Structure of RAP Antibodies (Specifically RAP-5) [EDIT] - Have just found not one but two papers that address my structure problem. However they concern RAP-1A, so I guess my question is now what is the difference in  structure and function of RAP-1A and RAP-5? Does anyone know of X-ray structure analysis being used to examine RAP-5?

original question

I'm a University Physics student writing a mock review article on what to me feels like a very 'un-physicsy' antibody - RAP-5.

Although my knowledge of Biology is pretty poor, research is going quite well. I've found a lot of papers from the 80s talking about conducting immunohisto(/cyto)chemistry experiments, most of them finding that RAP-5 can be used to determine whether a cell has the ras in it, so they are able to measure the percentage of cells that are neoplastic (I believe this means cancerous) and contain ras and the percentage of cells which are normal and contain ras. (the ras-gene being a proto-oncogene which on mutation can result in permanently switched on ras proteins (p21?), which results in proliferation of cells and therefore can cause tumors). This is all very nice but on first glance immunohistochemistry doesn't seem to involve a huge amount of physics (for my bio-physics assignment), apart from using an optical microscope.

I was hoping to be able focus a section of my article on the physical techniques involved in determining the structure of RAP-5. Although there seems to be plenty of literature on uses of RAP-5, I am struggling to find anything on the details on why it is able to be used in such experiments. In other words, I presume that its function is to bind on to an epitode specific to the ras protein (amino acids 10 -17 have popped up a few times) but I don't know if there is any imaging one can do to have a look at the structure and conclude 'yes this is why it binds to ras proteins and not to others'. Is there a technique that is likely to have been used to examine the structure of RAP-5? Is it's tertiary structure likely to be 'Y' shaped like other antibodies? Does it differ in structure from RAP1-4? (this book informs me that RAP1 and RAP2 have 60% sequence identity, but most sources seem to leave out RAP3-to-5, some evening telling me that the RAP family consists of RAP1A/B, RAP2A/B/C and no others!).

Also, if RAP-5 is an antibody, does this mean that it is produced in the body and gets involved in the ras protein signal pathway in order to reduce too much ras expression? (am I right in saying the amount of expression is the amount of protein the ras-gene is producing?) or is it only synthetically produced and used in experiments to measure the amount and location of ras proteins?

Also there seems to be little differentiation between the differences in the functions of each RAP. RAP-5 seems to be used quite a bit in experiments involving Ha-ras - but not exclusively. Do the different RAPs bind to different variants of ras? Ha-ras being the one unique to RAP-5.

The confusion that you're facing is because RAP-5 is actually known as RAB5C (GENEID). The ras superfamily (review) is divided into Ras, Rho, Rab, and Rap. But the Rap GTPases are divided only into two categories, RAP1 and RAP2. On the other hand, there are multiple Rab GTPases which include RAB5A and RAB5C.

There are a few crystal structures of both Rab5A and Rab5C in both human and murine forms.

Now, for RAP-5. RAP-5 is a monoclonal murine antibody which has no relationship to the RAP family of proteins. It's probably called RAP because Spandidos and Wilkie weren't thinking clearly when they named their antibodies RAP1-5. In this case, you're probably better off looking at the antibody Y13-259 which is probably called that since its the 259th antibody they tried.

To answer your questions, specifically, very few people have attempted to get a structure since it is an antibody and everyone knows what they look like. Secondly, the antibody is produced in a mouse and added to tissue. And yes, the RAP antibodies bind to different variants of Ras. Also, no one uses RAP-5 since anti-Ras EP1125Y seems to be more popular.

If you still want a crystal structure, I would hunt down the RAP5 patent and look up the peptide sequence. From there, you can look up similar structures in the IMGT database


What kinds of arousal can a human brain experience? I've been reading about the new phenomenon called "arousal addiction". The context in which this term is used is Internet, Porn and/or video game addiction(cummulatively Internet Addiction Disorder - IAD). Dopamine and Dopamine receptor D2 are sometimes mentioned, as being affected by exposure to a new, novel stimuli.

I'm interested if there are other forms of "arousal" that may involve more than just Dopamine. For example, I know that there are 4 neuromodulators in the human brain:

Dopamine
Serotonin
Choline
Noradrenaline

For example, if a person likes horror movies to the point of addiction, is it Dopamine, or is it Noradrenaline that the person enjoys? If a person is addicted to comfort foods, is it Dopamine or Serotonin?

Thank you!

Depends on what you mean by "addiction": defined, addiction usually requires both psychological and physiological dependence, but conversationally we sometimes only talk about psychological dependence (as in here, your muscles won't cramp up if you NEED a horror flick).

If a person enjoys horror movies, is it the suspense? Such a rush is caused by the well-known fight-or-flight catecholamine epinephrine (also known as adrenaline). This is the short-term stress response at play. Comfort foods are a whole other story, because it depends on the food as well. Carbohydrates can contribute to serotonin levels, yes, but I read a super-interesting study a couple years back about saturated fat causing a decrease in corticosteroid levels and this sought to explain why people eat fatty foods when they are stressed (I'll try to find this article for you). Tryptophan, an amino acid, is converted to serotonin, which is why turkey, milk, and other sources of trp can make one sleepy.

Awesome question! I'm going to try to learn more about this and find that article for you. Dopamine is the primary player in most conventional addiction-talk, as it's crucial to the reward circuitry that is usually discussed.


Which organism has the smallest genome length? Which animal/plant/anything has smallest length genome?

Since you said plant/animal/anything, I offer the smallest genomes in various categories...

(Kb means Kilobases, Mb means Megabases. 1 Kb = 1000 base pairs, 1Mb = 1000Kb)

Smallest plant genome: Genlisea margaretae at 63Mb (Greilhuber et al., 2006)
Smallest animal genome: Pratylenchus coffeae (nematode worm) at 20Mb (Animal Genome Size DB)
Smallest vertebrate genome: Tetraodon nigroviridis (pufferfish) at 385Mb (Jailon et al., 2004)
Smallest eukaryote: Encephalitozoon cuniculi (microsporidian) at 2.9Mb (Vivarès & Méténier, 2004)
Smallest free-living bacterial genome: Nanoarchaeum eqitans at 491Kb (Waters et al., 2003)
Smallest bacterial genome: Carsonella ruddii (endosymbiont) at 160Kb (Nakabachi et al., 2006)
Smallest genome of anything: Circovirus at 1.8Kb (only 2 proteins!!) (Chen et al., 2003)

Refs...

Chen, C.-L., Chang, P.-C., Lee, M.-S., Shien, J.-H., Ou, S.-J. & Shieh, H.K. (2003) Nucleotide sequences of goose circovirus isolated in Taiwan. Avian Pathology: Journal of the W.V.P.A. 32 (2), 165–171.
Greilhuber, J., Borsch, T., Müller, K., Worberg, A., Porembski, S. & Barthlott, W. (2006) Smallest Angiosperm Genomes Found in Lentibulariaceae, with Chromosomes of Bacterial Size. Plant Biology. 8 (6), 770–777.
Jaillon, O., Aury, J.-M., Brunet, F., Petit, J.-L., Stange-Thomann, N., Mauceli, E., Bouneau, L., Fischer, C., Ozouf-Costaz, C., Bernot, A., Nicaud, S., Jaffe, D., Fisher, S., Lutfalla, G., et al. (2004) Genome duplication in the teleost fish Tetraodon nigroviridis reveals the early vertebrate proto-karyotype. Nature. 431 (7011), 946–957.
Nakabachi, A., Yamashita, A., Toh, H., Ishikawa, H., Dunbar, H.E., Moran, N.A. & Hattori, M. (2006) The 160-Kilobase Genome of the Bacterial Endosymbiont Carsonella. Science. 314 (5797), 267–267.
Vivarès, C.P. & Méténier, G. (2004) Opportunistic Infections: Toxoplasma, Sarcocystis, and Microsporidia. In: World Class Parasites. Springer US. pp. 215–242.
Waters, E., Hohn, M.J., Ahel, I., Graham, D.E., Adams, M.D., Barnstead, M., Beeson, K.Y., Bibbs, L., Bolanos, R., Keller, M., Kretz, K., Lin, X., Mathur, E., Ni, J., et al. (2003) The genome of Nanoarchaeum equitans: insights into early archaeal evolution and derived parasitism. Proceedings of the National Academy of Sciences of the United States of America. 100 (22), 12984–12988.


Is it possible to genetically modify a plant at home? Would I be able to genetically modify a plant at home? What equipment will be necessary? I think it might be a fun change from the 'norm' of regular hybridisation, to try some inter-family gene insertion, instead of staying within a genus. Are some plants easier to modify than others?

Well, that depends on your home. ;) I think it is not an easy process.

There are two main methods that are used to genetically modify plants:

Using the bacterium, Agrobacterium tumifaciens, as a vector for the DNA. Agrobacterium has the ability to infect plants and insert DNA into a plant's genome. It causes crown gall tumours in natural infections. This method has mainly been used to modify broad leaved plants, such as sugar beet and oilseed rape, but is now also being applied to monocot species, such as maize and rice

Particle bombardment or biolistics where the DNA to be inserted is coated on minute gold particles and fired into plants cells. This approach is used for monocot plants such as maize and rice

Here I found simple step by step article, but lil bit old. may be there are new methods for this process.
How To Genetically Modify a Seed, Step By Step


How do racing pigeons know the way back to their roost? I have read that a standard way to do pigeon racing is that the male and female are separated and the pigeon races to its mate.

