). Genome-wide quantification of the effects of DNA methylation on human gene regulation. ELife, 7, e37513.
3: Sharifi-Zarchi, A., Gerovska, D., Adachi, K., Totonchi, M., Pezeshk, H., Taft, R. J., ... & Araúzo-Bravo, M. J. (2017). DNA methylation regulates discrimination of enhancers from promoters through a H3K4me1-H3K4me3 seesaw mechanism. BMC genomics, 18(1), 964.


What's the Evolutionary Purpose of Religion? I would imagine the answer to this question would be that religion tends to cause greater compliance of individuals within society, so it is pro-society. Plus these religions tend to incorporate some knowledge obtained by trial and error, an example of this is the fact that in Judaism the consumption of swine is forbidden which would be an evolutionary advantage seeing how swine is notorious for its parasitic constituents. Additionally religion offers an explanation for some of the phenomena that were once and still are poorly understood. Such things include near-death experiences. It also adds to motivation and tends to confer some other advantages such as a decreased rate of suicide due to the condemnation of suicide by the majority of religions.

In terms of genetic evolution, religion itself cannot really be considered to have an evolutionary advantage or disadvantage, as it is not anchored in any genes. This means that it is not an evolutionary trait and hence the principles of evolution do not apply to it. However, religion is a product of underlying capabilities of the brain (for example imaginative capacity?), and these are genetic and evolutionarily advantageous. Aside from this, asking for the 'evolutionary purpose' of anything is the wrong way to approach the topic, as things do not evolve to have a purpose but they simply evolve and stick around unless they produce a net disadvantage compared to a competing version of the same trait.

You could look at religion from a memetic point of view however, i.e. as an idea which competes with other ideas. The idea of religion has many aspects to it that would help it to 'survive', i.e. not be forgotten. These include the drive to tell other people about it, ease of understanding, the claim of exclusivity, addressing many social cravings, and filling in gaps of knowledge for which explanations are desired.


Are CN3, CN7, CN9 and CN10 the only Parasympathetic Cranial Nerves? It has been my thought for a long time that this is the case, but I am unsure currently, since the parasympathetic tract of colon sigmoideum does not seem to have connection with CN 10. It connects with pelvic splanchnic nerves.
Discussion about it here.

If there is no connection from pelvic splanchnic nerves to CN 10, like CN 10 running within the nerves, then my though must be wrong.

Are CN3, CN7, CN9 and CN10 the only Parasympathetic Cranial Nerves?

Yes, only III, VII, IX, and X are cranial nerves that carry parasympathetic autonomic neurons. The key phrase is "cranial." Pelvic splanchnic nerves also carry parasympathetics, but they arise from the pelvis, not the brain.


Amount of variation between a canonical gene sequence in various samples Suppose there is a GeneBank DNA sequence listed that produces a specific enzyme in a specific species of plant. e.g. A terpene Synthase.

Now if someone samples various trees of the same species would one expect to get the exact same sequence each time? Or is a certain amount of variation expected from tree to tree?

The drift behind my question is: Obviously not all tress of the same species are exactly identical in phenotype. So are the causative factors seen in sequence variations of various enzymes etc.? Or can we expect the various samples to have exactly identical amino acid / DNA sequences for particular genes / enzymes.

e.g.  e.g. Take this specific sequence: http://www.uniprot.org/uniprot/E3W202 If I sample from various trees of this same species and sequence this particular gene how much variation should I expect? Or would they be almost 100% identical?

Your question is quite vague so I can only give you a vague answer saying what I would expect given only the information of your question.

The vagueness mainly comes from the huge amount of functional sequences in the genome, particularly also in enzyme-coding genes, each being more or less conserved. You say

  I am surprised that there is no information of how much of a within species variation there is in enzyme sequence. I am having a hard time getting this info. too.

I would say that there is no feasible way of studying this question. You will find different selective constraints on every single enzyme and breaking this down to DNA this means that every single locus can be target of different selective pressures. And even if you figured out how to answer that question comprehensively for a given species (which probably will not happen), generalising it to every single species in every ecological niche, with every possible population history and so on is close to impossible. That is why one studies sequence diversity/conservation in model organisms and mostly on a per-gene basis.

In general, without knowing any background of a species and enzyme, I would however expect two things when looking at molecular variation between individuals of that species. These are merely based on general evolutionary principles and the nature of the genetic code. Keep in mind that these are trends, meaning that many genes will match these expectations but some definitely will not due to lineage-specific evolution.

First, I would expect generally high levels of amino acid conservation (but not always identity) especially in functional enzymes of core pathways. However, this depends on the function of the gene product. If the gene is a target of balancing selection, which maintains genetic variation within a population, there can also be considerable amino acid variation.

Second, there will generally be higher levels of DNA variation because of mutations with little or no fitness effect (synonymous variation or intronic variation which tends to have lower selective pressure).

To relate this to your last question: even though I would always expect a general amount of variation, even in the amino acid sequence of core enzymes, this variation will probably not be the main reason why you see different phenotypes. Phenotypic plasticity - the differential response of a given genotype to a given environment - is often stronger in plants than in animals as plants are stationary organisms. This plasticity will probably be the main cause of striking phenotypic differences between individuals.


Can anyone identify this bug? Spotted in Czech Republic. Our office was hit with cockroach infestation, so I'm afraid if I haven't carried one home.

It is German cockroach (Blattella germanica) with two dark parallel streaks on it's pronotum.
The one in your picture is a lady laying her ootheca.

It is a pest.
Here's it in different stages of life cycle.
Things you might like to know:

Blattella germanica occurs widely in human buildings, but is particularly associated with restaurants, food processing facilities, hotels, and institutional establishments such as nursing homes.
German cockroaches are omnivorous scavengers. They are attracted particularly to meats, starches, sugars, and fatty foods. Where a shortage of foodstuffs exists, they may eat household items such as soap, glue, and toothpaste.
The German cockroach reproduces faster than any other residential cockroach, growing from egg to reproductive adult in approximately 50 – 60 days.

Source: Wikipedia and different pest service websites.


Do snakes get dizzy? I've seen snakes get captured in sacks and I've wondered if the snake would get dizzy if the sack were twirled around.  I have not done any tests (and don't plan to) because snakes scare me.

Probably don't do any experiments that involve shoving reptiles in a sack and swinging them around your head, as someone will surely call the ASPCA on you.

The type of dizziness that is associated with spinning around is called "vertigo". From wikipedia:

  Repetitive spinning, as in familiar childhood games, can induce short-lived vertigo by disrupting the inertia of the fluid in the vestibular system

So then from a physiological perspective the question is, do snakes have fluid in their ears like people do? And a quick review of snake physiology seems to suggest that they do.

Thus, I'm going to put forward the tentative hypothesis that yes, snakes can get dizzy, but it's still probably very different from you think of as dizziness.


What is the name of this brown, "flat hat", fungus? I've seen this in October 2016 on Corsica (Island of France):

See https://commons.wikimedia.org/wiki/File:Gr-20-petra-piana-to-onda-08.jpg for more images and higher resolutions.

