Is some of the energy of food lost during digestion? I know that chemical energy of food is converted to heat energy to be used by the body in many metabolic reactions. Specifically, I know that the breaking down of bonds is what releases energy.

Does that mean that some of the energy of food is lost during digestion as enzymes breakdown large food molecules into smaller soluble ones? Or is it the common concept of losing energy during digestion because not all the food is absorbed and some are egested?

Typically, catabolic reactions such as the hydrolysis of food stuffs into their monomers is an exothermic process. This includes conversion of proteins into amino aids, starchs into monosaccharides and fats into fatty acids plus glycerol. As an example, hydrolysis of a peptide bond linking the amino acids in a protein liberates 8-16 kJ/mol of energy.
https://en.wikipedia.org/wiki/Peptide_bond

So, that means a certain amount of the energy in food is liberated in the gut. But this is very minimal compared to the amount yet to be liberated, and harvested, as the many other bonds in the monomers are further broken down during cellular respiration.

A bit of research from a few different sites suggests the gut temperature is not meaningfully higher that the core body temperature measured in, say, the anus or vagina. https://en.wikipedia.org/wiki/Human_body_temperature  Any heat liberated from digestion in the gut must be slow enough to be absorbed into the bulk of the body without accumulating in the gut.


What kind of a fly is this? I have a couple of new pictures of insects which I am really curious about. This is one of them. I found this fly near my cottage in Prague, Czech Republic.

It is fluffy with very long proboscis (almost half of an inch in length).

I found out that this is on of the most common specious from this family in whole Euroupe called Bombylius major. From wikipedia article (same with picture):

The adult is 14 to 18 millimetres (0.55 to 0.71 in) in length, squat and very hairy, with a wingspan of around 24 mm (0.94 in). It has dark patches on the anterior half of the wings and long hairy legs that dangle while in flight. The very long proboscis is used to feed on the nectar of many species of flower, especially primroses. While its wings continue to beat its front legs grip the flower and its long rigid beak is inserted to collect the nectar.[2] Despite its fearsome appearance, the beak is quite harmless.[2]
Bearing a mimetic resemblance to bees their body is stout and furry, with the top of the thorax being black and shiny and the pile either brown, yellow, or white. They have long spindly legs as well as a long rigid proboscis found in the front of the head. Their boldly patterned wings have a distinct dividing border through the horizontal middle between the dark and clear portions. Their antennae are typically very short and pointed. In the field they will be seen hovering and darting above bare ground or flowers, in an up-and-down movement, accompanied by a high-pitched buzz.


How does rho-dependent termination occur? Rho-dependent termination is not fully understood but there’s a brief description in almost every concerned book about it.
In Snustard and Instant notes-Molecular Biology it is written that, the rho protein binds a stretch of 72 nucleotides at the 3' end of the nascent RNA, which could be a recognition site and then moves along 5' -> 3' direction separating the DNA-RNA hybrid.
But how's it possible, rho binding to 3' end (which is not free) and moving in 5'-> 3' (if so it is sure to fall off!)?
Diagram from Berg showing something opposite, i.e. it has attached to the 5' end and is moving in 5' -> 3' direction.

What is the right thing?

There is no dichotomy in the two sources you have described. The text book you linked to says, exactly (emphasis added):

  Rho appears to bind to a stretch of 72 nucleotides near the 3'-end of the nascent RNA...

It doesn't say at the 3'-end, which is obviously impossible since the 3'-end forms a double-stranded hybrid within the transcription bubble.
Rho is not loaded at the 5'-end of RNA, either, but rather binds internally at cytidine-rich Rho utilization (rut) sites, which will be somewhere 5' of the actual point of transcription termination. As you mentioned, there is a lot of uncertainty in the process and, while a lot is known about rut sites, as far as I can tell there is no consensus sequence, thus making it difficult to systematically identify rut sites throughout the genome. I have found papers which identify rut sites in the 5'-UTR (1) as well as within the 3'-UTR, intercistronic regions and coding sequences (2, 3, 4).

Mechanism of internal Rho loading:

Koslover DJ, Fazal FM, Mooney RA, Landick R, Block SM. 2012. Binding and Translocation of Termination Factor Rho Studied at the Single-Molecule Level. J Mol Biol 423:664-676


Does a woman's G-spot actually exist? Does a woman's G-spot actually exist? Are there any research studies?

Links:

G-spot (Gräfenberg spot) at Wikipedia
U.S. gynaecologist says he has found the G-spot

The existence of the G-spot remains highly debated among researchers.  Two recent publications (Hines 2001, Kilchevsky et al. 2012) review studies of the so-called G-spot and conclude the evidence is too inconsistent to claim its definite existence.  Foldes and Buisson (2009) argue that the G-spot is actually just a clitoris that is richly  innervated. This would be consistent with the reported variability of G-spot presence or absence due to natural variation in innervation among women. (This last statement is my hypothesis offered without citation).

As noted by @Armatus in the comments, a few minutes following some of the Wikipedia links to the scientific journals (not the BBC, CNN, pop news sites, etc.) would give you lots of information about the G-spot. Still, I thought you question was worth typing up a brief answer for the sake of completeness.

Literature Cited

Foldès, P. and O. Buisson. 2009. The clitoral complex: a dynamic sonographic study. The Journal of Sexual Medicine 6: 1223–31.

Hines T. 2001. The G-Spot: A modern gynecologic myth. American Journal of Obstetrics and Gynecology 185: 359–62.

Kilchevsky, A, et al. 2012. Is the Female G-Spot Truly a Distinct Anatomic Entity? Journal of Sexual Medicine. 719-726.


How might gene clusters like the lac operon evolve? The obvious answer for a gene cluster is gene duplication and mutation of one or both genes. But the genes in the lac operon seem not be so functionally/structurally similar (as compared to the Hox gene cluster, for example), so I was curious as to how they ended up physically associated in the first place.

Operons, often but not always, contain clusters of genes (under the control of an operator region) which are involved in the same metabolic pathway. There have been several theories for how these groups of genes have arisen but the current feeling seems to be based around the regulation of the genes in question 1. To facilitate co-ordinated gene regulation there may have been strong selection for physical clustering of genes involved in a particular process. By being physically clustered this also means that all the genes within a given operon are probably subject to the same chromatin remodelling and will then be more easily switched on and off under the appropriate conditions i.e. all turned on when they are needed and switched off when they are not.

Operons with similarly arranged genes have been found in different micro-organisms, leading to the thought that the operon was an ancient and evolutionarily conserved arrangement [2]. The figure below from Fani et al. 2005 presents two possible ways of generating the current state of genome organisation for present day proteobacteria.

If the operon is an ancient arrangement we would predict high gene conservation within operons; but genome analysis of different micro-organisms shows this not to be the case (i.e. gene conservation is low and operons are pretty unstable). Accordingly, another author suggests that due to the lack of conservation, operon structure is pretty plastic and can change readily during evolution [3]. Indeed, Fari et al conclude in their paper that the histidine biosynthesis operon has been a construction or re-construction event from scattered genes and not from the descent of an ancient arrangement:

  Our model suggests that the his gene organization in the extant proteobacteria arose from a gene scattering in the genome of the proteobacterial ancestor. The model also predicts that all or most of the his genes (except for hisD) were monofunctional and that they underwent a progressive clustering and compacting which occurred together with gene overlapping and fusion events

They found, as you suggested, evidence for several gene modifications which included elongation, duplication and gene fusions. As for what caused the progressive clustering, see reference 1 again.

Obviously different operons are probably going to have formed in different ways in different organisms and I don't think we can rule out the 'ancient arrangement' argument completely. It's a pretty broad and confusing topic and there's a lot of literature, I hope the examples I picked and have listed are useful!

1 Osbourn, A. and Field, B. Operons. Cell. Mol. Life Sci. (2009) 66:3755–3775

[2] Fani et al. The Origin and Evolution of Operons: The Piecewise Building of theProteobacterial Histidine Operon. J Mol Evol (2005) 60:378–390

[3] Itoh et al. Evolutionary instability of operon structures disclosed by sequence comparisons of complete microbial genomes. Mol Biol Evol (1999) 16(3):332–346


What in soy are people allergic to and will these allergens be passed along if an animal that has eaten soy is consumed? I have two related questions about soy allergies and possible reactions.

What is it that are humans who have soy allergies actually allergic to? What is the allergen?
If an animal eats soy, are those allergens broken down or retained? Can the consumption of that animal cause an allergic reaction similar to direct soy consumption?

There are multiple soy protein allergens.  This has a pretty good review in the introduction.  Here is a list of some of the allergens (same paper).

Chickens on soy diets do lay eggs with higher concentrations of soy isoflavones than chicken on non-soy diets. (Edit: higher concentrations of soy isoflavones are also found in chicken tissues -- see ref 4 below.) References (originally found here) are:

Saitoh, S.; Sato, T.; Harada, H.; Takita, T. Transfer of soy isoflavone into the egg yolk of chickens. Biosci. Biotechnol. , Biochem. 2001, 65, 2220-2225.
Saitoh, S.; Sato, T.; Harada, H.; Matsuda, T. Biotransformation of soy isoflavone-glycosides in laying hens: intestinal absorption and preferential accumulation into egg yolk of equol, a more estrogenic metabolite of daidzein. Biochim. Biophys. Acta 2004, 1674 (2) 122-130.
Lin, F.; Wu, J.; Abdelnabi, M.; Ottinger, M.; Giusti M.M. Effects of dose and glycosylation on the transfer of genistein into the eggs of the japanese quail (Coturnix japonica). J. Agric. Food Chem. 2004, 52, 2397-2403.
Vargas Galdos, Dante Miguel Marcial. Quantification of Soy Isoflavones in commercial eggs and their transfer from poultry feed into eggs and tissues. Thesis. Ohio State University, Food Science and Technology Graduate Program, 2009; http://etd.ohiolink.edu/send-pdf.cgi/Vargas%20Galdos%20Dante%20Miguel%20Marcial.pdf?osu1236706764.