My understanding that in these cases the roost is several miles away from the release point. How does the pigeon know how to find the roost?

I have heard that sometimes they will hold up the mate in the air, but at several miles away, how would that help.

They find their way back even if they have been moved in complete darkness by using, indeed, magnetoreception. They can sense the direction of where they come from using the earth magnetic field. I believe there is still some debate about how magnetic fields are sensed by pigeons, the latest fashionable idea being that this is through a "warm" quantum process. I don't know if that's correct, but there is clear evidence that there are magnetic-sensitive cells in the pigeons nervous system (Wu & Dickman, 2007). This will only lead pigeons to the approximate location of their home, but once they are close enough they can recognize where they live visually. Pigeons are released everyday so they know the local environment of their home.

I'm quite sure this has nothing to do with the pigeons mates. This is probably some ridiculous idea people had in the middle-age and people kept repeating it because that sort of intuitively makes sense, but when you think carefully about it, it really doesn't.

Wu, L. Q., & Dickman, J. D. (2012). Neural correlates of a magnetic sense. science, 336(6084), 1054-1057.


Global Acidification or Warming Which poses the greater threat to ecology Global Ocean Acidification or Warming?

The issues of global ocean acidification and global warming are two symptoms of the same disease, too much carbon in the atmosphere. And they have 1 solution, put less carbon into the atmosphere. It doesn't really matter which aspect is the more harmful one, you can't treat one without treating the other.

If reducing carbon output were simple, we would have done it by now. However, it will most likely require radical changes to our energy infrastructure, with moves away from coal, oil, and natural gas and towards solar, wind, and nuclear power. It will probably require changes to our agricultural practices, and you should really watch Allan Savory's TED Talk for how those changes should be implemented.

People are very slow to change their habits, and short term profit is a powerful motivator against change, but I believe these we can and must solve these problems if humanity is to continue to thrive on Earth.


Abiogenesis: Beyond the research journals as a lead in to discussions on evolution I just came across this abstract:

  Aminoacyl-tRNA synthetases (aaRSs) are responsible for creating the pool of correctly charged aminoacyl-tRNAs that are
  necessary for the translation of genetic information (mRNA) by the ribosome. Each aaRS belongs to either one of only two
  classes with two different mechanisms of aminoacylation, making use of either the 29OH (Class I) or the 39OH (Class II) of the
  terminal A76 of the tRNA and approaching the tRNA either from the minor groove (29OH) or the major groove (39OH). Here,
  an asymmetric pattern typical of differentiation is uncovered in the partition of the codon repertoire, as defined by the
  mechanism of aminoacylation of each corresponding tRNA. This pattern can be reproduced in a unique cascade of successive
  binary decisions that progressively reduces codon ambiguity. The deduced order of differentiation is manifestly driven by the
  reduction of translation errors. A simple rule can be defined, decoding each codon sequence in its binary class, thereby
  providing both the code and the key to decode it. Assuming that the partition into two mechanisms of tRNA aminoacylation is
  a relic that dates back to the invention of the genetic code in the RNA World, a model for the assignment of amino acids in the
  codon table can be derived. The model implies that the stop codon was always there, as the codon whose tRNA cannot be
  charged with any amino acid, and makes the prediction of an ultimate differentiation step, which is found to correspond to the
  codon assignment of the 22nd amino acid pyrrolysine in archaebacteria.

Granted, this is a few years old, but I often find myself having to admit that "I don't know" when at the root of discussions on evolution.  That is, once abiogenesis has occurred, we can go on and explain the rich diversity of life, but sadly we really don't know much before that critical step.  Generally, those satisfied with "magic" as an answer posit their myths and fables, whereas I'd rather try to actually find out what happened.  Sadly, as the abstract shows, you actually need a level of education to understand papers such as this that is generally well beyond those who would deny the reality of evolution.

Does anyone have a collection of papers on abiogenesis that are more accessible and understandable to laypeople?

The fascinating field of abiogenesis is, as Nick Lane put it, "a wild west of ideas, theories, speculations, and even data". The stories we have involve a plethora of assumptions, there is no hypothesis where all or most of the pieces would fit together. Usually scientists agree it was RNA that played central role in the process, as the molecule could both carry the genetic code, necessary for hereditary natural selection, and catalyze basic biochemical reactions. Where the energy came from and how it was harnessed to maintain RNA (a rather unstable molecule) and perform work is still debated. A fermentation in a 'primordial soup' or a primitive form of respiration, perhaps through a thin iron-sulphur membrane, have been proposed as possibilities. The second gave a start to the iron-sulphur world hypothesis. Iron-sulphur minerals could catalyse the first organic reactions to synthetize sugars, amino-acids and nucleotides, and eventually RNA world, where natural selection could take over. Theories abound.

Usually reviews will give you a sound and approachable picture of the current thought on the matter. Take a look into Nick Lane's book and these articles, too.

Lane N., Origin of Life in: Power, Sex, Suicide: Mitochondria and the Meaning of Life. Oxford University Press, 2005. p. 94-104.
Russell, Michael (2006). First Life. American Scientist 94 (1):32.
Van Noorden R., RNA world easier to make - Ingenious chemistry shows how nucleotides may have formed in the primordial soup. Nature 2009
Check Hayden E. A never-ending dance of RNA - The recreation of life's origins comes a self-catalysing step closer. Nature 2009.
Cech TR. Exploring the New RNA World. Nobel Prize articles
Müller UF. Re-creating an RNA world. Cell Mol Life Sci. 2006 Jun;63(11):1278-93.
Lazcano A, Miller SL. The origin and early evolution of life: prebiotic chemistry, the pre-RNA world, and time. Cell. 1996 Jun 14;85(6):793-8.


Does xylitol kill all kinds of bacteria? Xylitol is known as a bad bacteria killer in human's mouth.
But I am curious about one thing.

Does xylitol kill all kinds of bacteria regardless of good or bad?

If so, Does xylitol kill bad bacteria more than good ones at least in human's mouth?

Xylitol does not kill any bacteria.

Xylitol is a sugar alcohol that bacteria happen to not be able to use as an energy source. In the absence of other sugars, bacterial growth slows. Therefore, its antimicrobial mechanism is bacteriostatic rather than bactericidal.

No antibiotic exists, or will ever exist, that kills or inhibits all kinds of bacteria.

One thing xylitol can kill is a dog – keep xylitol-containing products such as gum well out of their reach.


Why isn't suppression of immune system for organ transplant not as dangerous as AIDS? I've read that when AIDS symptoms show up, life expectancy is about two years if no treatment is applied. On the other hand, I've also read that people having an organ transplant need to take immune system suppressors for the rest of their lives so that their body does not attack the transplanted organ. So, if I understand well, it is a sort of induced AIDS. I do not understand then how it is possible for people with an organ transplant to live more than about two years.

Can someone explain with details the differences between the suppression of the immune system by medicine for organ transplants and the one due to AIDS?

Patients receiving immunosuppressive drugs do fall into the same category as patients with HIV-related acquired immunodeficiency - that is, they are all immunocompromised and face similar risks of infection, cancer, etc. The difference emerges over time: when the immunosuppression is controlled and monitored, a patient can retain some immune function, and a physician can help a patient adjust and rapidly respond to opportunistic infections. Drugs can be given in calculated doses; viral infections which disable the body's ability to stop viral infections typically only get worse. To elaborate:

HIV causes immunodeficiency by killing T cells. Firstly, it preferentially infects CD4+ T cells. This process can trigger an inflammatory response and (1) kill the infected T cell, as well as (2) bystander cells. Once the virus has successfully infected a CD4+ T cell, it can happily produce more viruses without killing the cell, which is how the infection can spread - or it can (3) rupture the cell membrane and kill the T cell. Finally, CD8+ T cells can notice that CD4+ T cells are getting infected by a virus and start (4) killing CD4+ T cells.

Immunosuppression after organ transplant can be more specific. It is typically achieved via a combination of drugs which can (1) reduce immune cell activation, (2) slow down immune cell proliferation, or (3) block the activating receptors on T or B cells. The amount and type of suppressants depend on the phase of treatment: induction of immunosuppression, maintenance, or treatment of transplant rejection.1 These drugs are also often administered alongside preventative antimicrobial drugs.

The immunosuppressants which are administered during the maintenance phase - i.e. for the rest of the patient's life - are often the drugs which dampen immune activation instead of eradicating all T cells, and are given at much lower doses. For example, calcineurin inhibitors block the [calcineurin-NFAT pathway];2 when this pathway is blocked, production of immune activators like IL-2 is reduced, and reduces T cell function.

TL;DR: "induced AIDS" is milder and more controlled than actual AIDS, and doctors work very hard to keep patients within a safe range of immune function/suppression.

PS: Good question! Made me think :) I've written some papers on organ transplantation before so am happy to do some digging to add sources.