Pretty sure (but not 100% certain) that it is a Amanita porphyria bk9845, which in german is called a "Porphyrbrauner Wulstling"

  Cap: 3-12 cm; convex, becoming broadly convex, often with a central bump; sticky at first or when wet; bald; appearing streaked radially; the margin not prominently lined; grayish brown to brown or purplish brown; often with scattered gray to purplish gray warts or patches.

Source:

amanita porphyria


If I stop consuming protein, will I still excrete urea? Will an animal that is not eating any aminoacids stop excreting urea (or whichever other form of excreting nitrogen)? If the body is not in a position to lose nitrogenated compounds, in which processes is nitrogen inevitably turned into waste products like amonia/urea?

Yes, you will still excrete urea, but the amount you excrete will be diminished. As you might expect, when the body is low on protein, there's a physiologic drive to hold onto as much nitrogen products as possible, in order to conserve the limited supply.

Normally, your kidneys excrete approximately 40% of the urea that is filtered through the glomerulus. (It's slightly more complicated, because there's both secretion and reabsorption that happens along the nephron, but that's approximately the end result.) However, in protein malnutrition, the kidneys reabsorb more of the urea, and that number can drop to excreting only 10% of the filtered urea. (Source) It appears that this is an active process to reabsorb the urea, rather than a passive effect from other effects that malnutrition has on the body.

However, the body isn't capable of stopping excretion of urea completely... there will still be some that is excreted. Urea transporters in the kidney aren't 100% efficient, but probably the bigger issue is that the body needs to use that urea to regulate other functions. Urea is important to the body's ability to concentrate urine, which in turn is related to the body's regulation of blood volume and sodium concentration. And in general, the body cares more about maintaining proper blood volume and tissue perfusion than anything else.


Why the scent of mouth gets dirty after not eating for a long time? After a long time of hard workout,not eating and nervousness makes your taste and scent of mouth very uncomfortable and bad why this happens and is there any way to prevent it?

This is caused by a build up of ketone bodies in your blood which lowers the pH of your body and can cause bad breath. Ketone bodies are a response of your body breaking down fatty acids for energy instead of glucose when in a low food intake (fasting) state. This is also true for morning breath since your body has been in a fasting state.
The way to prevent this is to eat the proper amount of calories needed for your body to function normally.


Is there any convincing evidence for the existence of nanobacteria? The existence of nanometer scale microorganisms has been proposed and used explain several phenomena  including morphological structures in a martian meteorite (ALH 84001) and implication in the formation of kidney stones (1).

Is there now any consensus in the biology community whether these are biotic or abiotic in nature?

(1) Kajander EO, Ciftcioglu N (1998) Nanobacteria: An alternative mechanism for pathogenic intra- and extracellular calcification and stone formation. Proc Natl Acad Sci U S A 95: 8274–8279

There are two convincing papers (1,2) arguing that the observed "nanobacteria" are in fact mineral/protein complexes and not any living organisms.

In (1) Martel and Young created very similar looking particles from calcium carbonate in vitro. The calcium carbonate precipitations can even look similar to dividing cells:

  After 5 days of serum incubation, a white precipitate formed and
  adhered on the bottom of each flask. When examined by scanning
  electron microscopy (SEM) and transmission electron microscopy (TEM),
  the precipitate was seen to consist of particles with a size ≈500 nm
  (Fig. 1 A, B, and E), an observation consistent with normal bacterial
  morphology, which peaks at one particular size specific to the strain
  on hand. Some forms resembled cells undergoing division (Fig. 1 D,
  arrow).

One strong argument against those nanobacteria being living organisms is that they don't seem to contain any nucleic acids. Of course non-DNA based organisms are theoretically feasible, but that would be an absolutely extraordinary discovery.

The autors of (1) also observed these particles after filtration through a 0.1um filter. They argue that this size could not be sufficient to contain all the cellular machinery bacteria need:

  Because an earlier workshop commissioned by the NAS had suggested that
  the minimal cellular size of life on Earth must exceed 200 nm in
  diameter to harbor the cellular machinery based on DNA replication
  (19), it is unlikely that nanobacteria represent living entities
  unless they contain some other type of replicating mechanism.

(1) Martel J and Young JD, Purported nanobacteria in human blood as calcium carbonate nanoparticles. PNAS 2008, 105(14):5549-54

(2) Raoult D. et al., Nanobacteria Are Mineralo Fetuin Complexes, PLoS Pathog. 2008, 4(2): e41.


Loss of antibiotic resistance due to long term storage How possible is it for antibiotic resistant bacteria stored for a long time to lose such resistance?

It is possible due to the fact that some antimicrobial resistance genes are induced by the presence of antibiotics themselves and are not promoted in the absence of a specific antibiotic, so the production of certain antimicrobial structures (enzymes, pumps, etc.) will be reduced once the bacterial medium is antibiotic free for enough time. This is sometimes refered to as "antibiotic pressure" referencing to some extent the genomic concept of selection pressure.

Take for example the phenomena reported in this paper's summary; they studied a patient hospitalized because of an infection by 2 K. pneumoniae strains. They knew beforehand that one of the strains was suceptible to carbapenems while the other one had a certain degree of resistance to this antibiotic. As the infection unfolded and a treatment with meropenem was administered, they took several samples and studied them via whole genome sequencing (WGS). They found out that the strain previously characterized as suceptible to carbapenems had acquired a plasmid (possibly by vertical transmission from the other strain) and hence now exhibited resistance to carbapenems, however when this strain was left in observation (and without being exposed to meropenem) it lost its previously acquired resistance.

In conclusion the sole presence of antibiotics induces resistance by different mechanisms in bacteria, but in some cases the lack of antibiotics in the medium can also revert resistance if this condition lasts for enough time. It is important to mention though that some resistance profiles will never be reverted no matter for how long the bacteria remains away from an antibiotic due to their nature. For example a gram-negative bacteria will always have instrinsic resistance to regular penicillin no matter what due to its cell structure itself (lack of a thick peptidoglican cell wall and presence of an outer cell membrane).


How does strength of a pulse related to EKG(ECG)? There are variabilities in the heart rate as well as strength of heartbeats. I want to know if one can predict which heartbeat will be strong or weak based on the corresponding EKG/ECG signal. I am interested in the displacement of brain due to the heartbeat, which probably correlates with the peak pressure, and total volume caused by the beat.

If there is such a correlation, which part of EKG would be related? The interval between P and R? The amplitude of QRS?

Human or primate information is preferred.

image from wikipedia

Higher QRS complexes particularly in the lateral leads would suggest hypertrophy of the left ventricle. This in turn would suggest a stronger pressure is in place, although it is not known whether this is because it is required (incompetent valves) or a physiological response to exercise (where the volume is likely to actually be bigger).

Alternatively, if it really is just displacement of the brain you're interested in, why not use an EEG taken with an ECG and measure if there is a variation with each heartbeat. Then you can tease apart whether this is due to pressure or oxygenation or many other things.

Otherwise you could place something overlying the carotid which will loosely, but perhaps more accurately, reflect the pressure and one could potentially calculate the volume this way once enough other factors are known.