However, I do not know whether this is enough to cause an allergic reaction if consumed. (There's plenty of anecdotal evidence, but no clinical studies that I know of.)


Who created the codon wheel chart (not as a table) I'm trying to find out who created or first used the codon wheel chart as far as we can know?
(I don't mean the tabular format)

It is very difficult to answer this one for certain but I think the codon wheel representation is sometimes attributed to Rosemarie Swanson who represented the amino acid code using Gray code (or reflected binary code).

Swanson's work actually went quite a bit deeper than the simplified codon wheels you find in ordinary textbooks (ordering by size of the amino acid and position within the chain as well). You can have a look for yourself here in her 1984 article A unifying concept for the amino acid code in Bulletin of Mathematical Biology.

DISCLAIMER: I do not claim that I know the answer to this question for certain nor can I. However, I cannot find official publications earlier than Swanson's 1984 paper showing a circular representation of the amino acid code.


What are the genus and species name of different breeds of dog? Can you refer me to a good source containing the genus and species name of different breeds of dogs?

All the different breeds of dogs - from Irish setters to greyhounds - are all part of the same species, canis lupus familiaris. The common, domesticated dog is actually a subspecies of the grey wolf. The different breeds do have different genetic characteristics (just as humans have, say, different eye or hair colors), but they're a all one and the same. The different names for different breeds are not like the scientific classifications of organisms via domain, kingdom, etc. They're just our choices.

References:

http://www.vetinfo.com/scientific-name-for-dogs.html
https://en.wikipedia.org/wiki/Dog_breed#Description
https://en.wikipedia.org/wiki/Subspecies_of_Canis_lupus
http://www.choosing-a-dog-made-easy.com/dog-types.html


Formation of splint bones in ungulates I do know that the splint bones are vestigial (reduced non functional toes in this case) , in odd and even toed ungulates. Is there any evolutionary reason of why is it so?
What were the conditions that lead to it?

One easy way to make an animal faster (especially if it is larger than a housecat), is to make the ends of the limbs lighter, the more mass there is near the end of a limb the more energy it takes to move it and the slower you can swing it, that translates into moving slower because you cannot get the limb back into position for the next step fast enough.

Because of this reduction in the mass and number of toes in lower limb is an adaptation we see over and over again in animals focusing on running speed. We see it in dinosaurs, we see it in ungulates and artiodactyls. We see five toes reduced to three then eventually one toe, or sometimes we see a reduction from four toes to two paired toes instead.

Source


Aquaporin and the exclusion of $H^+$ As I read in my textbook, aquaporins exclude $H^+$ when absorbing water, but where does this $H^+$ come from? Additionally, is $H_3O^+$ a liquid that looks like regular water?

It doesn't matter where the $H^+$ comes from in the context of this information. The textbook is just saying that the aquaporin is permeable to $H_2O$ but not to $H_3O^+$ (nor, presumably, to $OH^-$).

In any aqueous solution, especially in the presence of acids, some of the molecules will be $H_3O^+$. The pH tells you how many. It doesn't really make sense to think about what a solution of $H_3O^+$ would look like.


What goes wrong in the immune system that leads to autoimmune diseases As far as I understood so far, B and T cells are produced in the bone marrow, and during their maturing process in the bone marrow or Thymus, the are "programmed" to react to certain proteins. It is like giving them a particular key.

As I also understood, these "keys" are entirely created by random. Which means, that also "keys" are generated that match cells of the "host body."  Hence, if released into the bloodstream/lymph system, those B and T cells would attack the cells of the "host body."

As I understood further, there is a kind of a "security system" which checks if B and T cells are produced that would attack cells of the "host body." This security system would intervene and destroy those B and T cells before they are released into the bloodstream/lymph system.

As read lately - and I am not sure if I did understand this correctly - it is also possible, that B and T cells could also react to other cells even if the key doesn't match perfectly.

Now my questions.
Firstly, being an SW engineer interested in this topic is my understanding above correct?

Secondly, is it correct to say that autoimmune diseases are mainly caused by the following two points:
1. the "security system" in the bone marrow / Thymus failed, and therefore "bad" B and T cells were released into the bloodstream/lymph system
2. B and T cells react to other cells, even if the "key" does not match perfectly.

Your understanding of the process is basically correct. There are of course a lot more details to it, but that wouldn't be in the scope of the question. Do note that only T cells mature in the thymus (that's where the T comes from ^^), whereas B cells mature in lymph nodes and the spleen.

As for why autoimmunity occurs you also understood the basics, however the devil is in the details: wikipedia does have a much longer list of mechanistically different causes. While its often sufficient to explain immune recognition using 'keys' (T cell receptor / B cell receptor = antibody) and their respective 'locks' (peptides bound to MHC / antigens), the exact process of immune cell activation becomes important in autoimmunity, where cells are wrongly activated. This means that there are many possible points at which the 'security system' of the immune cell maturation can (or rather has to) fail to allow autoimmunity.

As for the cross-reactivity of cells: the difference between the binding of B cells (via antibody/B cell receptor to protein surfaces) and T cells (via T cell receptor to peptide sequences) means that in general T cells are much more likely to show cross reactivity - just because the possibility space of a 10-12aa peptide is much smaller than that of a protein surface (even though the probability is still very low).

Additionally - as stated in the comments to your question - both the immune activation pathway and the issue of cross reactivity, while principally understood, are not 'completely solved'. The immune system is insanely complex just by itself and the addition of interactions with both almost all human proteins AND proteins any kind of pathogen, mean that it will take quite a lot of time until researchers can figure out all the weird quirks caused by the 'wrong' combinations.


Why are women more susceptible to radiation? The answer to this question on the Space.SE indicates women are more susceptible to radiation in space than men.

Why is this the case? Is it merely that women have less muscle mass (which being more dense than fat) and therefore may receive a greater dose when exposed?

It's actually because of the greater risk "from breast, ovarian, and uterine cancers" (article).  There's a more scientific write-up here, and while I don't have access the abstract implies that a more rigorous update of the exposure criteria upheld sex differences.  From a more terrestrial perspective, The Nuclear Information and Resource Service (nirs.org) has this rather incensed piece on the issue.  They cite a 2006 NAS report which

  finds that harm to women (cancer) is 50% higher than the comparable harm to men from radiation doses that fall within the legal limit to the public over a lifetime.

Basically, it looks like females are more likely to get cancer from radiation, and once they do, those cancers are more likely to cause more harm.  According to the executive summary of NASA's 2014 in-depth report:

  [A] 45-year-old man has a 344-day limit versus a 187-day limit for a 45-year-old woman, due to radiation exposures on the space station that would be typical at the time of solar maximum.

The effect of body size, however, could be the opposite.  Taller women get more cancer, with that study showing a 16% increase in incidence for every 10cm (4in) height increase.  That increase, however, is among certain types, such as melanomas, and not the above-mentioned "breast, ovarian, and uterine cancers."  Males, being taller, could therefore get more cancer overall; it turns out males usually die more from most cancers, just not (obviously) "breast, ovarian, and uterine cancers."


Fisher's Geometric Model for Dummies Fisher's geometric model is still today one of the most important and fundamental model in evolutionary biology but it seems to me that most student in evolutionary biology don't really understand it (and I am one of these students). Such standard models are often found on wikipedia but in this case the wikipedia article (here) offers nothing more than a simple analogy.

According to Orr 2005:

  Fisher's geometric model shows that the probability $P_a(x)$ that a random mutation of a given phenotypic size, $r$, is favorable is $1-\Phi(x)$, where $\Phi$ is the cumulative distribution function of a standard normal random variable is a standardized mutational size, $x=r\frac{\sqrt{n}}{2z}$, where $n$ is the number of characters and $z$ the distance to the optimum.

Can you please explain what the Fisher's geometric model and the math behind it (how are these functions calculated)?

Fishers Geometric Model (FGM) is a theoretical prediction about the adaptation process in traits. There are a number of things to establish before attempting comprehend FGM. Firstly, shifts in an adaptive landscape, in natural scenarios, are generally quite small. Because populations have been evolving for such a long time and the small shifts in adaptive peaks it means that most populations should be near or on a local fitness optimum within the relevant landscape. The adaptive landscape comes from S. Wright, discussed in the Orr paper, where he spoke of a field of possible gene combinations" each with a fitness value, some combinations are fitter than others. Adaptive peaks represent the fittest combinations of all traits.

We can picture all of this using a single trait:

Here there is a local optimum (which is also global, Fisher assumed that adaptive landscapes are less rugged than Sewall Wright and had only one optimum) for the trait. The population starts at point A (the red ball), just off the adaptive peak for the initial fitness distribution (blue trace). Then selection alters (red trace), initiating a new bout of adaptation, making the population (green ball) further from the optimum.

From here lets imagine this is two seperate populations, the green population (A) wants to move along the red line to the highest point, the red population (B) along the blue line also for its own optimum.

If a mutation which has a very small effect arises then there is 50% probability in both populations that it will improve fitness (assuming no neutral mutation) because it will either be recessive or deleterious. This value is shown in box 2 figure 1 of the Orr paper.

Now if a large effect mutation was to arise in then there is less chance of it being beneficial for population B than for population A, this is because B is closer to its phenotypic optimum so a large effect mutation is likely to "overshoot" the optimum. (The black line illustrates where either population would end up after a large effect mutation in the direction of the adaptive peak). You can see this mutation would put population A very close to its peak (the red line) and population B would have a reduced fitness. This is summed up nicely in the opening to the Orr paper.