What decides the position of the node of Ranvier? The oligodendrocytes makes the myelin sheath in CNS and schwann cells make it in PNS. What decides where the oligodendrocyte or Schwann cell will attach and start forming myelin sheath? Is it genetically determined? Is it random? Is there any disease associated with improper positioning of node of Ranvier?

A combination of differentiation site, chemical guidance during migration, and signaling cues form a variety of sources.

  The final step in the generation of an oligodendrocyte is the
  development of a mature myelinating phenotype, and this is largely
  regulated by axonal signals. It seems likely that both soluble and
  cell mediated signals from adjacent axons are integrated into the
  developmental profile of oligodendrocyte precursors resulting in cell
  differentiation, up-regulation of myelin gene expression and formation
  of the myelin organelle. Candidates for axonally derived soluble
  factors include FGFs (Bansal et al., 1996 and Qian et al., 1997) and
  thyroid hormone (Barres et al., 1994a and Barres et al., 1994b), while
  axonal cell surface molecules such as L1, MAG, NCAM and N-cadherin may
  regulate formation of the myelin sheath (Payne and Lemmon, 1993 and
  Trapp, 1990).

http://www.ncbi.nlm.nih.gov/pubmed/12385864

I don't know of any diseases that just mess with positioning but there are diseases that kill oligodendrocytes (like multiple sclerosis).


How Plausible is Restoration of Cryonically Preserved People? I fear death (so much that I'll prefer a year/few of torture over death), and plan to sign up for cryonics. I would like to know how plausible it is, why the answer would be so, and if possible how many years away would revival be.

Thanks.

I have read a lot of articles on Alcor, and done several hours of research since yesterday. Mainstream Science seems to assign infinitesimal probabilities against, it, but the guys at Alcor (and other Cryonic institutes like Cryonics.org think they've got a case). It seems theoretically possible to me, but I don't want to but into too much hype—so how plausible is it?

Largely implausible, mainly due to damage from freezing. This type of damage even happens when food is frozen (although flash-freezing decreases it).

More feasible approaches for avoiding death would include machine-replacement parts, lab-grown transplants, neural backups, and regenerative gene modifications. I'm surprised no one has considered studying hibernation and how to add similar genes to humans that would enable hibernation.


Why aren't mitochondria and plastids considered symbiotes of eukaryotic cells? Mitochondria and plastids have their own DNA, their own membranes, and their reproduction is not tied to the reproductive cycle of the host cell. However, they are considered to be organelles rather than a separate species in symbiosis with eukaryotes. Granted, mitochondria and plastids are incapable of living outside their parent cells, and likewise eukaryotes are incapable of surviving without the help of mitochondria and plastids. But this is also true of many other symbiotic pairs in Eukarya. So where does the distinction lie? What makes mitochondria and plastids organelles rather than separate organisms?

I would say it has to do with the amount of mitochondrial or sequence that has been transferred to the host genome. As a consequence of all this information stored in the host genome, mitochondria cannot reproduce without the host. In this way, they are not their own organisms, but rather organelles.

Over evolutionary time, the line between organelle and intracellular endosymbiont gets blurry, but in their current state, mitochondria are organelles.

The same goes for for plastids, in general.


Do immature fruits perform photosynthesis? Most immature fruits are green: peppers, pine cones, plums, lots of them. I want to know if the green is from chlorophyll in the cells. Do the fruit cells perform photosynthesis? When you cover a green stem or leaf, it will turn pale and stretch. That is because the stems have little need for chlorophyll in the dark, which is why they are pale. They stretch because the auxins in the stems are not destroyed by the photons, and the stems stretch out and topple over. If a green fruit is covered, will it turn pale and stretch like that?

The green pigment is indeed chlorophyll, and the fruits do perform photosynthesis.   It's not just "fruiting" plants that do this either.  Some shading experiments i saw estimated that  up to 30% of the sugars assimilated into the barley ears (basically the grain) can come from photosynthesis occurring in those organs.


Why aren't the twin organs like both the eyes, ears, hands and legs lying both sides of a human body identical? Both the eyes are not identical in geometrical shape and size i.e. physical appearances of both the eyes of a person are different from each other. The same difference is observable in both the hands, ears.
I don't know which causes the difference in geometrical shape and size of the twin organs in the human body.
Any explanation will be greatly appreciated.

The topic you're looking into is fluctuating asymmetry, a broad field of study.  Among the free reviews this one is a bit old but well on topic.  The general idea is that there is "developmental noise", which is opposed by mechanisms for developmental stability.  The review covers a variety of conclusions people try to read in to these studies, often about the stresses on the organism or the mechanisms by which development is "canalized" to reach a specific goal.
The nature of the noise is usually presumed rather than proven, since many different factors are presumably adding up to make small differences.  We may assume (though I'm not always sure it is true) that mRNA, protein, and signalling molecules diffuse to reach their targets, which is to say they are subject to Brownian motion with random variations in timing.  The need for multiple factors to get together for a complex process like transcription or translation means that the number of copies of a protein produced under a given circumstance will vary.  An example of this in hypertrophic cardiomyopathy has been proposed to contribute to disease progression, due to random bursts of transcription in individual heart cells affected by the disease.


Name of dominant dinosaur I seem to remember reading some time ago about a dinosaur appearing very prominently in the fossil record, with continent-wise distribution. The layer is known specifically for having so many fossils of this dinosaur and might be named as such. Terms "cow-sized", "vegetarian", and "near to extinction event" come to mind. Does this ring a bell?

My memory might be so faulty that it could be an early amphibian, reptile or even mammal!

The closest example I can think of is Lystrosaurus, which was one of the most common animals in the early Triassic period. It was distributed across many modern continents, and was roughly the size of a pig or cow, depending on the species. Lystrosaurus was not a dinosaur, despite its name.

Excerpt from the Wikipedia page (emphasis mine):

  Lystrosaurus is notable for dominating southern Pangaea during the Early Triassic for millions of years. At least one unidentified species of this genus survived the end-Permian mass extinction and, in the absence of predators and of herbivorous competitors, went on to thrive and re-radiate into a number of species within the genus, becoming the most common group of terrestrial vertebrates during the Early Triassic; for a while 95% of land vertebrates were Lystrosaurus. This is the only time that a single species or genus of land animal dominated the Earth to such a degree


What directs macromolecules to their cellular locations For example I know that after transcription a mature mRNA is sent outside of the nucleus through the nuclear pore and then it goes to ribosome. But as for the free floating ribosomes that are out somewhere in the cytoplasm, how does the mRNA get to those organelles? Is there something else that attaches to the mRNA to help it? Even then I don't understand what force is helping a large molecule (mRNA) find and even larger macromolecular assembly (the ribosome).

This is fairly often question for molecular biology

  how does the mRNA know exactly how to get to those organelles

The secret to understand it, is that nothing knows where to go. Different molecules have different affinity to each other. Molecule A likes molecule B, but not molecule Y. Inside the cell, thermal fluctuations causes disorder that drives molecule A to bump into all kinds of molecules, including Bs, Zs, Ys, and others. However, when stumble upon molecule B, molecule A will very likely form some sort of stable complex with it. One example, is ribosome and mRNA.

When mRNA and ribosome join into complex, their inner parts can be considered in the same fashion: they will jiggle a lot around, but most likely jiggle will produce polypeptide, not, let's say DNA, or not cause mRNA to fall away from the ribosome.

So, you can say that mRNA tries to go everywhere it can, without any clear direction, apart from the fact that it will most likely form something stable (i.e. useful) with ribosome. Or maybe it will be mRNA degradation protein, such as ribonuclease.

PS: "will very likely form some sort of stable complex" means that in some reasonable time mRNA will find and bind to ribosome. However, it might take billions of years for ribosome to bind DNA and produce some sort of polypeptide.


Physiology of skin and leather: why do salt borders occur? I discussed a leather store about the white border aka salt border on leather shoes. They said that it is due to inner features of leather and you could try to add some fat/cream to push it back inside the shoes. I haven't yet understood physiology of skin here, "why does it act like that?" is the first doubt and then the second "does human skin act the same way?" -- I can see this kind of salt borders in gym clothes when they cry uncleaned but haven't seen them yet on my skin at least. The extra salty water from legs causes real damage, such as getting the inner fluids out, to the leather. When you do heavy training, the salty sweat in the human skin acts apparently the same way. So:

  how to manage the skin in living human skin and how does it differ from leather maintenance? What is the common physiological background with the different kinds of skins?

I try to answer it myself:

leather: you can add the fat/cream/etc only externally
living human ski: you can add the fat/cream-etc both internally (fatty food) and externally (lotions)

The two processes are quite different: On leather shoes no active transport takes place. The salt either comes with the snow (most likely most of it) when the streets get salted to avoid ice. Your shoe soaks up the salt-water mixture and when the water dries up, the salt stays behind. The other possibility (more for new leather shoes) is that water goes into the leather and dissolves salts, which remain from the tanning process of the leather. With older shoes I have never observed this "snow marks" in the summer when the shoes got wet in rain.
Using a wet cloth removes the salt, subsequent treatment of the shoe prevents that water can enter the leather.