Do birds change their diet before migration? Migration takes up a lot of energy, so I am wondering if birds (in my case mallards) change their diet / food preferences in the weeks before migrating. Do they select for more energetic foods to fuel up, or do they just eat more of the same foods to gain enough energy?

Apparently, yes. This article underlines the changes in diet in semipalmated sandpiper before its 3000 km-long migration:

  Near the beginning of their journey, sandpipers stop at the Bay of Fundy on Canada's eastern coast to gorge on mud shrimp, 1-cm-long crustaceans loaded with omega-3 fatty acids. Over 2 weeks, the frantic feeding doubles each sandpiper's body mass [and i]t makes sandpipers' muscles use oxygen more efficiently, enhancing the birds' endurance.

The authors experimented the diet on a similar species to disentangle the effects of the different diet from other effects, for example due to hormonal changes:

  To isolate diet's role, Weber and colleagues took exercise and migration out of the equation. They turned to the bobwhite quail, an unrelated sedentary bird that doesn't migrate and seldom flies. For 6 weeks, the scientists fed 40 couch-potato quails a combination of omega-3 fatty acids from fish oil. To the researchers' surprise, the quail's oxidative capacity - their muscles' efficiency at using fuel - shot up 58% to 90%.

This paper reviews the effects of diet changes on the digestive trait of migratory birds; however, it's quite old (2001).

I couldn't find any indication on mallard feeding prior to migration, but these links can be a start for further research.


Is there a term for tool use in animals? Is there a technical/scientific term that scientists use to refer to tool making abilities found in certain types of animals?

Reference http://en.wikipedia.org/wiki/Animal_cognition#Tool_and_weapon_use

Having read this article on tool use in Chimpanzees in full, I am inclined to say that if such a term existed then either the article itself or the titles of any of the 30 articles referenced would have included it.

Searching a couple of online biological dictionaries and ethology sites hasn't yielded anything either, therefore until someone else points out that I'm missing the obvious I'd say you're free to coin the term yourself!


What are these bulbous-ended filaments? Yesterday I noticed an array of filament type structures, each with a bulbous feature at the end, hanging off my car door. As can be seen in the first image, these structures are quite small (comparing to door handle/key hole). I live in Kentucky, USA. What are they?

They look like lacewing eggs, though related insects can have similar-looking eggs. Lacewings are beneficial insects; their eggs are laid on stalks, like this:

Edit to point to other questions and answers here:

Is this some sort of fungus?
What are these (eggs?) ? ( Location - India )


What voltage damages a neuron or a group of neurons? Neurons are stimulated for research and therapy purposes. How much voltage (current, duration, etc) can a neuron or a group of neurons, in humans, take without being damaged?

It probably mostly depends on how you stimulate them, when we probe the ulnar nerve in practical classes with a stimulator on the skin, then 20V seems about fine. Most students will handle 20V 100 ms pulses, but some will flinch.

If you have a neuron connected directly to an electrode (in a dish), then you will get decent responses from 50-100mV square voltage steps. Individual cells will respond after 10-40 mV (depending on cell type), much more than 150-300 mV will probably be problematic (and not physiological) for single cells.

It sounds like you need to read some early electrophys, start with the squid giant axon, then Neher and Sudhof were the gods for the start of my PhD.


Missing cells from immunopanning Why do I not have any cells left in my positive panning plate after transferring from the negative panning plate during immunopanning? I am trying to purify retinal ganglion cells from postnatal rats and use a Thy1.1 antibody harvested from a hybridoma cell line supernatant in the positive panning plate.

Following transfer of the cell suspension from the negative to the positive panning plate there are no cells in the pre-trypsinization supernatant, nothing stuck to the panning plate, and no cells in the post-trypsinization supernatant so I have no idea where they could have gone. Checking the negative panning plates however shows that there are many cells stuck to those plates, so could my RGCs have been lost at some point during the transfer and when?

Thanks v much in advance for your help.

Immunopanning in my experience takes an awful lot of optimization, but is worth it when it works.  I would plan, if you have the resources, to sac rats just for assay optimization before you even begin to try to get real data out (assuming your planning for a steady stream of primary cells).

That said, there are some real easy checks you can try do first.  Try to get a rough cell count on what you put on your negative plate (depending on your prep steps, that can actually be a bit tricky), and then count the cells again as you transfer the cell suspension to the positive plates.  If you don’t have any cells left, or you have very little cells left, then you might be losing all your population on your negative plate.

If you do have cells in suspension, I would start to question your positive plate.  Are you making them yourself or are you buying them coated? Which rat strain are you using?  Perhaps you need to titer your antibody concentration on the plate.  There are really a whole lot of steps in immunopanning that can be optimized.


Regarding the apoptosis mechanisms in cells and cancer If all the cells in a cancerous tumour had their apoptosis mechanisms 'turned back on' or reactivated or repaired by some 'yet to be discovered' process would this cause the tumour to 'self destruct' or be destroyed? Are there known processes that can repair or reactivate the apoptosis mechanisms in a cell?

The processes of apoptosis is not so simple, there is a lot of genes and proteins that participate in it. In cancer cells some of them mutate and not working properly.
Lack of apoptosis is the main problem in cancer. If cell not working properly, it dies. But not in cancer.
So theoretically, yes. If we will fix the apoptosis, the cell probably will die.
It's gene engineering direction. You need to target the cancer cell, and to change problem genes. It's really difficult processes. And every type of cancer has different mutations ...

Read this for example http://www.jeccr.com/content/30/1/87
(Journal of Experimental & Clinical Cancer Research )


What species of butterfly is this? Picture taken on 9-18-2018, near Helena, Mt Butterfly picture taken on the 18th of September 2018 at an elevation of 1800 meters (6,000 feet) near Mount Helena in Montana, USA.

That is a California Tortoiseshell google[https://www.butterfliesandmoths.org/species/Nymphalis-californica]


What is the biological basis for the perception of time? How is the "time axis" of memories encoded in the brain? I guess the time of the event could be "stored" with each event, but how is this translated into neurons etc.?

I'm no expert on the topic, but was about to find the following;

In mammals, the hippocampus region of the brain is one of only 2 regions with the capacity for lifelong neurogenesis (the creation of new neurons). This happens continuously with the creation of new memories and experiences (neurons are even created just to mark time passing - even if no memories are stored alongside - so that a perception of 10mins and 10secs is possible, even if nothing memorable happens). As new clusters of neurons are generated, they gradually differentiate and mature to become fully functional, and in this way time and memory are interlinked, and experiences are clustered together [1].

In a human study where individuals were asked to recall whether news events occurred within 1 week of each other (some related, some not), same-week and separation judgements were more far more accurate for related events. Unrelated events were essentially guesses, whereas deductions could be made about related events. [2]. This lends weight to the above argument that memories are clustered in the brain with temporal information embedded within.

The hippocampus is also involved in imaging the future. (Inconsistent) findings suggest that activation of the hippocampus allows mammals to conceive a scenario constructed from previous memories and experiences, and to store these for later use [3].