  "Precise adaptation is possible only if organisms can come to fit their environments by many minute adjustments"

So, descriptively, this is why we see a reduced probability of large effect beneficial mutations as we approach an optimum; we expect most bouts of adaptation to be due to small shifts in adaptive landscape and populations to start bouts near to the former adaptive peak.

The FGM expands this out beyond one trait (or, as Kauffman and Gillespie did, the sequence - with the latter seemingly being more successful than the former). As shown in figure 1 of the Orr paper,

This is a highly multidimensional space, with one dimension per trait, therefore more complex organisms by definition will have more complex spaces. The centre of this sphere is the phenotypic optimum, and each layer represents and adaptive movement, or substitution of the wild type as in the Maynard-Smith adaptive walks system. The red line shows the movement made by the population through this sphere.

And now for some math. (Refer to box two in the Orr paper). $P_a (\chi)$ is the probability that a mutation (of effect size $r$) is favourable. Thinking about what I discuss above, that is, $P_a (\chi)$ is the probability that a mutation will increase fitness, which must therefore be a product of the landscape complexity (the number of characters affecting the fitness), the distance from the population to the optimum, and the size of the effect. $\chi$ is the standardized mutation size, which accounts for the distance to optima, as $z$, the number of characters affecting fitness as $n$, and the effect size $r$. This means that $\chi$ = $r \sqrt{n} /2z$: therefore an increase in the distance to the phenotypic optimum ($z$) reduces the value of $\chi$ (thus increasing the probability that a mutation has a beneficial effect), whereas increases in $r$ or $n$ will decrease the probability that the mutation is beneficial (i.e. large effect mutations and high complexity). In the context of the above example, both populations have an $n$ of 1, and the values of $z$ vary - this means population A can tolerate a larger value of $r$, or in other words, population A is more able to make adaptive substitutions because it is further from peak fitness, thus more tolerant to large effects, than population B.

Difference between $r$ and $\chi$: $r$ is the raw value of effect size of a mutation, whereas $\chi$ is the standardized effect size. Assuming equal effect sizes the relative effect of mutations will depend on the number of traits affecting fitness (see the diagrams below), thus we have to correct for this.

How does complexity affect the probability of beneficial mutations? Look at the following diagram.

Each point represents a possible combination of traits when we have three traits affecting fitness, each with two possible incarnations (A or a [most fit and least fit respectively]). The outer green ring has one possible occupying combination (aaa) which is the least fit - it's the furthest from the optimal combination, the red point. On the green ring the probablity of increasing fitness with a mutation is 3/3 (because there are 3 possible mutations all of which increase fitness). Note, assume all changes are equal effect. If we change one trait to the A version we can have 3 possible outcomes (Aaa, aAa, aaA) which occupy the yellow ring. From the yellow ring a further single mutation has four possible outcomes, of which 3 can increase fitness so the probability of improving fitness with a mutation is reduced (3/4). In the blue ring there is a 1/4 probability of increasing fitness. Jumping to the red point, where all traits are A, every possible mutation will reduce fitness (0/3).

Bearing this in mind, lets change n (the number of traits affecting fitness) from 3 to 4. The least fit starts in the red ring (aaaa), from here there is a 4/4 probability of increased fitness via mutation. From the green ring there is a 6/7 probability. From the yellow ring there is a 4/8 probability of increasing fitness, and from the blue a 1/7 chance. Compare this to when n=3, from the blue ring there was a 1/4 chance, when n=4 it is 1/7 - there are more possible combinations and still only one fittest combination

Put another way; if we consider it in terms of single point mutations in a sequence, a mutation which affects 1 trait affecting fitness (n=1) then the probability it will increase fitness is drawn from the distribution of probable fitness effects. If the point mutation affects 5 traits then the effect is drawn from the distribution 5 times, and because we assume most mutations are deleterious and beneficial ones are relatively constrained to being small, there is a greater probability of reducing fitness when n>1.


The Semi-Conservative Model of DNA Replication: Question My Campbell's Biology textbook contains the following diagram related to the semi-conservative model of DNA replication proposed by Watson and Crick. I have highlighted where my confusion arises in red:

So, I understand what goes on in the first replication--that's pretty much straightforward. However, what I don't understand is why in the second replication, the light blue strand isn't paired with a dark blue strand. After all, aren't the light blue strand and dark blue strand complementary, per the results of the first replication?

After the light blue and dark blue DNA strands separate to serve as templates in Replication #2, why don't we see two dark+light double-helices?

I believe the reason you are having trouble understanding the concept is due to a poor usage of colors in the diagram. Don't focus on the colors, but on the concept. It's the same for both replication events. Each strand of a double helix is used as a template to make a new complimentary strand, giving rise to two new DNA helices from the original. In each new double helix, one strand should match that of the double helix it came from before, as it was the template and is the same strand. While the other strand, the complimentary strand, has been newly synthesized to match the complimentary strand. In this diagram, every newly synthesized strand is shown in light blue.

Start by looking at the first double-helix of DNA (navy blue). During replication, the DNA is unwound and each navy strand is used as a template to create the newly synthesized (complimentary) strand, which is shown in light blue. In this first all navy double helix, you have two navy strands that are each used as a template strand and new complimentary strands (light blue) are synthesized to match . This produces the second two helices (navy and light blue). They each have one strand from the original helix (navy), and one new strand (light blue).

The process is exactly the same for the second replication event, only, a new color was not introduced to show a newly synthesized strand, so one cannot differentiate between the original (template) strand and the new complimentary strand. Both are pictured as light blue.

For the final replication event, only focus on the top navy and light blue helix first. Just as before, the two strands are separated from each other and are both used as templates to create a new strand. The navy blue strand is used as a template for a new light blue strand to be transcribed. This produces the top-most helix, where the original strand is shown as navy and the newly transcribed (complimentary) strand is light blue.

Just as the navy strand was a template, the light blue strand from the bicolored helix is used as a template strand as well to create the second all light blue helix. This light blue template strand is used to synthesize a new light blue strand, creating the all light blue helix. One of the strands is the original light blue one from the navy and light blue helix, while the other strand is the newly synthesized one.

It might've been easier if they had used a different color for the final round of replication, like orange. Then to show the newly synthesized strands in the final round, the 1st and 4th double helix would consist of a navy (original) strand and an orange (newly synthesized) strand. The second and third double helices would then have each had a light blue (original) strand and an orange (newly synthesized) strand. This would have made it easier to understand where each strand originally came from.


what do I need to use for protein protein interaction network I would like to know what i should use to be able to build a PPI network. I have seen different structure for different techniques. for example sometimes the input look like this , each protein with another protein and a relationship

YAL011W YBR231C 0.804967
YAL011W YDR190C 0.790977
YAL011W YDR334W 0.840367
YAL011W YDR485C 0.815874
YAL011W YJL081C 0.574536

or sometimes I only see this

YAL011W YBR231C
YAL011W YDR190C
YAL011W YDR334W
YAL011W YDR485C
YAL011W YJL081C

what do I need to make a network ? and which structures normally used for making these networks.

If you are asking solely about data structure, the two data formats that you have given are essentially the same. Each row represents a PPI, so in a network a line (edge) will link the proteins (nodes) given in columns one and two. Column three is an edge score, but it can indicate a few things,  confidence in the interaction or strength of the interaction. Your network will for a single central node with 5 nodes linked to it in a wheel shape.

PPI networks may also be represented in Proteomics Standards Initiative Molecular Interaction XML Format. This provides a controlled vocabulary for programmatic access to data.

The choice of data structure, there are many, is yours but simple formats (as above) are often sufficient. It is important to be mindful of the meaning of the network, are the PPIs directional? Do you have estimates of interaction (edge) confidence? Do you have estimates of interaction (edge) strength?

Cytoscape will allow you to visualise a protein-protein interaction network (PPI) such as the two that you have given. The Bioconductor project provides a number of options for the visualisation and analysis of PPI networks in R.

If you want to create or build a PPI network from a single protein or list of proteins then Cytoscape, and possibly plugins such as Genemania, can also do that.

String is also useful for building PPI networks. The developers have focussed on a wide-range of species and their data export options will allow you to see the same network in a variety of data formats.


Evolution of bee hives How do the instinct to create a hive appeared in bees? Is there some evidence of
"intermediate" hives? With this questions i mean all the factors necessary to build a hive, including the social structure, the producing of beeswax and architecture.

I'm assuming you mean the distinct architecture and regular hexagonal shapes in bee honeycombs?

In fact, Charles Darwin spent a good bit of time with honeycombs.

First of all bees and wasps have a common progenitor and wasps also build combs and nests, albeit of paper/celluose as opposed to wax.  He was interested in how the perfect hexagonal lattice formed in the wax.

  Darwin tried three different experiments with bees’ cells at Down that he reported in Origin. In one, he put a thick block of wax into the hive. ‘The bees instantly began to excavate minute circular pits in it: and as they deepened these little pits, they made them wider and wider until they were converted into shallow basins, appearing to the eye perfectly true or parts of a sphere, and of about the diameter of a cell. It was most interesting to me to observe that wherever several bees had begun to excavate these basins near together, they had begun their work at such a distance from each other, that by the time the basins had acquired the above stated width (i.e. about the width of an ordinary cell), and were in depth about one sixth of the diameter of the sphere of which they formed a part, the rims of the basins intersected or broke into each other. As soon as this occurred, the bees ceased to excavate, and began to build up flat walls of wax on the lines of intersection between the basins, so that each hexagonal prism was built upon the festooned edge of a smooth basin, instead of on the straight edges of a three-sided pyramid as in the case of ordinary cells.’ (Origin, p. 223.) The cells were built up in a hexagonal shape when their bases intersected with those of other cells; but the pyramidal bases were apparently not built, since there was no pressure to accommodate cells on the other side of the wax, which was a thick block.