The skin is quite different: Here we have living cells and an active transport of water through pores when you body get warm. This is to cool you and prevent overheating and since the body fluids contain salt, so does sweat.


What's the difference between the terms "gene map" and "genome"? It seems some sites arbitrarily restrict "gene map" to only a single chromosome, but others don't. Supposing we don't restrict it to just a single chromosome, is it different from "genome"? Are these two terms just synonyms?

This question can be easily answered by reference to reputable sources on the internet, but as it is important to encourage the general use of the term, Genome, I shall cite examples.

Genome

  WHAT IS A GENOME?

  A genome is an organism’s complete set of DNA, including all of its genes

US National Library of Medicine, Genetics Home Reference

Genetic Map

  the arrangement of genes on a chromosome

Merriam Webster Dictionary

This is actually definition 3 of map in the dictionary — i.e. a variant on topological maps. The scientific usage is made clearer in the following:

Mapping

  DNA mapping refers to the variety of different methods that can be used to describe the positions of genes. DNA maps can show different levels of detail, similar to topological maps of a country or city, to indicate how far two genes are located from one another.

Nature Scitable

Distinction in a nutshell

A Genome is an entity — a Genetic Map is a graphical representation of features of that entity.

Hence the following sentence makes sense:

  There is no genetic map for the genome of Bacillus obscurus.

The two terms are certainly not identical. The confusion of the poster may relate to the practical limitations of representation such that often the map of only one chromosome is presented at a time.


Why is GenBank growth slowing down? https://www.ncbi.nlm.nih.gov/genbank/statistics/ shows the growth of the GenBank database is slowing since WGS (Whole Genome Shotgun) emerged. Is this happening because sequencing centers are submitting their data unannotated (WGS submissions are allowed to be unannotated assemblies)?

It is not really slowing down. The graph that you see in that link is semi-log. So the exponentiality of the growth has reduced. It is not surprising because we have much more data than what we had 10 years back but the rate is not going to increase at the same rate (10 to 1000 is a great change but 1000 to 5000 is not despite the fact the the number of new sequences is greater in the latter). However, new data is being continuously added and the linear growth has not saturated yet.

See these graphs that I replotted from the data in your link.

Nonetheless, the number of new sequences will also slow down in future because we would be approaching the maximum.


Hearing and neurons- do ears have a sampling period? From what I have read, outer hair cells in the human ear amplify incoming signals and inner hair cells "pick-up" the signals and generate action potential. However, neurons have refractory periods during which they cannot fire again. Does this mean that the human ear has a "sampling period" within which it cannot "pick-up" sounds?

Inner hair cells (IHC) do not fire action potentials themselves. It's the auditory-nerve that synapses with IHC that generates action potentials. The firing rate of the auditory nerve can be as high as few hundred Hz with a refractory period as short as 1 ms or so (depends on the animal).

However, it is important to note that the signal is not sampled at this rate. As you may know, the auditory signal is first transformed to the "frequency" domain through the physical structure of cochlea. Each inner hair cell therefore is roughly only encoding the relative strength of a frequency band. There are presumably inner hair cells in the human cochlea that correspond to a range centered around 18 kHz for example, but neither the neurotransmitters of the corresponding IHC nor the auditory nerve can fire at 18 kHz. Nevertheless, the amplitude modulation at this high frequency is what is transmitted.

Also, thinking of neural firing as a "sampling period" is not always a good analogy. There are debates about this, but it could be that precise timing of action potential carries large amount of information about the stimulus (perhaps not so much so in early auditory system.)

If you want to see some computational modeling work for inner ear, IHC, and auditory nerve, I recommend the Meddis IHC model:

C. J. Sumner, E. A. Lopez-Poveda, L. P. O'Mard, R. Meddis. A revised model of the inner-hair cell and auditory-nerve complex, J. Acoust. Soc. Am. 111 (5) 2002


Why draw blood from veins rather than arteries? Why draw blood from veins rather than arteries? Is it more convenient or safer?

Veins have several advantages over arteries. From a purely practical standpoint, veins are easier to access due to their superficial location compared to the arteries which are located deeper under the skin. They have thinner walls (much less smooth muscle surrounding them) than arteries, and have less innervation, so piercing them with a needle requires less force and doesn't hurt as much. Venous pressure is also lower than arterial pressure, so there is less of a chance of blood seeping back out through the puncture point before it heals. Because of their thinner walls, veins tend to be larger than the corresponding artery in the area, so they hold more blood, making collection easier and faster.

Finally, it is somewhat safer if a small embolism (bubble in the blood) is introduced into a vein rather than an artery. Blood flow in veins always goes to larger and larger vessels, so there is very little chance of a vessel being blocked by the embolism before the bubble reaches the heart/lungs and is hopefully destroyed. Blood flow in an artery, on the other hand, always moves into smaller and smaller vessels, eventually ending in capilllaries, and there is a chance that a bubble introduced by a blood draw (generally rare) or more commonly an intravenous line (IV) could block a small blood vessel, potentially leading to hypoxia in the affected tissues.


Can leukopenia in a person with an otherwise normal immune system lead to non-infectious diseases in the long-term? If a person has developed leukopenia as a side-effect of long-term use of anti-convulsant medications and his/her immune system appears normal otherwise (does not get infections any more often than a healthy person, and bone marrow biopsy did not indicate anything abnormal), does the condition need to be treated? Is it even possible to treat leukopenia effectively as long as the person is on anti-convulsant medication?

Does leukopenia increase a person's chances of getting some non-infectious diseases too? I know WBC is primarily responsible for fighting infectious micro-organisms, but does it have any significant role in cleaning up body's own malfunctioning or ageing cells?

Leukopenia is just a definition. In medicine, there's a saying:

  Treat the patient, not the numbers.

Numbers can mislead people, sometimes quite seriously. Definitions of leukopenia vary: some define it as less than 5,000 WBCs per µL of blood; others define it as less than 4,000.

Decreases in specific WBCs is usually described as neutropenia, lymphocytopenia, monocytopenia, etc. This, too, is important information, as each cell has a different function, and thus different results are possible.

In leukopenia, bone marrow biopsies are very informative. They reveal if the cause is a decreased production of WBCs due to destruction of precursor cells, replacement of marrow by other tissue, invasion of marrow by cancer, etc. If a bone marrow biopsy is normal, that is very comforting.

  does the condition need to be treated?

Most people with anti-epileptic drug (AED) induced leukopenia are just fine. Some common-sense precautions (such as avoiding other drugs which might also cause leukopenia, and checking a white count if you fall significantly ill) should be heeded. If your doctor is a neurologist, they should be thoroughly versed in the side effects of AEDs, as this constitutes a very large patient population for them. Some of the newer AEDs have a lower incidence of leukopenia. Talk to your doctor about the potential benefits and drawbacks of switching.

  Does leukopenia increase a person's chances of getting some non-infectious diseases too?

Theoretically possible, but not particularly likely.

If you are truly concerned, ask if you can get a referral to see a hematologist. They should be able to give you a real picture of the problems with long-term AED-induced leukopenia.

Remember: treat the patient, not the numbers. If you're healthy now, you're likely to continue to be so. Maybe you'll need more blood tests than others, but that doesn't mean you're not healthy. Talk to your doctors, not the internet.


Can Naegleria fowleri enter through the eyes ( example rinsing/splashing eyes with water) I understand that it primarily enters the body through the nose by by "feeding on the olfactory neurons in the nose" as answered here in a different question. Would the nerve cells in the eyes present a similar entryway?

In a 1987 article "Nonenteric Infections Acquired through Contact with Water", the author mentioned that "Infection of the ears, throat, respiratory tract, and cornea are also encountered" by virulent strains of Acanthamoeba and Naegleria fowleri. The only reference that implicates Naegleria fowleri is this one, but it doesn't mention modes of infection.

The long and the short of it is that Acanthamoeba infections can be acquired through contact with the cornea, but it's not clear whether Naegleria infections can also be acquired in this way.

n.b. The first link takes you to the JSTOR page.  In the event you do not have access, here is the PubMed page.


How does a gene "know" what to change to? Excuse my ignorance but I've always been curious about this...

For example, a frog is red, but it starts living in a green forest. Over time the frog becomes green to camouflage. But a gene can't see and I'm sure there's no mechanism for color info to be transmitted to individual genes from the brain. So how does a gene know to pick green over, say, blue?

Using your example, the gene doesn't know anything. Mutations cause some of the offspring of the red frog to turn green, some to turn blue, some to turn fluorescent yellow, and some stay red. Birds can't see the green ones as well as the others, so more green frogs survive and make more green frogs. The red frogs, the fluorescent yellow ones, the blue ones, mostly get eaten. After a few generations, almost all the frogs are green -- not because the gene knew anything, not because the mutations went in any direction, but because all the other changes were counterproductive and got eaten.

The gene doesn't know anything. It's just a bunch of chemicals that randomly react with cosmic rays, chance, whatever. Most of the changes are irrelevant or actively bad, and the frog that's carrying those particular chemicals doesn't survive. But sometimes the change benefits the frog carrying the particular chemicals and then the frog sends those chemicals down to its progeny.

Obviously this is hugely over-simplified. A short and simple intro to the basics of evolution is Understanding Evolution, by UC Berkeley.