Refs

Aimone, J. B., Wiles, J., & Gage, F. H. (2006). Potential role for adult neurogenesis in the encoding of time in new memories. Nature neuroscience, 9(6), 723-7. doi:10.1038/nn1707
Friedman, W. J., & Janssen, S. M. J. (2010). Do people remember the temporal proximity of unrelated events? Memory & cognition, 38(8), 1122-36. doi:10.3758/MC.38.8.1122
Addis, D. R., & Schacter, D. L. (2011). The hippocampus and imagining the future: where do we stand? Frontiers in human neuroscience, 5, 173. doi:10.3389/fnhum.2011.00173


Are there known minimal marine ecosystems that are stable? A more entertaining phrasing of the question would be "what would a marine ecologist put into a perfect aquarium?"

I was reading about Prochlorococcus, among other photoautotrophs, and found that they seem to get their nitrogen from ammonia, which must be produced by some other organism. This set me off wondering what different species I would need in a hypothetical aquarium (how big that would have to be is another question, I guess), such that a sustainable ecological equilibrium occurs (one different from everybody dead, I guess), only requiring sunlight and air from the outside.

I realize that I'll have to put other components like iron etc in the water, but let's say I only put some fixed amount in during setup. What exactly that would have to be is probably another can of worms, so let's keep that out of this question as much as possible.

Has there been research towards such model ecosystems, and are there known minimum configurations?

It's hard to give an authorative "no" to this answer. But maybe there's research that looked for such a system and failed, or maybe marine ecologists use model cultures in their labs that show instabilities (meaning the culture dies, you have to replace the water, or keep adding fertilizer, or keep removing some waste) which allow some generalizations.

This is the one I've heard of - Its a sealed acrylic globe that contains algae and brine shrimp.  There are quite a few references in the bibliography here to previous systems.
Of course, it needs sunlight, but all the elements are recycled.  Its really closed and has reasonable endurance.

The basic commercial version of his closed world -- sold under the label of "Ecosphere" -- is a glass globe about the size of a large grapefruit. My world #58262 was one of these. Completely sealed inside the transparent ball were four tiny brine shrimp, a feathery mass of meadowgreen algae draped on a twig of coral, and microbes in the invisible millions. A bit of sand sat on the bottom. No air, water, or any other material entered or exited the globe. The thing ate only sunlight.
The oldest living Hanson-world so far is ten years old; that's as long as they have been manufactured. That's surprising since the average life-span of the shrimp swimming inside was thought to be about five years. Getting them to reproduce in their closed world has been problematic, although researchers know of no reason why they could not go on replicating forever. Individual shrimp and algae cells die, of course. What "lives forever" is the collective life, the aggregate life of a community.

All of this is a real subject of research for those interested in creating entirely useful ecosystems.

It turns out that ecospheres scale up well. A huge commercial Ecosphere can weigh in at 200 liters. That's about the volume of a large garbage can -- so big you can't reach your arms around it. Inside a stunning 30-inch-diameter glass globe, shrimp paddle between fronds of algae. But instead of the usual three or four spore-eating shrimp, the giant Ecosphere holds 3,000. It's a tiny moon with its own inhabitants. Here, the law of large numbers takes hold; more is different. More individual lives make the ecosystem more resilient. The larger an Ecosphere is, the longer it takes to stabilize, and the harder it is to kill it. But once in gear, the collective give and take of a vivisystem takes root and persists.

Unfortunately larger systems that can support people have not been made yet.

Algae and man lasted a whole day. For about 24 hours, man breathed into algae and algae breathed into man. Then the staleness of the air drove Shepelev out. The oxygen content initially produced by the algae plummeted rapidly by the close of the first day. In the final hour when Shepelev cracked open the sealed door to clamber out, his colleagues were bowled over by the revolting stench in his cabin. Carbon dioxide and oxygen had traded harmoniously, but other gases, such as methane, hydrogen sulfide, and ammonia, given off by algae and Shepelev himself, had gradually fouled the air. Like the mythological happy frog in slowly boiling water, Shepelev had not noticed the stink.

Here is an academic reference you can use to start looking around if you like...


Where does meiosis II of oogenesis end exactly in tuba uterina - uterus? I know that metaphase II ends at ampulla tuba uterina, but I am not completely sure where the telophase II ends. Is it in the triangular section of cervix uterii?

I just have an intuition that the thing is not ending at the ampulla, since there is some time to get to the uterus. The thing must happen before implantation to the uterus, since the egg is blastocyst at the stage.

2. When does meiosis II of oogenesis end exactly?

The location is exactly tuba uterina infundibulum, source, since the processes results in the following things before LH peak:

  The correct placement of the uterine tube infundibulum upon the
  ovarian surface
  The rupture of the follicle wall and the flow of the
  follicle fluid with the oocyte into the infundibulum
  The inhibition of
  the maturation of further follicles


What is this little owl-like bird? I was walking outside (location: Netherlands) and just saw this little bird:

Unfortunately I had to take a long range picture with my cell phone so the quality is quite bad, however I hope still someone can identify this species. Personally I think it escaped somewhere as we have never seen it before and also did not seem to be scared of us.

This looks a lot like a double-barred finch (Taeniopygia bichenovii). Your note about this being an "owl-like" bird is supported by it's less common name, the "owl finch", so named for the dark ring around the face.

 Source: Wikipedia; Credit: Glen Fergus

If this is in fact the bird you saw, you're right that it's not native to your country (or continent or even hemisphere!). The Taeniopygia genus is in the Estrildidae family, and it only contains two species native to Australia! According to Wikipedia, T. bichenovii is found:

  in dry savannah, tropical (lowland) dry grassland and shrubland habitats in northern and eastern Australia

You can read more at eFinch and The Atlas iof Living Australia.


Difference between 'fitness' and 'fitness effects' Term 'fitness' is pretty obvious, but, often 'fitness effects' is commonly used in many research articles in the field of evolutionary biology.

I suspect that 'fitness effects' has a different meaning than just 'fitness'. I found that it's really difficult to find the distinction between the two terms just by googling.

So, if some expert in the subject is reading, please clarify.

Fitness

Fitness is some function of the probability of survival and fecundity for a given genotype. Fitness is therefore a single value per genotype.

Fitness effect

A fitness effect is a component of fitness. For example, for a given bi-allelic locus, the fitness effect of allele A is -0.05 in comparison to the allele B, meaning that the allele A is deleterious and the allele B is beneficial. There is a fitness effect for each allele, for each trait and, if you interested in  genetic interaction (epistasis) and genetic-environment interaction, then there can be a fitness effect for each gene and each trait in each genotype in each environment.

Example

It is typically common to assume a model of $n$ loci, where the fitness effects at each loci are $1$, $1-hs$ and $1-s$ for the three genotypes AA, AB and BB respectively (diploid population). $s$ is the selection coefficients and $h$ is the dominance coefficient. The fitness of the individual is often obtained by multiplying out the fitness effects at each loci. The worst possible fitness is therefore $\left(1-s\right)^n$.


Where is the H+ ion in this step of glycolysis coming from? (from Fundamentals of Biochemistry by Voet, 5th ed.)