This seems to have a built in burrowing behavior in how the lattice forms that eventually turns into hexagonal shapes.

BTW this topic is very similar to the evolution of spider webs, which is also fascinating.


Difference between haemocoel and coelom I am looking for an embryological perspective on the following question.
I know about coelom derivation, but I want to know how haemocoel is derived and how it is fundamentally different from coelom.
True coelom is formed by the cavity formed in mesoderm. It is lined by mesothelium on both sides, whereas on the other side pseudo coelom is cavity which is lined by endothelium and mesothelium. However, the formation of haemocoel is not clear to me.
I have looked for in many books, but I have not been able to find an embryological perspective and what happens to coelom in which haemocoel is present.

I was looking for the same thing and i found the answer in the anatomy of molluscs
you can clearly see that coelom is different from haemocoel and coelom is greatly reduced.
Haemocoel is a pseudocoelom it is a body cavity but not lined with mesoderm at all sides


Would modifying the human microbiome to digest cellulose be worth it? I've read that cellulose has a lot of calories that go unused. I was wondering how practical it would be to incorporate a bacteria capable of suggesting cellulose into the human gut.

I would say that it is worth it if a human could gain a substantial amount of calories by digesting cellulose in a "normal" diet. To compute the amount of calories, I would like estimates for how fast bacteria can process the cellulose (like half life per billion bacteria) and how efficient the process would be.

Then given the average duration of the digestive process and a reasonable bacteria population, estimates could be made on how much energy could be gained by digesting the cellulose in an average diet.

You really need to understand how cellulase would effect metabolic systemic homeostasis before anyone can answer that. It's an interesting question. At first glance, one could consider that cellulase would allow disproportionate glucose intake, ultimately making fat a smaller % part of the diet. If unchecked, this could lead to a reverse Randal effect inhibiting fatty acid metabolism thus altering adipokine synthesis leading to a range of negative, if not, species detrimental effects such as reduced capacity for reproduction (as an example between altered biosynthesis and crosstalk between leptin and estrogen). This may have presented a problem for early humans, because in essence, cellulose could have acted as the very first mcdonalds convienience if we were capable of digesting it. I'm sure I'm missing many complications that would have occurred if early humans had this capacity, but it's a nice thought experiment.

And regarding the mathematical induction, forget about it, you can't induce a conclusion on potential alterations within the mammalian digestive system from only the enzyme kinetics of cellulase found in bacteria.


Research from the early molecular genetics era that supported protein as the primary carrier of genetic information? I can't seem to find anything on my own. Surely there were experiments performed (possibly using bacteriophages) that managed to come to this conclusion?

Specifically I'm interested in anything pre-Hershey/Chase.

It’s difficult to be convincing with a negative answer, but I venture that the answer to your question is that the idea that protein was the genetic material was not supported by any experiments, but was a supposition based on the conventional wisdom that proteins were more complex and therefore more suited to the job.

I suggest that you should be thinking earlier than bacteriophage and Hershey and Chase. Bacteriophages only came into genetic research after the war, and the Hershey/Chase experiment (1952) was only a rigorous confirmation of the conclusion of Avery et al. in 1944 (mentioned in this Scitable article). The system that Avery et al. used (bacterial transformation) went back to Griffiths in 1928 and must have been the first that allowed any sort of experimentation in this area. And I think it was more a question of working out what was happening than devising an experiment to distinguish between protein and DNA as the genetic material.

To my mind this illustrates something about how science progresses. It is often dependent on advances in technology and changes in the conceptual framework in which scientists work. (Sometimes — e.g. Mitchell’s Hypothesis — it needs the experimental results to change that conceptual framework.) Coming back to the Hershey/Chase experiment, this was performed when the balance of scientific thought had already changed to DNA as the genetic material.

Footnote: It’s earlier than you think

I generated the Google ngram below to put the term you use, ‘molecular genetics’ into historical perspective.

This shows that the term ‘molecular genetics’ was hardly in use at the time of the Hershey–Chase experiment and Watson and Crick’s postulate of the structure of DNA in the early 1950s. I think that this reflects the fact that the concept was not current. The more popular term, ‘molecular biology’ gained currency on the basis of the structural work on DNA and proteins, and the name of the journal in which much of the work was published (Journal of Molecular Biology). The question is assuming a state of science that did not actually exist before the 1950s.


How to design an experiment with scent triggered memory recall in humans? I've recently learned that scents can trigger memory recall in humans, and am thinking about setting up an experiment where I would attempt to induce memory recall through exposure to scents.

In order to help reduce the amount of experimentation required to actually trigger recall, I'm interested in - What kinds or qualities of scents have been demonstrated to trigger memory recall in humans? Are they pleasant smells/unpleasant,  sharp or subtle?

Is there any information about how long of an exposure is needed to trigger such recall? Is it 2 seconds, 15 seconds, an hour?

Scents can make memory recalls. We experience this very often, like when we repeatedly smell a good perfume in ,say a shopping mall , and when some person uses it too, we recall the memory of the shopping mall. This hqppens especially when the smell is associated with a very good or very bad incident.

For an experiment, you can expose yourself or someone to a particular smell ,either very good or very bad at any one time, like during examination or holidays for a couple of times. Next when the person again smells the scent he/she will be reminded of the previous exposure.

As regards to how long the exposure is required to trigger recall,it depends upon how strong the smell is (subtle smell takes ponger time) , how good/bad the memory is (very good or very bad memories will be recalled faster) and ofcourse on the memory associativity power of the person.


Central of Dogma? reverse transcriptase says No I know what a reverse transcriptase is but I'm not sure why it is suggesting that the central dogma may be wrong -- RNA first then DNA instead of the well-known sequence of DNA -> RNA -> protein

Go to wikipedia and look reverse transcriptase. All your questions will be answered. But to answer your question, reverse transcriptase is an enzyme that uses RNA molecules as a template to make a DNA version of said RNA. ie the flow of information from DNA to RNA is reversed.

The central dogma... is a terrible name. It was an idea state in the 1950s that information flows one way from DNA to RNA to protein. The use of the word dogma is an ill choice to use. Because science does learn new things. And given that DNA was only just discovered in the 1950s....ie the same decade... the word dogma is a bad idea. SHould have waited a few more decades first

Anyhow... the discovery of reverse transcriptase allow information to flow back from RNA to DNA. The discovery of siRNA.. mean RNA can control DNA. The discovery of prions... lead to current work now where pre-existing proteins can be templates for the folding of newly synthesised protein. DNA methylation allows epigenetic inheritance. Ie changes of certain protein levels (say during starvation) in your body can leave inheritable marks on your DNA (which will then affect the behavior of those gene in your children).

The central dogma now (if it still is used) has a lot more lines leading up and down the chain.


Why are some bodily fluids more of an infection risk than others? Whilst on a recent refresher course it was highlighted that when considering risk of exposure to infection from bodily fluids we should be aware of two distinct risk levels:

High Risk:

Blood
Semen
Vaginal Secretions
Diarrhea

Low Risk:

Saliva
Vomit
Urine
CSF (Cerebrospinal fluid)

Why is it that some bodily fluids are a greater infection risk than others?  Is it related to the fluids themselves or the species of pathogen that are located within them?

This is just about where the pathogens can be found that are dangerous to people.

Vomit is highly acidic and less accommodating to microbe growth. Similarly saliva has many immune components in it as well as digestive enzymes that keep most microorganisms down.

Urine and CSF are actually quite sterile as they come from environments that are highly filtered - the kidney is an osmotic processor that essentially is a molecular filter and does not allow cells to pass, the spine is highly insulated from the blood and other direct exposure to microorganisms.

Compare that with the 'dangerous' list and you have organs that are open to human pathogens.  Venerial disease like HPV is so common that what - about 1 in 5 people under a certain age carry it.  That is a pretty high expectation of a biohazard.  most infections and viruses are blood bourne - influenza, cold, as well as any bacterial infections.

Feces is always a dangerous thing to handle as the digestive tract is rich in nutrients and essentially directly open to external bacteria and fungi.  (and its not acidified like the stomach).  Also parasites like tape worms and other multicelled animals! yum!

Diarrhea is often caused by an infection of some sort, so its just more likely a hazard, but feces is always a place where you might find a pathogen.

This is not to say that the 'safe' list is totally safe.  Its just less likely to bear disease causing agents.


How do cold conditions help organ transplants? Body organs are kept cold in-between explanting them from the donor and implanting them in the new host. How do these cold conditions help organs to stay viable while they haven't fresh blood, energy and oxygen supply?

This paper actually goes into the whole history of organ transplants.

In short it seems to have the following effects:

preservation - usually with a specific solution to help.
slows down extracorporeal ischaemic damage
slows down hypoxic damage
slows down the metabolism (energy consumption) and thus the need for oxygen that blood provides.

Remember that the cooling doesn't allow the organ to live indefinitely, and may only work for a few short hours depending on the organ.

I highly recommend reading the paper if you'd like to know more about organ transplant. They went into great detail about the past and present and the abstract also says they discuss new techniques about to be don't in clinical trials.


Star-like organism seen in microscope I found this strange star-like thing while observing a slide of onion root somatic cells. I don't know that it is; I even doubt if it is an organism. It has conical arms directed  radially outwards all over it's body. It wasn't moving. If it was indeed living,  maybe I had killed it while flaming the slide. Anyway, I am interested in knowing more about this  unexpected guest of mine. Can anyone tell me what it is ?

It may be a stellate trichome from a plant.

You can find other ones by taking swabs from the onion and nearby plants.

cool images here

wiki info about trichomes


Protein purification methods Which of the following methods would yield the most purified protein fraction?

A. Salt precipitation

B. Charge separation

C. Affinity purification

The first one is the most commonly used, is it the best ?