Information Gene HBA2 Gene : HBA2? hemoglobin alpha 2 (Homo sapiens)

I don't find any tissues (or organs) in which the expression of this gene is strongest? What is the size of the gene (promoter off) encoding this sequence?

You mention that you "started in bioinformatics", so perhaps you might feel more comfortable taking such an approach to better characterize where the promoter for HBA2 might be.

As @Bitwise mentioned in his comment, "the promoter" is not a well defined region. Often times "we" take the promoter of a gene to be some arbitrary (2-4) kilobytes upstream from the TSS. With more high throughput data coming online (especially from ENCODE), we are starting to get a better picture of where the functional regulatory elements of genes might be.

By combining data from several different high-throughput assays across a variety of cell types, the human genome has been segmented into broad regions of interest. You might start by looking for where the "Predicted promoter region including transcription start site" segment is for HBA2.

I'd also take a closer look at the DNase-seq data in this "promoter region" across as many cell lines as they have processed for you to look for regions that are differentially occupied in hopes of identifying more precisely which parts in the promoter region might be important for the gene's expression (this would, of course, require you to connect DNAseq data with gene expression (RNA-seq) data).


Terms related to megasporogenesis Well, I am not able to understand the exact difference between megasporocyte and archesporium. Also I'm not quite able to get, how or precisely from where do these arise?
Please help.

In relation  to angiospermic megasporogenesis, archesporium cell is the precursor of Megasporocyte.

  Archesporium is defined as   the cell or group of cells from which spore mother cells develops

  The megasporocyte is the cell(or the tissue) which directly produces
   the megaspores.

In most angiosperm, the nucellar tissue within the ovule first differentiates into a single archesporial cell, the ancestor of the Megaspore Mother cell(MMC). In certain species, this archesporial cell may itself act as the MMC undergoing meiosis to produce the megaspores. in such cases, the archesporial cell and the megasporocyte (another name for MMC) is the same.

But in some species, the archesporial cell first undergoes a periclinic division producing two cells which further produce the parietal layer (covering of the megaspore) and a single sporogenous cell. This cell acts as the MMC, and is the megasporocyte.

Thus the archesporial cell may or may not be the same as the megasporocyte. It could be the ancestor of megasporocyte.


Is drinking your urine an effective way to stay hydrated in a hostile environment? There are quite a few stories about people trapped or otherwise incapacitated resorting to drinking their own urine in an attempt to stave off dehydration, ignoring the long term consequences, my problem with this idea is that the main cause of death when dehydrated is kidney failure, resulting from the buildup of urea and uric acid when the body can't package those chemicals with water to execrate them. Because of this, I'm tempted to assume that drinking your urine (without somehow purifying it) is a futile action as you are consuming both the water and the exact chemicals you need to remove with the water. I'm however not confident with this analysis, so any sources on the subject would be appreciated.

Drinking urine could help you stay hydrated a bit longer, maybe a day, but only when you are well hydrated at the start. You could get about 0.5-1 liter extra water this way. This doesn't work anymore when you start drinking urine the 2nd or 3rd day without water - the amount of urine will be very small and will be too concentrated at that time.

A man, drinking his urine has survived for 6 days under the ruins of the earthquake (Slate.com). However, people have survived for as long as 8 days without water or drinking urine: a 7 and 11 years old kids under the ruins of 2010 Haiti earthquake, and a 35 years old woman trapped in a lift.

According to Guyton and Hall Textbook of Medical Physiology:

...to excrete an average amount of waste products, let's say 600 mOsmols, your kidneys need to excrete at least 500 mL of urine, because they have a limited ability to concentrate urine.

If you drink 1 liter of urine with 600 mOsmols of waste products, you will need to excrete 500 mL of urine to excrete those 600 mOsmols and additional 500 mL to excrete 600 mOsmols from your normal metabolism. So, drinking 1 liter urine forces you to lose 1 liter of water, which means no water gain.

If you are very well hydrated at the time of first urination, your urine will be more diluted, so containing less than 600 mL of urine (minimally about 50 mOsmols/kg according to Wikipedia). Drinking such urine can provide net hydration, but your next batch of urine will be much more concentrated and will provide much less hydration. At the point when the kidneys need to excrete more water to eliminate the waste than you have drunk by urine, you will be in the negative water balance.


Overexpression by integration of an additional copy vs promoter exchange In Becker et al (2011), the authors increase the expression of several genes through different methods. For some genes (e.g., lysA, ddh), they achieve overexpression by integrating an additional copy of the gene and its flanking regions. On the other hand, for other genes (e.g., lysC, dapB, fbp, and the tkt operon) they take another approach and instead replace the native promoter with a strong constitutive promoter (Psod or Petfu).

Is there an advantage of one technique over the other? Why was one technique preferred over the other one for certain genes?

Modifying promoters can give finer, more targeted control of expression than changing copy numbers. In the paper you referenced, for the ddh gene, it sounds like they just wanted to boost production of that protein, so making a second copy made sense. But with some of the other genes, they wanted to alter metabolite fluxes through a more complex pathway. Copying a whole operon would not achieve this, because then you would just get two pathways doing the exact same thing. But even copying the one or two genes in the operon that you want to investigate might change their relation to the other genes in the operon. Bacterial operons are generally organized such that the genes for the transcriptional regulators are located adjacent to the genes they regulate. This proximity is necessary for the proper functioning of the operon, and if you copy a gene, depending on where you put the copy, it may not function as it usually does. In these cases, it's better to mess with the promoters because you can leave the organization of the operon largely intact.


How does the colinearity of the HOX genes determine the body plan of an organism? I was recently reading about colinearity in the HOX genes that give an organism its high-level body plan (where the order of the HOX genes on the chromosome follow the head-to-tail order of body segments, such that the head gene comes before the thorax gene, comes before the abdomen gene, etc).

I'm really just a layman  interested in this stuff (only completed A & P I), but I was under the impression that the location of genes on a chromosome has no bearing on the expression of those genes or phenotype of the organism -- in other words, that genes can be anywhere on any chromosome.

Do we understand how the order of the HOX genes ends up being expressed as the order of the body segments? Do we know why the positioning of these genes matters when the order of other genes don't?

Quoting from some parts of Sean Carroll's book - Endless forms most beautiful, I have tried to provide you with an answer but, remember that this can never suffice for the reading of this great book.

Yes, we do understand how the hox genes' expression is regulated.

From page 126-127

  ......The establishment of these Hox zones and their subsequent action
  in sculpting the different forms of repeated parts is the fundamental
  genetic logic upon which the modular forms of large,biletarian animals
  is built.

  The genetic logic relies on genetic switches at two levels. One set of
  switches belongs to the Hox genes themselves. these switches activate
  each Hox gene in different zones that will become different modules of
  the animal. Another set of switches contain signature sequences that
  are recognized by Hox proteins and that control how other genes are
  expressed in different modules.

  In both arthropods and vertebrates, the Hox genes are developed in
  zones along the main body axis. The distinct zones of each Hox gene's
  expression domain are governed by genetic switches, and seperate
  switches control Hox gene patterns in different tissues such as the
  ...... Because of the logic of the genetic switches, the cells that
  belong to one module express different Hox proteins or combinations of
  Hox proteins than those in adjacent modules....

Let us take an example of Ubx gene which leads to formation of wings in the 2nd and 3rd thoracic segments of  drosophila. This gene is turned off in the first thoracic segment  but in the second and third segments, it is turned on. This regulation can be achieved because of the genetic switches which in turn can be switched on or off by activators and repressors. These activators and repressors are unevenly distributed in the embryo and so regulation of switches in different parts of the embryo is possible.


How many organisms have ever lived on Earth? I've looked for some information on this, but couldn't find anything useful. Has there been any noteworthy attempt to estimate the sum amount of individuals of all species that have ever lived on Earth?

it is impossible to know the exact number so here is my gross ballpark estimate of an upper bound -  i.e. the maximum number of organisms that could have lived on earth in the extreme best case scenario. in practice it is probably much less, but this is to get an idea of what kind of numbers we are dealing with.

The earth's volume is about 1.08321 * 10^12 cubic kilometers =  1.08321 * 10^21 cubic meters

The crust of the earth is 4-8km and the radius is about 6,353km giving around 1% of the total volume available for life.

Hence, the volume available, i.e. the volume of the crust is about 1.1 x 10^19 Meters.

An average-size bacterium such as the rod-shaped E-coli is about 2 micrometers long and 0.5 micrometers in diameter. Hence, the volume is roughly:

(2*10^-6)*(0.5*10^-6)*(0.5*10^-6) = 0.5*10^-18 meters

Hence, if the entire volume of the crust of the earth were entirely filled with e-coli bacteria, there would be:

(1.1 x 10^19 meters)/(0.5*10^-18 meters) = 1.3*10^36 bacteria on the earth.

Bacteria take time until they reproduce. If they reproduce faster than they grow, they will become reduced to zero size, so there must be a balance between growth and reproduction.