In this step of glycolysis, I'm not seeing where the $\ce{H+}$ ion on the product side is coming from. It seems to me that the G3P's aldehydic H is replaced by phosphate, and that H is given to $\ce{NAD+}$ to make NADH. So where is the extra $\ce{H+}$ coming from?

Although texts such as Berg et al. tend to refer to inorganic phosphate, $\ce{P_i}$,  as orthophosphate ($\ce{PO4^{3-}}$), the term inorganic phosphate is used because in aqueous solution at pH 7.6 several phosphate species exist, the predominant one being $\ce{HPO4^{2-}}$. If this is regarded as $\ce{P_i}$, then it is the source of the $\ce{H^{+}}$, and the equation balances.

Note added by David:

On checking I find, in contrast to Berg, Lehninger’s book defines $\ce{P_i}$ as monohydrogen phosphate ($\ce{HPO4^{2-}}$), and Fersht actually writes the equation of the reaction (16-1) with $\ce{HPO4^{2-}}$ rather than $\ce{P_i}$.


What gases are needed for humans to breathe? I will be beginning a science project about sustaining life on space stations. I already know that pure oxygen is harmful for humans but would $O_2$ + $CO_2$ be enough for humans to breathe in or do humans need other gases as well?

Why not look at the existing space station as an example.  The International Space Station (ISS), a starting article is "Breathing easy on the space station" (NASA), while this article does not discuss the amounts of various chemicals, it looks at the process about how the chemical balance is maintained - an important point related to your question is that carbon dioxide is filtered away.

The second article "Breathing on the Space Station" (e-missions), discusses the actual percentages of each component.  It states that the chemical composition of the space station air is ideally similar to Earth's atmosphere.  With 78% nitrogen, 21% oxygen and 1% water vapour on the space station (Argon is in the Earth's atmosphere, but appears to be unnecessary on the space station).

I hope this helps.


What are some examples of interbreeding between species that are separated by 5 million years or more? Interbreeding is constrained with that the offspring shares the gene pool of the parents. What are some examples of interbreeding that has occurred, where the two species were separated by 5 million years or more?

I depends a little bit about what you mean by interbreeding. In any case, my answer won't be fully satisfactory.

Horizontal gene transfer

If you are referring to any exchange of genetic materials than, you can have a look at Salzberg et al. (2001) who report 40 genes that were horizontally transferred from bacteria.

Elysia chlorotica is sea slug which is able of photosynthesis thanks to a horizontal gene transfer (Schwartz et al., 2014)

Typical interbreeding

If you are thinking about some kind of more common type of inbreeding, then you might want to consider

mule who is the hybrid between a male donkey and a female horse. Donkey and horse share a common ancestor that is about 4.5 millions years old (according to Live Science). Mules are often sterile but some of them have been fertile (Rong et al. 1988; see also this article from the Denver post; thanks @iayork)

Platanus × acerifolia is a hybrid between Platanus orientalis and Platanus occidentalis. Platanus are a rather old genera with fossils of 115 millions years old found (from wiki). However, I don't know how old is the common ancestor between P. orientalis and P. occidentalis

There are plenty of other examples in wikipedia > hybrid but I failed to find good estimate of common ancestry for those who may have had a common ancestor older than 5 millions years but it probably exist given that the mule example is already 4.5 millions years old.


Structure and reactions of the cofactors of oxidoreductases such as ferredoxin I have seen the word flavoprotein being used in place of ferredoxin in few places and vice-versa. I have not found any source that mentions them both together and explains the relation between them.
Examples I have found are:
FAD-Flavin Adenine Dinucleotide/Ferrodoxin Adenine Dinucleotide
FNR-Flavo protein NADP Reductase/ Ferredoxin NADP reductase
Is there any relation between the two? Are they the same or do they serve the same purpose?

Summary
Enzymes catalysing oxido-reductive reactions (oxidoreductases) do so with the aid of non-protein molecules (prosthetic groups or cofactors) at their active sites. The three main types of such prosthetic groups or cofactors are iron–sulphur clusters, derivatives of flavin (FAD and FMN) and nucleotide derivatives of nicotinamide (NAD and NADP). The groups of proteins incorporating these type of cofactors are often referred to by the general terms ferredoxins (also iron-sulphur proteins), flavoproteins, and NAD(P)-linked oxidoreductases, respectively.
Introduction
The vast majority of enzymes are proteins, linear polypeptide chains folded into specific but irregular spheroidal shapes. In addition to interacting with the reaction substrates, the amino acid side-chains of the polypeptide chains participate in the actual reactions catalysed by many enzymes, and in many cases are sufficient for the catalytic properties of enzymes. However for the catalysis of some sophisticated reactions, additional non-protein molecules are required — metal ions or organic molecules — known generally as ‘co-factors’, ‘co-enzymes’ or ‘prosthetic groups’. This is the case for the various enzymes termed oxidoreductases, which catalyse oxidation/reduction reactions, involving the transfer of electrons.
Nucleotide derivatives of nicotinamide in NAD(P)-linked oxidoreductases
The cofactors found most frequently in oxidoreductases are nicotinamide adenine dinucleotide (NAD) and nicotinamide adenine dinucleotide phosphate (NADP). The pyridine ring of the cofactor is the electron acceptor, and the oxidized and reduced forms are termed NAD+ and NADH, respectively.

[Own diagram]
Proteins with bound NAD or NADP (non-covalently) are the most common type involved in oxido-reductions, and have systematic names composed of the cofactor, substrate and ‘oxidoreductase’. e.g.
Systematic Name: lactate:NAD+ oxidoreductase
Common Name: lactate dehydrogenase)
Flavin Nucleotides in Flavoproteins
The other common cofactors in oxidoreductases are flavin adenine dinucleotide (FAD) and flavin mononucleotide (FMN). The isoalloxazine ring is the electron acceptor, and the oxidized and reduced forms are termed FAD (FMN) and FADH2 (FMNH2), respectively.

[Adapted from section 14.3 of Berg et al.]
Proteins containing FAD or FMN are called flavoproteins, and are less abundant than NAD(P)-linked oxidoreductases, and a few of them actually perform non-redox reactions. Example of nomenclature:
Systemic name:  short-chain acyl-CoA:electron-transfer flavoprotein 2,3-oxidoreductase
Common name: short-chain acyl-CoA dehydrogenase
Iron–Sulphur Clusters in Ferredoxins
Whereas the above two oxidoreductases are common in intermediary metabolism, those containing iron–sulphur clusters (some of which are known as ferredoxins) tend to be involved in more specialized and ancient reactions, such as photosynthesis, tagged in the question. The diagram  shows one particular type (2Fe–2S) of iron–sulphur cluster and its covalent attachment to the ferredoxin through cysteine residues. 4Fe–4S stoichiometries are also found, as well as some others.
The electron transfer involves changes in the oxidation state — Fe(II)/Fe(III) — of the iron.