In my protein purification experience, affinity purification is the most selective purification strategy. This makes sense because affinity tends to be very specific, and only one protein should in theory be preferentially separated by the column. Think how specific the antibody-antigen interaction is compared to the differences in, say, charge between proteins (which could be very slight). When I was purifying proteins I would pretty much always start with affinity purification. If more purity was desired after the affinity purification step, I could perform salt precipitation or charge separation on the affinity-purified sample, which had already been cleared of major contaminants/nuisance proteins by affinity purification.


How do neurons form new connections in brain plasticity? I've been reading about brain plasticity and how the brain can "rewire" itself.

One of the things that is not clear to me - how neurons can establish new connections. Does this rewiring mean that neurons can "disconnect" from other neurons to reuse existing dendrites?  Or do neurons grow new dendrites to make these new connections, adding to existing ones?

Thank you for your input!

I haven't read anything particularly about dendrites being reshaped, though I would expect them to be as flexible as other parts of the cells.

The more commonly discussed topic (in my literary experience) is reshaping of the axon's branches before forming synaptic terminals. These branches are not fixed even in adults - neurons can grow new and retract old branches, attaching (synapsing) to other cells in new places and removing old connections (see Wikipedia: Synaptogenesis).

Additionally to this actual change in the number of synapses, individual synapses can be regulated in their signal strength by adjusting the number of neurotransmitter receptors in the postsynaptic membrane (Gerrow&Triller, 2010, also see Wikipedia: Synaptic plasticity)


Enzymes and Digestion If biological enzymes (protease,amylase,lipase etc.) just speed up the reaction (in the digestion process), then what actually digests the food?? (I'm a secondary student)

I suspect that the question reveals an incomplete understanding of enzymic catalysis and could more generally be rephrased as "If enzymes just speed up biological reactions, what makes the reactions proceed in the first place." The simple answer to this is the fact that the thermodynamics of the reaction are favourable, i.e. the reaction involves a negative change in (Gibbs) free energy.

So what is stopping the reaction proceeding at a reasonable rate without catalysis? The fact that the thermodynamic path of reactions involves an activated state with a higher free energy. In most cases this is sufficiently large that it acts as a barrier to spontaneous reaction. You can get over the activation barrier by e.g. supplying heat (i.e. supplying activation energy) but this is not possible in living organisms. Enzymes act by lowering the activation energy (energy barrier) or raising the ground state (which in effect decreases the activation energy).

One should realize that "just speeding up the reaction" is generally increasing the reaction rate from being negligible to biologically sufficient. So what makes the reaction go is a combination of the reactants being there with a favourable chemistry and the enzyme being there in the right place to deal with them.

If you are unfamiliar with this basic reaction chemistry see:

http://www.ncbi.nlm.nih.gov/books/NBK22384/#A1100

and the image below from Wikipedia.


How do humans perceive time? We can see length, and other physical quantities. We can perceive through our other senses like (temperature through thermoreceptors, weight through pressure receptors etc.). But how do we "sense" time?

The nature of time has been discussed for millenia. We don't know exactly why or where time perception exists, but we do have some information on how it is perceived.

The circadian rhythm is basically in place to help us sleep, wake and perform tasks in a 24 hour cycle of light. Robbed of light, and the melatonin it's absence produces, the rhythm shifts considerably.

Vision is a powerful cue for the passage of time. Bees have an extremely sophisticated ability to predict the sun's location at a given moment (they can count the moments). While I doubt the same is true for humans, our eyes give us a great deal of information about the passage of time: the time in a 24 hour period (the position of the sun, moon, stars, shadows, etc), and the time in a year, the time in a lifetime. Witnessing the passage of time, according to physicist Paul Davies, we observe how the “later states of the world differ from earlier states that we still remember.”

Besides the important input from our eyes and memories, we also have internal timekeepers.  A study decades ago on short order cooks (I can't seem to find it) found that an experienced cook can keep internal time to the second, and can keep multiple "stopwatches" going in his head: the scrambled eggs, the toast, the pancakes, the grilled cheese sandwiches all take a certain amount of time, and short order cooks can tell when that time has passed with extraordinary precision.

The fact that the fluids flow at different rates tells us that we perceive time differently under different circumstances. Time perception is surprisingly prone to measurable distortions and illusions.

  The importance of our temporal experiences for daily living is strikingly documented in individual neurological cases where patients report of an accelerated progression of time and, consequently, have troubles in adequately interacting with the environment, i.e. driving a car. Psychological research has shown that cognitive functions such as attention, working memory as well as long-term memory determine our temporal judgements. Moreover, drive states, moods and emotions, as well as factors of personality influence duration estimates. For example, time intervals are judged to be longer when we pay more attention to time and when the load of varying experiences stored in memory is higher. Our subjective well-being also strongly influences how time is experienced. Time speeds up when we are involved in pleasant activities, but it drags during periods of boredom. Thus, our sense of time is a function of the intricate interplay between specific cognitive functions and of our momentary mood states.[1]

Where exactly time is perceived by the brain is unknown, but several areas keep appearing, most prominently, the cerebellum, the right posterior parietal cortex, the right prefrontal cortex, as well as fronto-striatal circuits. All have been implicated as the neural substrates of a potential timekeeping mechanism. The inner experience of time[1] gives a broad overview. The conclusion is worth reading.

To further support that the where is not known, consider the following:

  Studies done in humans also support the hypothesis that striatum and its afferents are involved in interval timing. Recent fMRI data showed that timing network could involve cortico-striatal loops, including premotor and supplementary motor areas, frontal operculum and dorsolateral prefrontal cortex, and temporal and parietal cortices, as well as the putamen. Imaging studies in humans, lesion studies in humans and rodents, and drug studies in rodents all point towards a central role of the basal ganglia in interval timing. The anatomy of the basal ganglia suggests that information is proceeded through cortico-striato-thalamic loops. Severe deficiencies in reproducing temporal intervals were also found in Parkinson’s patients, therefore, further supporting the hypothesis of basal ganglia involvement in interval timing. There are also lesions data suggesting that the timing network is much widely distributed. Lesions of the nucleus basalis magnocellularis, a cholinergic nucleus in the basal forebrain with projections to the frontal cortex, induced a progressive, proportional, delay in peak time response (memory pattern). This effect is believed to be related to altered temporal memories [42,43] due to change in acetylcholine (ACh) level. Lesions of the frontal cortex produce similar memory patterns, whereas lesions of the hippocampus or fimbria fornix, a basal forebrain cholinergic nucleus with projections to the hippocampus, result in memory effects translated into an advance of the peak time response. These experimental findings undoubtedly support the hypothesis of a distributed interval timing neural network.[2]

For a fun but non-scientific look at time, the NYT has written an understandable article.[3]

The final answer is that no one knows for sure.

The Experience and Perception of Time
1 The inner experience of time
2 Why noise is useful in functional and neural mechanisms of interval timing?
3 Where Did the Time Go? Do Not Ask the Brain
 Time and the Brain: How Subjective Time Relates to Neural Time
Human time perception and its illusions


Identifying Promoters in Non-homologous Sequences within the Same Organism In this paper, the authors cloned a GPD promoter for use in driving a GFP gene from Lentinula edodes using a set of provided primers. The primers were derived from the following accession GQ457137.1 containing the GPD gene for this organism.
In fact, there are three accessions in GenBank containing gpd promoter sequences for Lentinula edodes, each of varied size and homology to the aforementioned sequence used in the paper.
I am working on defining a transformation protocol for Psilocybe cubensis (of which there are no published transformations) and I would like to design some primers as done in the paper above in order to clone the GPD promoter for this organism from its DNA; however, just as with L. edodes, there are multiple accessions of GPD in psilocybe cubensis: KM273235.1 and KT067727.1
In my case; however, there is no literature referencing either of these accessions and so I don't know which of these accession I could or should use to design my primers.
I have the following questions:

Why does the same promoter within the same organism have such varied sequences?
If the promoter sequence varies even within the same organism, the how can anyone extract the promoter with certainty since the organism may carry a different sequence for the promoter?
Generally, I'm trying to find the GPD promoter for P. cubensis (or any strong promoter) and clone it for use in my plasmid for transformation. I'm stuck as to how to go about finding a suitable candidate.

Thank you.

Why does the same promoter within the same organism have such varied sequences?

While there may be other reasons, the fact that the same species has several genes encoding GPD proteins is an indication that this enzymatic activity is important for different mechanisms, times or conditions. For example, I mentioned in a comment to one of your previous questions that the three GPD-encoding genes in budding yeast (TDH1, TDH2 and TDH3) are expressed during different growth phases. Therefore, although the proteins encoded by these genes might share both sequence homology and function, their promoter regions most likely will not. We even expect their promoters to be different, to allow for such differential expression. Put differently: if the three TDH promoters were all highly similar, we would expect them to also be active at the same times, effectively rendering the three genes redundant.
There is therefore no reason for assuming that promoters driving the expression of two different genes will share any homology, just because the encoded proteins happen to share function.

If the promoter sequence varies even within the same organism, the how can anyone extract the promoter with certainty since the organism may carry a different sequence for the promoter?

The only way of knowing exactly what region upstream of a gene that regulates it's expression (i.e., what functional elements that defines its promoter) is to characterize the promoter region. This is way beyond the scope of your work. What we tend to do in budding yeast when we clone an uncharacterized promoter, is to simply take 1000 bp upstream of a gene's start codon, and assume that this includes all elements necessary for proper regulation of the gene in question (e.g. possible transcription factor binding sites (TFBSs), transcriptional start site (TSS), etc). 1000 bp is a relatively safe length in budding yeast, since the distance between genes rarely exceeds this, and we tend to assume that promoter regions don't overlap neighboring genes' coding regions. But this might be different in your species. Also, if you know the location your gene's TSS, this would be a safer reference point than the start codon.