Under ideal conditions the E-coli bacterium would divide every twenty minutes. source

Let's say we have the maximum number of bacteria on earth dividing every twenty minutes. Somehow, they divide and then one dies so that the population is stable. (hypothetically)

The age of the earth is roughly 4.5 Billion years. Much of that time, it was not colonised, but just to give an upper bound let's assume it was colonized the whole time.

There are 525600 minutes in a year so this give

4.5 ^ 10^9 * 5.3* 10^5 = 2.385 * 10^15 minutes

Dividing by twenty minutes gives 1.1925 * 10^14 total reproductions.

Hence, the number of organisms that ever lived if the entire volume of the crust of the earth were entirely filled with e-coli bacteria reproducing at the maximum of every 20 minutes would be:

(1.2*10^14) *  1.3*10^36 bacteria = 1.56 * 10^50 bacteria

This is an highly exaggerated gross estimate of the maximum number of organisms that ever lived in the extreme best case scenario. In practice it is probably 5-15 orders of magnitude less than this but we get an idea of the kind of numbers we are dealing with.

UPDATE: A more realistic number

The number of bacteria currently on earth is about 5*10^30 forming a biomass which exceeds that of all plants and animals. source.

According to this source cited by the previous wikipedia article:

  Most of the earth’s prokaryotes (bacteria) occur in the open ocean, in soil, and
  in oceanic and terrestrial subsurfaces, where the numbers of cells are
  1.2 × 10^29, 2.6 × 10^29, 3.5 × 10^30, and 0.25–2.5 × 10^30, respectively. The numbers of heterotrophic prokaryotes in the upper
  200 m of the open ocean, the ocean below 200 m, and soil are
  consistent with average turnover times of 6–25 days, 0.8 yr, and 2.5
  yr, respectively. Although subject to a great deal of uncertainty, the
  estimate for the average turnover time of prokaryotes in the
  subsurface is on the order of 1–2 × 10^3 yr. The cellular production
  rate for all prokaryotes on earth is estimated at 1.7 × 10^30 cells/yr
  and is highest in the open ocean.

Hence we have about 1.7 x 10^30 New Cells/year

Multiply this by the estimated 3.5 Billion years (3.5*10^9) when the earth was colonized and we get

  5.95 * 10^39 Bacteria that ever lived. of course there were other organisms, but as above even the biomass of bacteria exceeds that of
  all plants and animals combined so their effect on this number is
  negligible. Likewise, the life conditions were surely not ideal at all
  times, so this number may be lower still.

For some perspective, the estimated number of atoms comprising all of planet earth is about 1.33 * 10^50 according to this source.

ESTIMATE OF NUMBER OF MAMMALS THAT EVER EXISTED

The upper bound for mammals is as follows.

The surface area of the land of the earth is 149 million square kilometers.

Let us consider if the entire land area of the earth was completely covered with mice.

A mouse is typically 10cm from nose to base of tail and about 5 cm wide=0.1*.05=0.005 square meters. So we get 200 mice per square meter.

Hence, if the entire land area of the earth were covered with mice the world population of mice would be:

149*10^12 square meters * 200 mice per square meter = 1.788 * 10^15 mice

Mice typically produce a litter of 6-8 young and a female can have 5-10 litters per year. source

Let's say we have this maximum population reproducing in a stable manner. i.e. for every new mouse, an old one dies.

Hence the total number of new mice per year would be:

1.8 * 10^15 * 8 young * 10 litters = 1.44*10^17 new mice per year.

Mammals appeared around 200 million years ago (source), so that makes

1.44*10^17 new mice per year * 200 million years

= 2.88 * 10^25 total mice.

In practice mice need space and resources and compete with other mammals which take up space and which reproduce less frequently. Likewise, deserts and polar regions are less inhabitable, and sometimes there are periods of droughts, and they don't always reproduce at the maximum rate etc. so the total number is probably about around 4-10 orders of magnitude less than this.

So it is probably something like 10^20 total mammals ever existed.


Are neurotransmitters part of the endocrine system? I was speaking with a substitute teacher of mine, and we were discussing whether neurotransmitters are part of the endocrine system or not. My class just spent an entire semester on the topic of the endocrine and nervous systems. From my knowledge, they are not part of the same system, because they function very differently and they are not activated by the same triggers. Does anyone have any info on this subject? I am interested what the case is an why.

Short answer
Synaptic signaling can be seen as a type of paracrine signaling, and is hence not an example of an endocrine system.

Background
Khan Academy has a nice accessible overview on this confusing topic:

Paracrine signaling
Signalling between nearby cells that are near one another van occur through the release of chemical messengers that diffuse through the intercellular space. This relatively short-distance communication is called paracrine signaling. Notable paracrine signaling occurs during development, where growth-hormone gradients regulate the differentiation of the various tissues.

Synaptic signaling
A unique type of paracrine signaling occurs between neuronal cells, namely synaptic signaling.

Autocrine signaling
Autocrine signaling refers to cell signaling to itself. Like paracrine signaling, autocrine signaling is important during development, but also in tumor metastasis.

Endocrine signaling
Communication over longer distances often occurs through the circulatory system is called endocrine signaling. Often it occurs through the release of hormones into the bloodstream. Hormones are produced and released by specialized cells and target cells in distant parts of the body. Endocrine glands include the thyroid, hypothalamus, and the pituitary, among others. For example, the pituitary in the brain releases growth hormone that affects growth and other functions throughout the body.

Juxtracrine signaling
Cells can also interact via direct contact. For instance, gap junctions in animals and plasmodesmata in plants allow for a direct communication between cells by forming tiny channels, allowing small compounds and ions to cross the cell's membrane to a neighboring cell. It occurs for instance in the brain.


Pyrimidine bases + genetic variation I don't understand this question, hoping someone can help!

One of the following bases does not belong among pyrimidine bases:
 - Uracil
 -  Adenine
 - Cytosine
 - Thymine

I thought that everyone was bases, expect that uracil is in RNA, and that in DNA it is replaced by guanine.

Also one more question:
Which of the processes would never contribute to genetic variation within a bacterial population?
 - Transformation
 - Meiosis
 - Mutation
- Transduction

I have a hunch that the right answer is mutation, but I don't know why. If you know the answer, it would be very helpfull if you could explain why :-)

You are correct - they are all bases. However there are two types of bases. Purines and pyrimidine bases. Purines have two ring systems, while pyrimidines have only one. With this hint, I think you will be able to find the answer to your first question.

As for your second question. Can you give me a definition for what a mutation is? I think if you are able to define this word you will know why that answer is incorrect.

Also, bacteria are incapable of performing one of the four processes that you have listed - and that particular process, is therefore the correct answer to your second question.


In Sanger sequencing, why do we resort to cloning? Why doesn't PCR suffice? I understand that in Sanger sequencing we can clone our fragments with the help of e.g. bacteria to make multiple copies of our fragments for further analysis.

I also understand cloning can be a bottleneck in Sanger sequencing - and partly prompted the development of NGS methods.

But doesn't PCR do just that, make multiple copies?

What am I missing?

The error rate of PCR is still very high in comparison to natural bacteria DNA replication of its plasmids.

Natural bacteria DNA replication has an error rate of approximately 1 in 10 billion, and the best PCR polymerase commercially available (Q5 from NEB) has an error rate of approximately 1 in 1 million.

Therefore, cloning fragments into bacteria and sequencing the cloned plasmids ensures that you have the correct sequence for further downstream experiments, since the error rate of natural plasmid replication is far lower. With PCR, you are likely to have some errors introduced due to the higher error rates. This becomes more and more likely with increasing numbers of PCR cycles as well as increasing PCR amplicon lengths.

The fact that the PCR amplicon sequences correctly does not mean that DNA cloned from the PCR amplicon is correct. Therefore, if the PCR is intended for downstream experiments, it is best to sequence the cloned plasmid instead of the amplicon.

In addition, as WYSIWYG has pointed out in the comment, having the PCR amplicon cloned into a plasmid would also allow for the plasmid's regions flanking the cloning site to be used for sequencing. This allows standard sequencing primers on the plasmid to be used, instead of having to design new sequencing primers for each PCR amplicon.

Furthermore, since Sanger sequencing requires the primers to bind ~50-100bp upstream of the region to be sequenced, cloning the amplicon into a plasmid would also allow short amplicons to be sequenced in a single read, instead of requiring a forward and reverse read for sequencing a PCR amplicon.


What is (roughly) the net charge of the DNA in an average human cell? I was wondering about what general range for the net charge of DNA in human cells is in Coulombs.  I imagine that kind of thing would be hard to measure but could be approximately calculated/estimated.  Could you approximate it by taking the average number of base pairs in the human genome and multiplying it by the charge of a phosphate group?  Would you have to multiply by two as well because there are two phosphate groups attached to each base pair?

That reasoning seems to work for Harvard's bionumbers database. They use a charge of -2 per base pair, and then estimate the linear charge density as 2e / 0.34 nm, where 0.34 nm is the length of a base pair. There are approximately 3.08 billion base pairs in the human genome, so you could run the same calculation: $2e \cdot 3.08 \cdot 10^9 = 9.86 \cdot 10^{-10} C$.


Why the total phosphorylation of certain neuronal proteins decrease during development? Looking at the effects of RIM1a which is a protein involved in neurotransmitter release. Any ideas as to why its total phosphorylation decreases as the rats develop?