[Adapted from section 19.3.3 of Berg et al.]
The figure also provides a good illustration of the relationship between a co-factor and the protein in which it resides.
Example of nomenclature:
Systematic name: hydrogen:ferredoxin oxidoreductase
Common name: ferredoxin hydrogenase
The situation here is complicated by the fact that iron–sulphur clusters are found in other proteins besides those termed ferredoxin, including some specialized oxidoreductases involved in the electron-transport chain, and in nitrogenases. The term ferredoxin is historical rather than systematic.
Differences between these oxidoreductase cofactors
The specific roles played by these three cofactors in oxidoreductases is a topic of its own. However, it should be mentioned that an important difference is their standard reduction potentials, the biochemical background to which can be found in Section 18.2.1 of Berg et al., available online.
Ferredoxin-NADP+ reductase (FNR)
Electron transport occurs between the different cofactors in certain circumstances, one of which is photosynthesis where electrons are transferred from ferredoxin to NADP+. The enzyme catalysing this — Ferredoxin-NADP+ reductase — uses the third type of cofactor — FAD!


Real time PCR parameter CT When puting a real time PCR, parameter CT, which means threshold cycle, is used. What does it mean really? according to wikipedia "The number of cycles at which the fluorescence exceeds the threshold is called the threshold cycle (Ct)"
could anyone put it in conext?

Realtime PCR uses a fluorescent dye which binds to double-stranded DNA and thus allows to measure the growing amount of DNA by each cycle. The DNA added to the reaction also binds the fluorescent dye and makes some part of the fluorescent background. When the PCR reaction starts, it takes a while until enough DNA is synthesized to go over the background and to be able to reliable distinguish the signal from the noise. I think this becomes clearer, when you look at the image below (from the NIH):

The Ct is the point where the signal can be distinguished from the background when it enters the exponential grwoth phase. The no template control stays below this threshold.


Can virus resistance be acquired through generational exposure? If I have a squash plant that has a mosaic virus of some kind, and I breed its descendants (via seed) for generations, each with exposure to the same virus, will future generations be likely to eventually obtain resistance to the virus, and if so, how long would this typically take?

It seems to me that this might be how the resistant plants would have first developed resistance, but I could be wrong.

Perhaps the answer is in natural selection. Over many generations, if these plants are constantly exposed to the same virus, one of them may obtain a mutation or something similar that allows it to be resistant, thus that plant will have higher survival and growth rate and thus more seeds.

The current plant itself may also adapt to the presence of this virus (perhaps in growth patterns, etc.) over a long period of time.

As for the time for the genetic resistance to take place, it is almost impossible to say as it is almost completely random (and would also depend on what other plants you may pollinate it with as an already resistant plant would, of course, cancel the need for a mutation).

I hope this helps.


C Form DNA Base Pairs Per Turn How does C-DNA have 9.33 base pairs per turn? The number of base pairs should be quantised. How can it be a decimal?

There is no requirement that DNA should have a whole number of base pairs per turn. As a thought experiment, say you have a helix of dsDNA with 10 base pairs that completes one helical turn (ie it has 10 bp/turn). Now, twist that DNA along its axis so that it completes 1.5 turns. There is still only 10 bp and thus 6.67 bp/turn (which you should notice is a decimal).


How a nerve impulse reaches the correct destination? Say your brain wants to retract your right hand.

If there is some information coding playing a major role here, then what is the mechanism to find the correct path to reach the correct muscle?

Or is it every part has a single nerve connecting to the brain?

Any difference when it comes to withdrawal reflex comparing to brain initiating action? i.e. how the reflex round trip reaching the correct muscle?

OK, I think I can answer at the right level now.

Firstly, a nerve is a bundle of neurons, each neuron is like a fibre. So the sciatic nerve in the leg will carry fibres from the spinal cord to the muscles in the leg, like a data cable might connect many computers in an office to a server on another level.

Each neuron will form connections with a specific area on a specific muscle, at a specialised synapse called the "neuromuscular junction". When a signal travels down that particular neuron, it will release neurotransmitters that activate that particular muscle region. So by sending signals to the right neurons, the muscle to be activated and how much to activate it can be selected by the CNS.

A nerve impulse is a slightly misleading term as it refers to the collective activity of signals within the many neurons of the nerve, so an individual neuron won't register on an impulse. The signals in neurons are called "action potentials".

There is some information coding in the frequency of action potentials within neurons, but it is used to control the response of the muscle, rather than locate the correct muscle.

Wikipedia is pretty good on the subject if you know where to look:

neuron

withdrawal reflex

sciatic nerve


What is the motivation behind fluorinated pharmaceuticals? From what little research I've done, it appears that a significant portion of modern psychoactive drugs are fluorinated in one way or another (for example, Buproprion, Fluvoxamine, or any number of other antidepressants).

What is the motivation behind the addition of these groups? My initial guess would be that it either increases blood-brain barrier clearance or reduces the drug's metabolism, but I've been unable to find papers supporting either idea (or papers on the subject at all, for that matter). Any books/papers illuminating the subject would be greatly appreciated.

Fluorine has a combination of unique chemical properties, which makes it very useful in drug design :

It is small, such that replacing a C-H with a C-F is often possible, from a sterical point of view. Halogens, which share some of the other desirable properties of fluorine, are much larger.
It is very electronegative: it will attract electrons strongly, which allow polarising, stabilising or destabilising various moieties.
It is not found in natural products (except for trifluoroacetic acid), which means our metabolising apparatus, result of evolution by exposure to such products, can have difficulty dealing with it: thus ut makes drugs more resistant to degradation.

With these properties, you either start with fluorine in mind, to make  molecules that mimics transition state of reactions involving non-fluorinated compounds (thus, enzyme inhibitors), or mimic the peptide bond (but not cleavable as easily); or you add it later to a compound that already work for additional activity, or less clearance.

There are many good books and reviews, but you could start with this one.


Why is Paracetamol so great? Every time I get ill (cold, flu etc) I take a couple of these wonderful tablets for up to 4 times a day and I, eventually, get better.  What exactly is paracetamol?  Why is it so effective and is it really not harmful as my doctor would have me believe?

Paracetamol is a pain killer, it does not treat the cause of your illness, it only alleviates the symptoms. From its wikipedia page:

Paracetamol [...], chemically named
N-acetyl-p-aminophenol, is a widely used over-the-counter analgesic
(pain reliever) and antipyretic (fever reducer).

So, paracetamol does not make you better. Your immune system makes you better. Paracetamol just makes you feel better while you are waiting for your immune system to get an infection under control.
You should be aware that it is only safe in small doses and a toxic dose is not that much more than the recommended one (source):

Risk of severe liver damage (ie a peak ALT more than 1000 IU/L)
Based on the dose of paracetamol ingested (mg/kg body weight):
Less than 150 mg/kg - unlikely
More than 250 mg/kg - likely
More than 12 g total - potentially fatal

Again from wikipedia:

While generally safe for use at recommended doses (1,000 mg per single
dose and up to 4,000 mg per day for adults),[6] acute overdoses of
paracetamol can cause potentially fatal liver damage and, in rare
individuals, a normal dose can do the same; the risk may be heightened
by chronic alcohol abuse, though it is lessened by contemporary
alcohol consumption. Paracetamol toxicity is the foremost cause of
acute liver failure in the Western world, and accounts for most drug
overdoses in the United States, the United Kingdom, Australia and New
Zealand.