Generally, I'm trying to find the GPD promoter for P. cubensis (or any strong promoter) and clone it for use in my plasmid for transformation. I'm stuck as to how to go about finding a suitable candidate.

My guess is that the authors that cloned the GPD promoter from Lentinula edodes either already knew that this specific gene is highly expressed and therefore selected its promoter; alternatively they might have cloned all GPD promoter variants, and then simply published the one that they saw worked best.
If you don't have any information about the expression of the GPD-encoding genes from your species, any decision as to which promoter to choose will inevitably be more or less guesswork. It seems to me that the evolutionary distance between Lentinula edodes and Psilocybe cubensis is way too large to make any direct inferences. Nevertheless, with the lack of better options here is what I suggest:

Try to identify which of Psilocybe cubensis's GPD proteins is most similar (in terms of sequence homology) to the protein the authors chose for their Lentinula edodes GPD promoter. This might indicate that these are direct orthologs, and with a bit of luck may also share similar relative expression patterns and/or levels. You could also do a similar matching with the Tdh3 protein from budding yeast, since TDH3 is indeed a very strong promoter (article behind paywall, but easy to find elsewhere). If you still don't know which of the promoters to choose, proceed with both candidates and see which one works best (although that means doubled cost and effort).

Once you have identified your candidate GPD gene, you define an appropriate region upstream of your gene’s coding region as the promoter region. This can be arbitrarily picking 1000 bp, or the entire intergenic region, as @Cholpisit suggests.

Design your primers for cloning this region into your target vector, upstream of GFP.


Can anyone tell me what type of worm this is? I sure hope you can see this picture. Need to know what type of worm this is. Found one in July and one just now inching its way across my tiled floor. I live in Florida. It is one color all the way around, dark red.

I can't see the head clearly but based on

1: it is a big worm cruising around on land
and
2: you have never seen one before

I bet on this

From linked article.

  The flatworm (Platydemus manokwari) has few natural predators outside
  of New Guinea, and it likely will have no predators in the United
  States, Justine says. It gobbles up soil-dwelling invertebrates like
  snails, which could have a big impact on the environment.


Glycosidation and glycosylation I read somewhere that the function of Golgi bodies is glycosylation and glycosidation. What is the difference between the two? I searched google but it gives complex answers.

Glycosylation is a controlled process that involves a carbohydrate being attached to a hydroxyl or other functional group of another molecule. I think you meant to say glycation instead of glycosylation, and that is a random process that involves free sugars attaching to proteins.

https://www.neb.com/faqs/2015/04/10/what-is-the-difference-between-glycosylation-and-glycation


Is complete dominance actually a genotypic process? An example often stated for codominance is blood groups, where both alleles version of the protein is expressed and can be found in the cell membrane.

An example of incomplete dominance often given is of red and white flowered snapdragons giving pink flowered offspring because enzymes for both pigments are transcribed and translated and the mixing of these pigments gives the intermediate phenotype.

In both these examples both alleles are transcribed and translated.

In the text-book mendelian situation of a dominant and recessive allele are there actually a cellular mechanisms by which a 'dominant' allele silences the 'recessive' allele and inhibits it's translation, transcription or both? If so are there any well characterised examples?

Or are all alleles actually codominant at the transcription/protein level? e.g like in many recessive gentic diseases where both the mutant and the normal protein are present (cystic fibrosis, sickle cell anemia etc) but the activity of the normal protein gives the 'healthy' phenotype.

"Or are all alleles actually codominant at the transcription/protein level?"

Yes this is the right idea. Generally all alleles are transcribed independently (with some exceptions like in females where one X chromosome is inactivated). And the dominant and recessive phenotypes are in a sense extreme cases of codominance. The terms are used for describing phenotypes and depend on thresholds of activity. In the snapdragons example we can associate 2 functional enzymes EE with the red phenotype and white (lack of red pigment) associated with 2 nonfunctional enzymes ee. But one E is not enough to make the red pigment so we see some red pigment and a pink phenotype.

Now consider a yeast cell with 2 hexokinase genes (H). With two inactive proteins (h/h), the cell will grow slowly. Now let's say that H is a very efficient protein and that glucose transport into the cell is rate limiting so one active H has the same phenotype as having 2 H/H, so H/H is the same as H/h thus H is a dominant allele and h is recessive because one H is past the threshold of activity for fast growth on glucose. h is recessive because h/h genotype is needed to see the h phenotype. Hope that helps.


Elevated position effect on recovery times from upper respiratory infections at rest? In nursing school, they advice for people with upper respiratory infections to be in a slightly elevated position at the head region when sleeping.
My intuition of the reason is that the lymphatic drainage to the venous arch works better; gravity helps to drain the lymph to the venous system; not only the heart.
Bacterial infection of the pharynx occurs in a prolonged exposure of the concentrated lymph.

I got today exact information about exact positions to relieve the body most when sleeping:

5-10 % angle to relieve body most, while gravity helping to suck the lymph from the throat; can be helped with the hormone motilium (domperidone)
more than 10 % is for other conditions

Is there any studies about the effect of elevated sleeping position on the recovery time from the upper respiratory infection?

Physiology

My conjecture.
The slightly elevated position causes greater venous return (work against gravity by smooth musculature and thoracic pump).
Why this is happening this way is partially based on my question here about Fast standing and the heart's insufficient accommodation of the increased venous return.

where the venous return reacts first the change in the position from supine by shifting the VR1 to VR2.
The stroke volume increases initially to SV1 to SV2, while the end diastolic volume from EDV1 to EDV2.
The increased stroke volume cannot be maintained long time so the cardiac output shifts to the right from CO1 to CO2.
So the initial stroke volume SV1 is the same as SV3 (not in the picture).
However, the EDV has increased (EDV3 >> EDV1) which increases much the lymphatic drainage.
Lymphatic drainage is not dependent on the stroke volume.
Increased lymphatic drainage then again increases the circulation of lymph.
This then again supports the recovery from the upper respiratory infection where the fine regulation between

the thoracic pump,
respiratory pump, and
smooth musculature

determine the final effect of the body position on the recovery times.
The size of the thoracic cavity puts some limitations, for instance.

Cardiology

In some cases, the upper respiratory infection can cause myocarditis.
This will decrease the functioning of the heart and cause possible

premature atrial contraction, and/or
premature ventricular contraction.

Elevated position helps small arterioles of left ventricle supply preload.
Otherwise, ectopic beat can be heard or also called "epics beat" which is sign of the two previous conditions.

The nurse is educated to listen to the patient and ask for possible jolts and flips in the chest.
Elevating position in such a case can help because of better supply for preload in the left ventricle.

Pathophysiology

Upper respiratory infection is often acute respiratory infection (acute respiratory distress syndrome).
There is an increased permeability of the vessels.
The fluids and plasma proteins are going through alveoli.
Acute hyaline membranes are formed.
Cytokines play a big role in this process.
To maintain lymph retention, the result of increased venous return compensates.

These patients can breath normally in the sitting position.
There are also other reasons for the infection:

overweight - the greater intra-abdominal pressure $\to$ more liquid diffused into the lungs OR other organs are suppressed.
Big chest suppresses lungs such that the architecture can change.

Pharmacology

There are different drugs which effect is dependent on posture and position of the body.
Hypertension is a common disease which amount increases during ageing in population.
Let's take hypertensive drugs as a case study.
Peripherally acting sympathoplegic drugs are generally dependent on posture more than centrally acting ones.

In hypertension treatment, the peripheral acting sympatholegic drugs are used often in combination with diuretics.
Blood pressure can be under control when blood volume is 95% of normal, but much too high when blood volume is 105% of normal.
So this study should be considered with no hypertension and hypertension.

Sources

For Pharmacology, Basic and Clinical Pharmacology, 11th edition, Katzung et all.


How long will a vegetable live for after being harvested? I understand this might depend on the types of vegetables, but is there an average or studied specifics? Does it die immediately? Is there a way to precisely diagnose death in plants? If so, what are the conditions for it?

The short answer is that as long as the vegetable/fruit is fresh looking - i.e. the cells have not disintegrated - they will be respiring, many cells will be functioning quite normally, and the plant is still technically alive. In cases where the part of the plant we treat as a vegetable is a part intended for reproduction (e.g. a seed, or a tuber like a potato) the plant will keep growing.

The point at which the plant dies is not clearly defined like it is in animals, but generally if you can still eat it, it's still alive.

Death in plants is quite different from that in animals - we refer to it as senescence. The key difference is that it happens to tissues and organs which can die and separate from the organism. Individual leaves can die without the plant's health being affected. Once this has happened to all the parts, the organism is considered dead, but if there is any respiring tissue left, it's still alive.


Branch length in phylogenetic trees I know this is a very basic question, but it is not too clear to me what is the unit of measure of branch length in phylogenetic trees.
I have come to understand that it is usually expressed in number of substitutions/site/some unit of time.
What is that "some unit of time"? Generations?
Does it depend on what method of tree construction I am using (NJT, MP, ML)?

Thank you for your time.

When you estimate a phylogenetic tree, be it by likelihood, parsimony, or distance (like NJ), the lengths will be given in units of substitutions per site, with no time information. For example from here:

  The units of branch length are usually nucleotide substitutions per
  site – that is the number of changes or 'substitutions' divided by the
  length of the sequence (although they may be given as % change, i.e.,
  the number of changes per 100 nucleotide sites).

To transform these lengths into a time scale, further information is necessary. For example assuming that the molecular clock is valid, or instead using relaxed clock models that describe how each branch length l=r x t can be decomposed into a rate r and a time t. Since in many cases the rate is not constant along the tree (i.e. the clock is not valid), an inferred phylogenetic tree is not ultrametric (i.e. the sum of branch lengths from the leaves to their MRCA is not constant).