Many thanks

Image; https://i.gyazo.com/16170fd79bd1f96517e028dfa2e70fbf.png

Paper; http://www.cell.com/cell/pdf/S0092-8674(03)00727-X.pdf

Here are a couple Wikipedia articles that might help out:

Critical period - Critical period: the idea that certain types of plasticity in the nervous system occur only at certain "critical" times.

Long-term potentiation - LTP, talked a lot about in the paper you linked: it's a mechanism for strengthening of synaptic connections.

Synaptic pruning - # synapses/strength of synapses tend to decrease from adolescence to adulthood

The paper you linked talks a lot about the role of phosphorylated RIM1a in LTP. Without knowing more specifically about this protein, and from just a glance at the paper you linked, I'd suspect that RIM1a is phosphorylated during periods of increased LTP, particularly earlier in development, and as animals age and their brains go into the synaptic pruning phase, LTP is downregulated overall, and one of mechanisms could be the lack of phoshporylated RIM1a.


Why does the human brain not overfit when training at some task? One of the problems that occur during (artificial) neural network training is called overfitting. The error on the training set is driven to a very small value, but when new data is presented to the network the error is large. The network has memorized the training examples, but it has not learned to generalize to new situations.

The human brain does not overfit when training at some task, but becomes better and better instead. Why? Or conversely, why do artificial neural networks overfit when are trained too much, in contrast with the human brain?

I would say the human brain overfits all the time! Gambling addiction,  superstition and anxiety disorders are all examples of overfitting. We are optimized for seeking patterns and avoiding threats. Our brains mess this up all the time! But having said that, one of the major differences between the human brain and a neural network is the amount of information that's being supplied. Neural networks overfit in part because of limited data sets. Our brains have nearly unlimited data sets available, and this provides us at least the opportunity for some self correction.


How much pollen is needed to pollinate a flower? Assuming 100% of the pollen gets delivered to exactly the locations it needs to pollinate a female flower, how much pollen is needed to pollinate a flower? If it's more than one unit of pollen, what, if anything, prevents more than one plant's pollen from pollinating the flower?

If we need an example plant to answer this question, let's assume zucchini. For instance, if you plant a zucchini in the middle of a spaghetti squash and an orange-fleshed squash, is there any likelihood at all that you'll get a single zucchini pollinated by both in one generation (such that the next generation of cross-pollinated zucchini would be both stringy and orange-fleshed instead of just one or the other)?

A single ovule in a fruit is pollinated by a single grain of pollen. So, in theory, a fruit with n seeds can be pollinated by n grains of pollen. In reality, of course, not every pollen grain makes it to the ovules, but if we treat your assumption as true, then a flower can be fully pollinated by as many pollen grains as there are ovules in the flower.

If you plant your zucchini and cross your zucchini flower with pollen from spaghetti squash and orange-fleshed squash, you will end up with a zucchini fruit filled with seeds that are either half spaghetti squash or half orange-fleshed squash. If you planted the seeds from that zucchini, you would end up with some individual plants that have spaghetti-squash traits and some with orange-fleshed squash traits. You would not end up with any plants with both stringy and orange-fleshed fruit.


Did birds descend from a single or multiple species of dinosaur? It seems like there are mixed results because sometimes I read about a single missing link, like an archaeopteryx that somehow single-handedly explains all modern-day birds, but then I see conflicting articles about how different birds are descended from different dinosaurs like a t-rex or a velociraptor and so on. Which theory is correct? Did birds all descend from one common ancestor or multiple?

The answer is "one common ancestor", but I'll expand.

All organisms descend from one common ancestor so that question is not quite well-posed, but what you are actually asking I think is whether birds all descend from one common ancestor that was a bird, or whether their common ancestor wasn't a bird, which implies that different branches of birds became birds independently. In other words, are birds a "polyphyletic" group or a "monophyletic/paraphyletic" one (the difference between the latter is whether all of that common ancestor's descendants are birds, or whether it also had descendants that aren't birds).

The answer to that is that modern birds are monophyletic: they all descend from a common ancestor that, itself, was a bird. (and that common ancestor doesn't have any descendants that aren't birds)

But modern birds aren't the whole story - their group originates in the Cretaceous, and there are many groups of birds that are clearly recognizable as birds but also aren't modern birds - they might have teeth, they have subtle but unavoidable skeletal differences, etc. Like Enantiornithes and Confuciusornis. In other words, modern birds absolutely, unambiguously have a common ancestor that was itself a bird, which isn't hard because animals we would recognize as "birds" were already common by the time it appeared and the ancestor of our modern birds was just one of them. Whether those older, "extended" groups of birds themselves descend from a single species is harder to tell because fossil evidence is all we're going on, and it's even harder to tell when we go closer to the origin of birds and they no longer look unambiguously like birds. But at that point it's not so much a matter of "did this group originate from one ancestor or several" but "are these fossils that we've been putting in this group as closely related as we were assuming?" and "did this trait that these different fossils have evolve in their common ancestor, or did they evolve it independently, and what about those other fossils that seem related but don't have the trait: did they lose it from the common ancestor who had it or are they a sign that the common ancestor didn't have it to begin with?". Like, you might get different answers depending on how you define "bird". BUT paleontologists these days like monophyletic groups, so whichever groups they call "bird", those will have a common ancestor that was a "bird".

The Wikipedia page for Avialae expresses some of the issues with what "bird", or "Aves" means in the context of paleontology. To quote:

  Aves can mean those advanced archosaurs with feathers (alternately Avifilopluma)
  Aves can mean those that fly (alternately Avialae)
  Aves can mean all reptiles closer to birds than to crocodiles (alternately Avemetatarsalia [=Panaves])
  Aves can mean the last common ancestor of all the currently living birds and all of its descendants (a "crown group"). (alternately Neornithes)

"Avialae" is one of those "extended groups of birds", in that paleontologists will often refer to any member of that group as "birds", but there's still a wide gap between "Avialae" and "Neornithes"; some stepping stones on that gap:

Neornithes (modern birds) are part of
Euornithes (birds have a certain articulation oriented like modern birds, as opposed to Enantiornithes, or "opposite-birds", who have it the other way, in addition to other differences like having teeth; note this page has a cladogram), which is one branch of:
Ornithothoraces (all descendants of the common ancestor of Euornithes and Enantiornithes), which is part of
Avebrevicauda ("short-tailed birds", to distinguish them from long-tailed Avialans like Archeopteryx) which is part of
Avialae, which as mentioned is basically birdinosaurs that could fly like Archeopteryx but it doesn't stop there because that's part of
Paraves, a group of dinosaurs that by and large had wings and feathers including the four-winged dinosaurs like Microraptor gui, which if we saw today we'd recognize as not like other birds but would we recognize as not a bird, really? That's part of
Pennaraptora, which is the first group to contain names that we definitely think of as not-birds; this group contains birds as well as Oviraptor and Deinonychus, but to quote the page:

  The earliest known definitive member of this clade is Anchiornis, from the late Jurassic period of China, about 160 million years ago.

And Anchiornis, as its name suggests, is bird-like, feathered wings and all. This is where we get into "wait, Velociraptors were basically like turkeys?" reactions (Deinonychus is Jurassic Park's "Velociraptors").

(also these points are where the groupings become disputed, or fast-changing, or ambiguous between groups that are defined based on phylogeny, or similarity, or others and you can get different results depending on which group's Wikipedia page you look at; for example the Wikipedia page for Theropods puts Avialae directly under Maniraptora).

Pennaraptora is part of Maniraptora, which also contains your velociraptors, and Maniraptora is part of Coelurosauria which also contains your Tyrannosaurs. At this point we have clear non-bird dinosaurs, although it's likely they all had feathers.

I don't know which articles you read saying some birds would have descended from T-Rex and others from Velociraptor; that seems completely counter to what we know today of bird evolution, even if we extend "birds" to "Avialae" or even "Paraves". In fact the only way it would work is if we call T-rex or velociraptor themselves "birds". What you could have is conflicting articles about how close birds are to T-rex or Velociraptor; that part of the family tree is based entirely on fossils and so new fossils can change our understanding of how things are related... But the current phylogeny that makes, say, Avialae a group that's quite a few nodes away from velociraptors, and both of those a couple of nodes away from T-rex, seems quite robust. We have found many, many bird and proto-bird fossils in the last few decades that have clarified the picture on that scale (you can get an idea of how many by clicking the various links).

One thing those many, many bird and proto-bird fossils also made clear is that the traits of modern birds (feathers, wings, toothless beaks, etc) didn't evolve in a simple line from non-bird to bird. Many of those traits evolved convergently in several lineages, were lost in some, maybe regained in others, and feathers in particular turn out to be a widespread dinosaur feature that cannot be considered a uniquely bird trait anymore (unless we want to call T-rexes "birds"). Still, saying "beaks evolved several times" or "feathers evolved several times" doesn't mean that birds, let alone modern birds, evolved from several different ancestors. It can mean that the common ancestor of birds had lots of variously bird-like more-or-less distant cousins living around the same time.