I am sure someone else can explain the pharmacokinetics and details of action of paracetamol. I just wanted to point out that paracetamol can be dangerous and should be treated with respect.


Which one is better to use for water stress experiment GWAS or RNASeq? This is my first time in this area of research. I am working on 95 varieties of bambara groundnut. I have done the agromorphological characterization of these varieties as well as the genetic diversity using DArT markers. Based on the charaterization result, i have selected 10 varieties to be subjected to water stress with the objective of identifying genes that are responsible for tolerance in this plant. My challenge now is:
1. bambara groundnut does not have a reference genome, so will i be able to use GWAS in getting these genes from the result of the DArTSeq.
2. Bearing in mind that the whole 95 varieties characterized were not subjected to water stress, do i need to set up another experiment entirely for the water stress and go ahead to make use of RNASeq to get the genes?
3. It is obvious that some genes will be upregulated and some will be downregulated, how do i identify these genes and how do i know if they are expressed at the onset of stress, during, or after stress?
4. when is the appropriate time to take my samples, i was considering taking at 50% flowering stage. Is this good?
Any help and insightful articles will be greatly appreciated.

bambara groundnut does not have a reference genome

This is your biggest problem if you want to do any sequencing based analysis. Neither GWAS nor RNAseq data analysis are possible without a reference genome (or at least transcriptome).
Depending on the availability, quality & similarity of reference genomes from related species it may however be possible to construct a reference transcriptome for your species from RNA sequencing data you get from RNAseq experiments. I'm whether it's feasible (or indeed possible) to try the same with genome sequencing data, since with only 10 individuals/strains you may only be able to get huge linkage groups for GWAS analysis.

Either way I'd highly recommend you to talk with someone (i.e. from your institute) who has experience in doing RNAseq or GWAS on plants, when planning this. (The experience with platns important, mammalian/model system genomes are much better studied and generally have less genome duplications, so analysis of plant data comes with its own set of baggage)

  Bearing in mind that the whole 95 varieties characterized were not subjected to water stress, do i need to set up another experiment entirely for the water stress and go ahead to make use of RNASeq to get the genes?

If you want to use RNAseq to find genes that are differentially expressed between states of water stress and no water stressin the same plant/species you will need to compare samples taken from corresponding conditions. This is only possible with RNAseq data.
Another approach could be to do some other experiments to determine which plants show a phenotype when exposed to water stress, and then look for correlations of this phenotype with (sequence) isoforms variants [GWAS like approach, possible with RNAseq or genomic sequencng data] or with expression levels of certain genes [again only possible with RNAseq data]. In thsi approach you need to be aware that your sequencing data either represents the ground state of all plants (no stress) or a potentially stressed state and missing one of these may mean that you can't find genes that change expression levels based on stress.

  It is obvious that some genes will be upregulated and some will be downregulated, how do i identify these genes and how do i know if they are expressed at the onset of stress, during, or after stress?

First, while most analysis tools will always give you some values for up- or downregulation, that does definitely not mean that these values are always meaningful. Only proper statistical testing can tell you which up/downregulation is somewhat reliable (it still wont tell you if its biologically meaningful) and depending on the quality of your data and the actual biological differences you may not be able to find anything.
Secondly, if you care about the timepoint of expression for specfic genes, you will need to some time series experiments. (Doing that for the whole RNAseq/GWAS would be very expensive, so ideally you first identify some candidate genes and then study their specific expression profiles with easier methods).

  when is the appropriate time to take my samples, i was considering taking at 50% flowering stage.

If you are not an  expert on the species you#re working with, I'd again highly recomment you to speak with someone who is.


Comparison of humans and other primates in milk production amount Do human females produce more milk (relatively to average child weight weight) than other primate females? Are human females more likely to feed several children through breastfeeding than other primates?

P.S. I am asking this, because it's what my antropologic hypothesis predicts: some women refused to nurse (and breastfeed) children born by them, so "nurses" - other women - fed those children. This, of course, would require those women to have extra (more than needed to feed their own children) amount of milk.

The comparison to non-human primates and the behavioral question kind of threw me, but I think this is an X-Y problem. If you're asking:

  Are humans capable of producing more milk than they need to feed their own offspring

The answer is yes

There is some data I don't think we'd be able to get anymore, but in Chapter 5 of Nutrition During Lactation, they break it down.

  Several studies indicate that potential milk production in humans is considerably higher than the average intake by single infants. Kaucher and colleagues (1945) measured maximum milk output with intrusive and tedious mechanical methods to extract all the mother's milk and reported that production averaged almost 1,200 g/day at 6 to 10 days post partum. This level is much higher than the 500 to 700 g/day consumed by breastfed infants at the same age (Casey et al., 1986; Saint et al., 1984).

Kaucher's methods may not have been particularly good, because others showed limits more than twice that

  Women who express surplus milk for a milk bank have been shown to produce as much as 3,000 g/day (Macy et al., 1930).

As my wife and many lactating mothers who use a breast pump will be able to confirm, this isn't a relic of the 30s and 40s. If you keep pumping, you keep getting milk.

  In two separate studies, milk production increased by 15 to 40% when a breast pump was used to remove additional milk after feedings (Dewey and Lönnerdal, 1986; Neville and Oliva-Rasbach, 1987).


Is there any evidence of blue jays preying on other birds? Are blue jays known to prey on other birds?  I've found that they are known to raid nests of eggs and young, but have not found any evidence of them actually preying on other birds.

Background:  A few years ago while raking leaves this time of year (late Oct/early Nov) the head of a house sparrow fell on me.  I looked around in the spruce tree I was under and saw a blue jay eating the rest of the house sparrow.  This was approximately 10 feet from my bird feeders.  I can't say that it wasn't dead beforehand, but it's proximity to the feeders made me wonder.

Yes! This article gives an account of a Blue Jay killing and consuming a Cedar Waxwing, and further it clearly states that at times Blue Jays do predate on fledgling and adult birds, and gives a hefty amount of sources to back that up, if you're in the mood for further reading.


Are all hybrids infertile? I'm familiar with the concept of hybrid infertility, but my question is: Are ALL hybrids infertile, or is it just so extremely unlikely that the chances are basically nil that they can actually produce a viable sperm/egg?

Thanks.

Species definition

The whole problem is based upon your definition of hybrid and therefore your definition of species. If a hybrid is the offspring of two individuals belonging to different species and if we define species based on reproductive isolation, then a hybrid can, by definition, not be fertile.

However, we often call two lineages as being two different species even if they can reproduce. To get into more difficulties we could differentiate between pre-zygotic and post-zygotic reproductive isolation assisted reproduction.

You should definitely have a look at the post How could humans have interbred with Neanderthals if we're a different species? for a discussion on the concept of species.