There are software packages, most notably BEAST, that explicitly model a strict or relaxed clock for you, and then can return the branch lengths in arbitrary time units. "Arbitrary" means that the numbers by themselves do not have special meaning, and will reflect your choice for instance of the prior. In which case they can represent year, million years or generations (http://beast.bio.ed.ac.uk/faq#Evolutionary_rates_and_time_scales).


Can silverfish climb and produce silk? I am equally disgusted and fascinated by the "Silverfish" (Lepisma saccharina) that we regularly find in our UK home. I tried searching for information on the internet but they seem poorly understood.

We only ever find them on the work surface in the kitchen when we switch on a light at night. They are presumably feeding off food residues - but they never seem to be found in the most obvious place, among the crumbs under the toaster.

When caught by the lights, they run for cover but never, ever climb. You would think them unable to climb at all but then how have they reached the work surface?

The other day there appeared a new twist; 2 "husks" hanging from silk threads between 2 containers, maybe 8cm from the surface. If they were caught and eaten by a spider, why did it take them to a rudimentary web when it (presumably) caught them on the surface? There was no sign of a spider around. The only other possibility I can see is that they somehow suspended THEMSELVES from the silk and this was a moulting behaviour. Thus they now CAN climb - and very well - and also produce silk!
Can anyone explain the mystery?

According to a paper by Walker et al. (2013) (found by googling "silverfish + silk", so not very hard to come by), silverfish can indeed produce silk. The paper also mentions that silverfish (Thysanura) and bristletails (Archaeognatha) use silk to transfer their sperm, and they also use it for "...tactile cue during courtship (Sturm, 1956)". This webpage (from NY State University) explains that male silverfish will deposit a spermatophore on a silk thread that is vertically suspended, and the spermatophore is later picked up by a female.

  Abstract:
  Silks are semi-crystalline solids in which protein chains are associated by intermolecular hydrogen bonding within ordered crystallites, and by entanglement within unordered regions. By varying the type of protein secondary structure within crystallites and the overall degree of molecular order within fibers, arthropods produce fibers with a variety of physical properties suited to many purposes. We characterized silk produced as a tactile stimulus during mating by the grey silverfish (Ctenolepisma longicaudata) using Fourier transform infrared spectroscopy, polarized Raman spectroscopy, gel electrophoresis and amino acid analysis. Fibers were proteinaceous-the main component being a 220 kDa protein-and were rich in Gln/Glu, Leu, and Lys. The protein structure present was predominantly random coil, with a lesser amount of beta-structure. Silk fibers could readily be solubilized in aqueous solutions of a mild chaotrope, sodium dodecyl sulfate, indicating protein chains were not cross-linked by disulfide or other covalent bonds. We conclude that entanglement is the major mechanism by which these silk proteins cohere into a solid material. We propose silks used as short-term tactile cues are subject to less stringent requirements for molecular order relative to other silks, allowing the random coil structure to be favored as an adaptation promoting maximal entanglement and adhesion.

The linked paper contains several references that should be useful if you want to look deeper into how silverfish use silk.

From what I've seen, they don't use silk for climbing. Silverfish can usually climb rough surfaces, but not smooth surfaces, which is why they are often found trapped in sinks, bathtubs etc.


Does a zygote express all genes? If a zygote has all the cytoplasmic determinants and all the specific transcription factors, does that mean that all genes in the genome are expressed?

The short answer is that no, a zygote doesn't express all genes simultaneously.

A zygote is like any other cell, in that it represents a distinct phenotype. And like any other cell, this phenotype is maintained by tight regulation of gene expression patterns. Check out this paper, for a nice description of the process of embryonic gene activation.

An important way in which the zygote differs from other cells, and which might be what drives your question, is that the zygote has the potential to differentiate into all the other cell types found in the body. This process of differentiation is also very tightly controlled in terms of gene expression.


Is telomere length a reliable measure of health/lifespan? Several companies are commercializing tests for telomere length such as this one here. I understand the basic mechanism for why telomeres shorten during DNA replication, but how good is the evidence that telomere length is a reliable indicator of healthspan/lifespan?

I disagree with Ctina.  So many factors go into determining loss rate, activity of telomerase, gene conversion or unequal exchange at chromosome ends, etc to ever say that length is a function of age.  There is far more variation between individuals and between cells within an individual than aging ever shows.  Here is one study:

Das B, Saini D, Seshadri M. Telomere length in human adults and high level natural background radiation. PLoS One. 2009 Dec 23;4(12):e8440.

however I've seen similar studies published elsewhere.  Telomere length as diagnostic for age is very poor at best.  Here's an article that gives a formula, but acknowledges the R2 is 0.04, which is useless: http://preview.ncbi.nlm.nih.gov/pubmed/18378481


How can the following data regarding flower phenotypes be explained? $$\begin{array}{c|c|c} \hline
\text{Parents} & F_1 & F_2\\ \hline
\text{Blue}\:\times \text{white} & \text{All blue} & \text{196 blue, 63 white} \\
\text{Blue}\:\times \text{pink} & \text{All blue} & \text{149 blue, 52 pink} \\
\text{Pink}\:\times \text{white} & \text{All blue} & \text{226 blue, 98 white,
77 pink} \\ \hline
\hline
\end{array}$$

From the above data, it is likely that this is more complex than simple Mendelian inheritance. My guess is that there is epistasis at play here, but I can’t figure out what is really happening. What are the phenotypes of the parents? What genetic loci are involved and which traits are dominant?

(I was thinking blue ($B$) was the dominant epistatic flower color allele—$BB$ or $Bb$ would give blue regardless of the other color allele, and $bb$ would allow the expression of color dictated by the other gene, which has pink ($P$) as its dominant allele. This doesn’t work, as seen in the third row.)

Can anyone lend their aid here?

(The data was taken from here, question 32 in the sample multiple choice.)

Because it seems you might be studying for a test, I will try to not answer directly but show the beginning of a chain of logic that might be more useful.

Let's review the very plain evidence. blue crossed against other colors leads to 3:1 ratios of blue:other. So it seems that blue is dominant in those cases. But when you cross those colors against each other, you get silly nonsense, a 3:1.2:1 ratio or something.

So, based on the linked answers, you are justified in thinking that genetics determines flower color, just because of the simple Mendelian pattern of the first 2 crosses. But things don't work for a straightforward monogenic trait in the pinkxwhite cross.

Let's now analyze your explanation. You say: "I was thinking blue (BB) was the dominant epistatic flower color allele—BB or Bb would give blue regardless of the other color allele, and bb would allow the expression of color dictated by the other gene..."

But look at the parents and offspring of the third cross. You say blue is dominant- but it is in fact expressed in the offspring of non-blue parents! So blue can't both be dominant and be the "controlling" epistatic gene. So now: let's consider some other similar possibilities:

1) blue = dominant and is controlled by another locus (recessive or dominant?)

2) blue = recessive and controls another locus (recessive or dominant?)

Do any of those hypotheses match the data?

A final observation: I find it always helps to add up all the combinations of phenotypes (if possible; for example the ratio of (blue+white) : pink, etc.) to see if anything looks like a familiar ratio.

I hope that is useful (and not too late to be helpful in studying, if that is your goal).


Do sulfate reducing bacteria help during the formation of the mineral dolomite in low temperature environments? Do sulfate reducing bacteria help during the formation of the mineral dolomite in low temperature environments?

Wikipedia says

  The actual role of bacteria in the low-temperature formation of
  dolomite remains to be demonstrated. The specific mechanism of
  dolomitization, involving sulfate-reducing bacteria, has not yet been
  demonstrated.

I wonder if someone has any updates on this. The reference given in the Wikipedia article is from 2000, from a source titled suspiciously "Journal of Conference Abstracts". Now it's 2013 and maybe someone else has found out something new.

The appropriate answer seems to be that bacteria help somewhat sometimes, maybe.

The evidence for this appears to be mixed, and appears to have been historically controversial.

One old-ish paper claims that bacteria (and more importantly, Archaea) are necessary at least under some conditions. Another somewhat later paper including some of the same authors claims to have found conditions for abiotic dolomite synthesis in the laboratory.

It appears that in terms of mechanisms, the relevant process may involve the proper state of magnesium ions, to which apparently microbes contribute via extracellular polysaccharides:

  Literature values for carboxyl group density are not available for all bacteria involved in dolomite formation, however Braissant et al. (2007) demonstrated disordered dolomite phases forming in the presence of the EPS of sulfate reducing bacteria with a carboxyl group density of ~10-3 moles g-1, similar to our values. We suggest that these carboxyl groups promote desolvation of the Mg ion, known to be a kinetic inhibitor in dolomite precipitation (Wright and Wacey, 2004), but are needed in a high density for nucleation to commence.

However, what process exactly is generating geological dolomites appears to be still a matter of debate, and also here, with some suggestive evidence in favor of microbes affecting that process.


Can females be recreated from male DNA? A chromosomal male is XY and a chromosomal female is XX. Now imagine if, one day, this world has only males - is it possible to "recreate" a female by using two X chromosomes from two different males?

Short answer
Technologically yes, but practically no, because there would be no surrogate mother available to bring the artificial XX zygote to term.

Background
Theoretically a cell with two male Xs can be generated, given that it is technically possible to shuttle single chromosomes between cells (Paulis, 2011).

However, assuming that in your future world oocytes are available from oocyte banks and sperm from sperm banks just like they are today, then the artificial combination of two Xs from male cells wouldn't be necessary in the first place, as regular IVF could be used.

Note that in both the chromosome transfer and IVF scenario, a female would still be necessary to implant the zygote. Until artificial wombs become available (they are not), it is impossible to generate females without females.

Reference
- Paulis, Methods Mol Biol (2011); 738: 57-67


Reasons for the HIV-1 epidemic So, the HIV-1 jump to humans occurred as early as the 1920s, but the AIDS epidemic didn't start until the early 1980s.

Some things I don't understand about this:

Why the delay?
What is needed for a successful zoonosis transmission in the first place?
If Bushmeat practices (eating meat from non-domesticated animals, in this case HIV-infected fruit bats) have been the same for centuries, why has HIV only really spread in THIS century?

if Bushmeat practices (eating meat from non-domesticated animals, in this case HIV-infected fruit bats) have been the same for centuries, why has HIV only really spread in THIS century?

We can't really rule out the existence of similar epidemics in the more distant past. In fact, almost certainly they were transmission events from bushmeat (not necessarily of the same virus). The thing that made 20th century different, as the other commenter rightly says, is the mobility. Previously, such transmissions would have lead to local epidemics which would have run their course - leaving super-controllers or individuals with immunity and killing everyone else. And since most of the African cultures haven't left a written record we wouldn't know about such isolated local epidemics. Not to mention that in the unlikely event of such records existing they would hardly be scientific - the disease would be most likely attributed to "evil spirits" or some other supernatural cause.

So, it is really the mobility, the public policies (mass vaccinations by colonial authorities that used the same syringes repeatedly) and the fact that we can retain information in a much better way which make the HIV epidemic different than the ones that almost certainly have happened in the more distant past.


Why would a snake follow a kayak? We live on the shore of Kentucky Lake in Middle Tennessee and kayak often.  A common snake here is the Northern watersnake.  Observing several of these snakes over a period of ten years, I am puzzled by their behaviour in several respects.

The snakes appear in March when it's still cold, much earlier than other snakes.  They repeatedly return to the dock or the pontoon boat even after being forcibly removed. The other snakes here are shy and usually don't return once frightened away.  This year, twice, Northern watersnakes have followed my kayak.  They change course towards me and speed up to keep up.

My basic question is, Why would a snake follow a kayak?

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

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

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

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


Why not self pollination for finding the genotype instead of test cross? Test cross can tell us what's the genotype of a plant is. But we can know that even by self pollinating the plant. For example,
If a garden pea plant has the genotype TT, then self pollinating them will give all tall plants.
If the plant has the genotype Tt, then self pollinating them will give both tall and dwarf plants in 3:1 ratio.
So we can simply say that by self pollination if all the plants are of same type then the parent plant is homozygous. If the plants are in ratio them the parent plant is heterozygous.

Because for test cross you need to phenotype far less progeny to be reasonably sure about parent genotype. Lets say you decide to phenotype N progeny. If the tested parent is heterozygote the random chance of you getting all N plants tall is (1/2)N for test cross and (3/4)N for self pollination.

So for example if you decide to phenotype N=8 progeny plants in case of self pollination (3/4)8=10% of your heterozygous parents will be wrongly assigned as homozygous which is error too high for almost anything serious. In case of test cross (1/2)8=0.4% of your heterozygous parents will be wrongly assigned as homozygous. To achieve the similar level of accuracy with self pollination you would have to phenotype N=19 or N=20 progeny plants.

The difference does not seem like much when testing one parrent but if you need to test many the costs will add up.


Bug Identification: what type of bug is this small ant-like bug? It's not an ant; do you know what it's called? Found some in the building different times.

Edit: Size is 4mm (length) x 1mm (height)

It looks like a ground beetle (family Carabidae)


What type of insect is this? Is it ant or something else? I was sitting under morning sunshine when I saw this:

At first, I thought that it is a common Indian black ant. But it was moving much faster. Also, it seemed to have 2 (or probably more) eyes (sorry, couldn't take images as 'twas too fast). The most surprising part was when it leapt over the chair WITH A WEB! (just like a spider). Also, its mandibles(?) are much bigger than an ant's. Is it some kind of hybrid of ant and spider. I recently read that in some caves new varieties of spiders, which look like beetles (or maybe opposite) have been discovered. Is this related to them?

Details: I found it in Northern Plains, India. Its length is almost 1 cm (maybe bigger) and breadth is about 0.5 cm (actually slightly smaller than that).

Such a queer species. I thought it was an ant. But it is actually a spider.

These spiders belong to Salticidae family,commonly called ant-mimicking spiders / jumping spiders.

  They are  Batesian mimics of ants, such as Sphecotypus in the Clubionidae.

They do not feed on their model organisms and keep them at an acceptable distance.

This one is from Myrmarachne sp. There are more than 20 species found in India.

Source:

Wikipedia
Myrmarachne


What is this fossilized claw found in a Belgian forest? What is this fossilized claw found in a Belgian forest? It is 14.5 cm long and 2.5 cm in diameter.

Looks like the proximal end of a rib of a large mammal (cow, horse, deer). Without information about how large it is, it is not possible to get closer to an identification. It's not a claw and very likely not a fossil. It just looks old and dirty.

Here's a horse rib cage (from https://www.rodnikkel.com/content/saddle-tree-blog-from-shop-and-desk/the-rib-cage/):

Ribs in the 4-7 range seem to be a good match for shape but not as much for roundness.


How do I look for pathogen in water with a microscope? Is it possible? I am a 9th grade student from Manila and we're currently working on an investigatory project. We want to know how effective SODIS or solar water disinfection is. The purification method claims to be able to kill pathogen. We've just finished our methodology; we have not done to experiment yet.

There's one thing that concerns us: is it even possible to see pathogen in water using a microscope? We raised our concern to our teacher and at first she believes it is possible. However, she said that she was not sure because she mentioned that some stuff (I forgot what) are "cultured" before checking for pathogen like  bacteria.

Yes your teacher is right. In a microscope you can see microorganisms. Now the question is to identify them as pathogens.

I guess what your teacher has in mind is to use specific culture mediums for different pathogens and see if anything is growing there, then you have a positive.

You could also do a PCR. This is extracting the DNA and amplify specific genes that you know belongs to pathogens.

But the most currently trendy analysis is metagenomics. Basically, you exctract the genetic material from the sample, then sequence and compare against public databases. This methodology allows the identification of everything that is there pathogens and non-pathogens.


Do aquatic plants have stomata? I am wondering if aquatic plants have stomata or not. I know that non-aquatic plants have stomata to release water(transpiration) and oxygen, and to take in carbon dioxide. Do aquatic plants also have stomata, and if so do they take in water through their stomata? If water is taken in through their stomata, wouldn't other substances such as dissolved salts get in the plants vascular system too? Does the aquatic plant use this salt or remove it, and how would they remove it?

Note: I am talking about fully submerged aquatic plants such as kelp.

According to the book Stomatal function (Zeiger et al, 1987), many aquatic angiosperm plants have stomata (since they have evolved from terrestial plants), while some have reduced or complete loss of stomata.

However, the book also states that:

  ...aquatic plants living underwater are devoid of stomata. Leaves that float in water, which are common in ponds, have stomata on their upper surfaces but lack them on the surfaces in contact with water.


Are there statistics on Sickle Cell Traits based on country of origin? And where was it originally from and how does it spread?

Thanks.

For "where does it come from and how does it spread?", why not read Wikipedia?  Short answers: (1) malarial regions of sub-Saharan Africa; (2) movement of people and genetic introgression.

Googling 'sickle cell "country of origin" turns up, for example:

"Sickle cell disease in areas of immigration of high-risk populations: a low cost and reproducible method of screening in northern Italy" Blood Transfus. 2014 Jul; 12(3): 346–351. doi:  10.2450/2013.0188-13 PMCID: PMC4111816

Country    Selected     Enrolled/   Enrolled/
                        negative    Hb variant
-----------------------------------------------
Ghana      241 (51.4%)  112 (47.1%) 53 (57.6%)
Nigeria    152 (32.4%)  77 (32.4%)  29 (31.5%)
Guinea      15 (3.2%)   8 (3.4%)    4 (4.3%)
Cameroon    13 (2.8%)   10 (4.2%)   1 (1.1%)
Senegal     12 (2.6%)   8 (3.4%)    1 (1.1%)
Ivory Coast 10 (2.1%)   9 (3.8%)    1 (1.1%)
Other       26 (5.5%)   14 (5.7%)   3 (3.3%)
Total      469 (100%)   238 (100%)  92 (100%)

"The burden of sickle cell disease in Cape Town", South African Medical Journal 102(9), 2012 Wonham et al. http://www.samj.org.za/index.php/samj/article/view/5886/4421

Distribution of sickle cell disease patients by country of origin. Up to 93.1% (n=54) of the patients were originally from other countries in Africa, mainly from the Democratic Republic of Congo (62.1%, n=36).


Binary fission in amoeba When a parent amoeba undergoes binary fission, two amoeba are obtained. Are those two amoebas, both daughter, or 1 parent and 1 daughter?

In binary fission, the fully grown parent cell splits into two halves, producing two new cells. After replicating its genetic material, the cell divides into two nearly equal sized daughter cells. The genetic material is also equally split. The daughter cells are genetically identical (unless a mutation occurs during replication).

Source: Binary Fission - Wikipedia

This corroborates with what I was taught in school as well.

A quick Google Image Search also shows that most diagrams on the subject involve one parent producing 2 daughter cells.


Can the Na+/K+ pump backwards to generate ATP? The standard physiological direction of the Na+/K+ pump is to export 3 Na+, import 2 K+, and hydrolyze one ATP to ADP. Can it be driven backwards, importing 3 Na+, exporting 2 K+, and generating ATP? Does this happen in normal cells, and in what conditions?

All enzymes can theoretically catalyze the reverse reaction.

Researchers have driven the Na+/K+ ATPase to synthesize ATP with artificial ion concentrations:

  We have studied the apparent affinity for K at its intracellular discharge sites by measuring the rate of ATP synthesis as a function of the internal K concentration in resealed red blood cell ghosts, where the Na-K pump is driven in reverse by the downhill efflux of K and influx of Na…