In practice

In practice we often call two lineages as different species even though they are not reproductively isolated. In such cases, yes hybrids are fertile. In fact, hybrid can even have a very high fitness, a phenomenon called heterosis (aka. hybrid vigour). A historically important example is one described by Darwin in The Variation of Animals and Plants under Domestication; the hybrids between the common pheasant and domestic fowl are larger nd more resistant than both parents.

Note also, Haldane's rule that states if in a species hybrid only one sex is inviable or sterile, that sex is more likely to be the heterogametic sex. This is for example the case of the Yakalo (hybrid of yak and bison).

There are also cases where the hybrids are reproductively isolated from both parent species and end up creating a third species. This is called hybrid speciation.


Can someone help me identify this queen ant? I found this queen ant near a river on the 14 july in Braga-Portugal, it was on a river bank, and it measures around 8 mm. Can someone help me identifying the species? thank you for your time :)

The small space between the thorax and the abdomen indicates this queen has only one petiole segment (no post-petiole). The large size and absence of an elongated first abdominal segment indicates the subfamily Formicinae. The morphological features necessary to go further with a formal identification are not visible, but from the general aspect of the ant it is likely to be a Lasius or a Formica.

See ref below:

  Seifert, Bernhard. Die Ameisen Mittel-und Nordeuropas. Lutra Verlag-u.
  Vertriebsges., 2007.


Why is AUG the initiation codon? Is there any reason why AUG is the initiation codon?
Can’t translation start with different codons?

A good question (if a little mixed up on transcription vs. translation!)

AUG is not always the start codon, but whatever the codon is it will always code for Methionine (or fMet, but still a variation on Met), even if the codon codes for a different amino acid otherwise. A  separate transfer RNA (tRNAi, the initiator tRNA) is used for the arrangement of this first step, guided by eIF2 [in eukarya].

In this respect it's less a question of "why AUG" than "why this specific initiator tRNA", the answer being that it's got certain sequence elements and modifications that distinguish it from the elongating tRNAs which bind elongation factors and hence are targeted to the ribosomal A and B sites instead of the ribosomal P site (with function being dependent on form, basically it's shaped to set up transcription rather than to elongate an existing nascent chain polypeptide).

  "Identity elements appear to finely tune the structure of the initiator tRNA, and growing evidence suggests that the body of the tRNA is involved in transmitting the signal that the start codon has been found to the rest of the pre-initiation complex." — Kolitz and Lorsch, 2010

The other start codons are just from natural chemical variation (or evolution, whichever way you want to look at it) giving rise to different codon-recognising protein shapes.

The machinery for starting translation works, and as such is "conserved" - evolution has kept it, and that's why it is always the same codon (more or less). Archaea have a very similar shaped tRNAi acceptor stem, and is an equally good ligand, which shows how ancient the system is and gives an idea of how fundamentally difficult it must be for an organism to change a system like this through mutation (3.5 billion years of evolution can't be wrong! etc. haha).

Not to just gloss over the part where I said that non-AUG codons get used too (in yeast and mammalian cells), the following is from a study in which it was found changing 1 (and only 1) of the AUG bases still permitted translation initiation:

  "Naturally occurring misrecognition indicates that discriminating two base-paired near-cognate codons from the perfect three-base-paired AUG
  codon is subject to mistakes. Mutations in translation
  initiation factors, such as eIF1 and eIF2b, further increase the levels of these mistakes.

  Two base-pairing interactions between non-AUG codons and the anticodon of
  the Met-tRNAi are sufﬁcient to trigger translation initiation, suggesting that wild-type eIF1 plays a role in
  monitoring proper base-pairing interactions when scanning for the AUG start site. It would be predicted that
  the Met-tRNAi, not a cognate tRNA matching an individual non-AUG codon, is used in translation initiation at these non-AUG start codons.

  The translation initiation complex will bind only the Met-tRNAi as
  opposed to other tRNAs because Met-tRNAi has unique
  sequence and structural features that allow it to be
  loaded onto eIF2 of the ternary complex and enable it
  to ﬁt into the P site of the ribosome" — Maduzia et al, 2010

Basically the consensus is that it's not really possible to say why the methionine codon, "it's just a structural thing", which is a bit of a circular argument really.


What bird is this seen trekking in Nepal during descent on Manaslu circuit? What bird is this seen trekking in Nepal during descent on Manaslu circuit?

You found an Alpine accentor (Prunella collaris). It's a bird of mountain areas in the Paleartic.

Here is a picture for comparison:

The only similar bird in the area is the Altai accentor (Prunella himalayana), but you can tell it apart because your bird does not have streaked flanks and the more uniform grey head (in your picture it is clearly visible the supercilium)


Can one dendrite pass through another? While tracing dendrites on EyeWire I encountered the following situation. They belong to an Orientation Selective Ganglion Cell.

It's the first dendrite I've noticed with such a clear 'hole' in it, though which another dendrite passes.

Is it possible for one dendrite to pass through another? Perhaps I shouldn't have 'connected' the top part with the bottom part?

I can't think of any reason that would explicitly prohibit a dendrite from travelling through a space created by another dendrite's branching pattern. In non-EM images of dendritic branching patterns I don't think I have ever observed dendritic loops, but of course, that has nothing to do with whether or not they occur. Nonetheless, I think there are more likely explanations for what you are seeing in these particular images.

As shown, the upper and lower parts of the "dendrite" in the first image do not look like a continuous structure. I would guess that you are looking at a synapse or some other contact between two different processes in the first image. The 3-4'o'clock connection in the loop suggests this interpretation. Can you see vesicles in the images around those connections?

The other dendrite that shows up in your second image might be a glial cell or some other cell's dendrite that participates in the synapse. Alternatively, the other dendrite may just be a chance passing of two dendrites that don't interact functionally.

Of course, it could be that you and the computer have just completely misunderstood the data. My understanding of the Eyewire interface is that the computer guides a lot of the identification and doesn't easily allow you to see the surrounding areas so you can't track structures all the way to their sources. In such a situation, it seems probable that you would end up with ambiguous instances like this that you would have a hard time resolving without more information/expertise. But maybe Seung or one his colleagues can come weigh in on that?


Purpose of poly(A)+ RNA? I am learning RNA-seq analysis. I always encounter this phase "poly(A)+ RNA". After searching, I got this: "Most messenger RNAs contain a poly(A) tail, while structural RNAs do not. Poly(A) selection therefore enriches for messenger RNA. The technique has proved essential for construction of cDNA libraries."

Does it mean that when constructing the cDNA, we always use the ones with a A's tail? Then other RNAs like tRNA are filtered and not used to get their cDNA? I do find some RNAs records on UCSC where microRNAs are included.

When we say poly(A)+ RNA library, what is the difference between normal one? Or normal RNA library is a poly(A)+ RNA library? Thanks.

One of the primary reasons to use poly(A) selection is to eliminate the massive amount of ribosomal RNA (rRNA) present in the samples.  The alternative is to use ribosomal RNA depletion kits / techniques to remove as much rRNA as possible before sequencing.  Without rRNA depletion a large proportion (~60-80%) of the reads would map to rRNAs.

poly(A) selection also reduces the amount of pre-mRNA in the samples, which reduces the number of intron aligned reads.