"bead" on a string theory of genetics, source? Thomas Hunt Morgan was a pioneer in genetics and proposed the now false model of genes being "beads" on a string. These beads being indivisible and responsible for a single phenotype, if I understand correctly.

Does anyone know of a good, reputable source of information on this theory that would be sufficient to use as a citation? I would use wikipedia, but it is disallowed.

If the Cold Spring Harbor Laboratory is considered a reputable source (it should be), you can check out their Defining the gene page which has an overview of the beads-on-a-string theory, and how it was disproved by Seymour Benzer. You could also try to find Benzer's original paper, although it doesnt seem to be available online.

Related and possibly helpful:

Benzer's page on Cold Spring Harbor website
Evolution of Genes and Genes in Evolution - very interesting paper from 1959 on genes/genetics, look on the fourth page (marked 18) for the bead-on-string theory


Are more molecules of ADP than inorganic phosphate returned to the light reaction in photosynthesis? During the dark reaction, 9 molecules of ATP are consumed for every 3 carbon dioxide molecules, yet only 6 molecules of inorganic phosphate ultimately leave the cycle. Does that mean that there is a greater concentration of ADP than inorganic phosphate returning to the light reactions?

Not 6, but 9 molecules of Pi are formed in the Calvin cycle, from the conversion of 9 ATP to 9 ADP:

Source: Columbia University


Can a bacteriophage be used to treat bacterial diseases? Some bacteriophages reproduce using the lytic cycle which ends with the destruction of the host bacterial cell. I was wondering if theoretically this could be used theraputically to treat bacterial diseases.

Yes, this is possible and is researched as an alternative to antibiotics. It has been used experimentally before antibiotics became widely available. Research was abandoned when antibiotics became widely available. See for example here and here for reports on this.

Today bacteriophages are researched for the treatment of bacteria which have a lot of resistances against antibiotics like Mycobacterium tuberculosis, Enterococcus faecalis, Staphylococcus aureus, Acinetobacter baumannii and Pseudomonas aeruginosa. See the references for more details (the first article also contains a nice historic overview of the field):

Bacteriophage Therapy
Bacteriophages: an appraisal of their role in the treatment of
bacterial infections
New ways to treat bacterial infections


CD spectra of Porin molecules? Can anyone please help me how will the CD spectra or graph of porin molecule look like. Porin molecule has 14 beta plated structures joined by some random coil, but it's very confusing to draw it. Can anyone please help me?

CD (circular dichroism) spectrum of porin will look like CD spectra of most beta-sheet-reach proteins. You can look, for example, paper on PorB protein (Minetti et al, JBC, 1998) where authors present CD spectra of one of porines:

Circular dichroism spectra of recombinant PorB class 3 protein as a function of SDS. Standard solutions of PorB rclass 3 protein (1.0 mg/ml) dialyzed against a buffer comprised of 10 mM sodium phosphate and 0.05% zwittergent 3-14 and incubated with varying concentrations of SDS (0-1%) at 25.0 °C for 24 h prior to spectroscopic analysis. Far UV CD spectra are recorded for rclass 3 in the absence of SDS (solid circles) and at the following SDS concentrations: 0.15% (open triangles), 0.25% (solid squares), 0.30% (open diamonds), 0.40% (solid triangles), 0.45% (open circles), 0.50% (solid diamonds), and 1.0% (open squares).


Why do cows (and other hooved animals) need a hierarchy? Clearly numerous animals have a hierarchy - hereditary one.  For example, I understand zebras have a pecking order, and must map this hierarchy from highest to first in line and lowest to last in line when traveling, and they can be brutalized for breaking this hierarchy.  (Interestingly, they allow looser rules for their young.)  (Reference.)

Cows apparently spend inordinate amounts of time with certain other animals, and avoid others still. (Reference.)

My question is: why do animals need the hierarchies and alliances?  Because human adults tend to make friends with people based on the kind of people they are.

I would imagine that they may have signals that indicate competing survival strategies (for example, a man with thick, tattoo covered arms vs a man in a tie) and that these likenesses try to propagate at the expense of others by forming alliances using organisms that possess these attributes (very vaguely akin to "the selfish gene.")

Or does it have something to do with advertised fitness?  I just have to wonder how grazing animals manage to compete over food.  Does it control access to reproduction?

Could not fit in a comment...

There are several issues with your question.

The correct question is not why such species need something but rather why it occurs in this species. In other words, why did a hierarchy evolved in a given species?
It is unclear to me why your are interest in cows (or other grazing animals) rather than any other species that has some kind of hierarchy and therefore your question is a bit unclear.
There are several questions in your post. A post should always be limited to one question.
I personally have never heard of the concept of "advertised fitness". How do you define it?
I am not sure how much you are interested in the evolution of social traits and especially about reputation and how much you are interested in Machiavellian intelligence. In any case, you may probably want to read about the evolution of social traits (kin selection, it may take you some time) and about the social selection pressures for the evolution of cognition, such as Machiavelian intelligence.

For all those reasons I vote to close. But I hoped that those comments can help you to clarify your post and to seek for more information.


Photosynthesis regulation I read about the regulation of Calvin cycle by thioredoxin which activates key enzymes essentially by converting disulphide linkages on inactive enzymes into sulfhydryls. Another regulatory mechanism is the pH control. The enzymes work at a slightly alkaline pH which is established as soon as the proton gradient is set up by the light reactions. But aren't these two mechanisms contradictory: at alkaline pH, the sulfhydryls $-SH$ groups, being acidic, will dissociate by giving up a proton and will be more stable in the dissociated form.
In general I fail to understand how pH will decide which bio-compounds will dissociate into proton or hydroxyl.

Your question conflates two separable events, a redox process and an acid-base dissociation.

The interconversion between disulfides and free sulfhydryls is a redox reaction, governed by the redox potential of the surroundings. The importance of redox potential to the -S-S- <> -SH equilibrium is illustrated by the difference between the cytosol and the lumen of the endoplasmic reticulum (ER). The cytosol is reducing and so free thiols are prevalent (there are usually no disulfide bonds in cytosolic proteins) whereas the ER lumen is oxidising, and the formation of disulfides in secreted proteins is promoted. The redox potentials of the two compartments is set primarily by the ratio between oxidised glutathione and reduced glutathione.

The thiol group in cysteine residues of proteins typically has a pKa of around 7, so it will indeed have some acidic character at slightly alkaline pH, dissociating to form a thiolate group. This doesn't however promote the reformation of disulfides, and in any case if it is important for a protein to have an undissociated thiol, then the environment of the specific cysteine residue can be adapted to raise its pKa. Note however that it is also possible that the thiolate form may be compatible with (or even required for) the function of the enzyme.


Do transcription factors bind to both strands of DNA? Do transcription factors (or generally proteins) bind to only single strand of DNA or both strands? Since it can have non covalent bonds to both strands in theory. I would like to know the mechanism. Any reference books, papers or links will be helpful.

The short summary is that typical TFs bind and read both strands together, as a basepair sequence. Some proteins instead recognise a site on the helix by its shape and flexibility. ssDNA-binding proteins obviously bind one strand but they do this in a non-specific manner.
RNA-binding proteins recognise the sequence on a single strand by inserting intercalating planar residues between bases! All of this binding is non-covalent.
Transcription factors recognise sites in dsDNA, with DNA-binding domains. The rest of the protein might surround (partially, to varying degree) the negative outer surface of the dsDNA double helix with positively-charged surface, in order to hold it on to DNA as it scans (perhaps) along its length.
DNA-binding domains: major groove

The following domains are found in many transcription factors, and they all recognise both strands. More correctly, they recognise basepairs and their orientation. The first 5 pages of this lecture slideshow demonstrate that the chemical groups on the side of basepairs, accessible in the major groove, allow proteins to distinguish A:T, T:A, C:G & G:C by the order of hydrogen-bond donors, acceptors, and a methyl group.
Hence, TFs recognise a sequence of basepairs - oriented such that one strand is (e.g.) pTpCpApG, and the complementary strand is pCpTpGpA; and the bulk of the protein may 'sit' on one strand or the other - or a nearby gene may locally define one strand or the other as the coding strand but this does not mean that this one strand is read.

Zinc fingers probe the major groove with reading helices.
Helix-turn-helix motifs do much the same.
Leucine zippers also do much the same.

These are common domains that all recognise basepairs in the major groove by interactions with residues on a probing aplha-helix.
TATA-binding protein: minor groove
TATA-binding protein (TBP) is a different, interesting case. It binds the 'TATA-box' via the minor groove, where the exposed chemical groups only distinguish [A/T] from [C/G], but not their orientation. This means that the sequences on each strand cannot be easily read from the minor groove. TBP instead recognises the shape and flexibility of the double-helix at the TATA-box, 'grips' it by the minor groove and bends the DNA, which aids the melting of the strands to the transcription 'bubble'.

The TATA-box sequence is usually pTpApTpApApA on the coding strand upstream of the transcriptional start. This is the convention when giving the sequence of a TF-binding site, but you couldn't say that TBP actually reads TATAAA - it doesn't!
Here is another, similar set of lecture slides.
Even better, here is the same material covered in a popular textbook.


Online phylogenetic tree of human lineages I am looking for a source of information about the diversity of human lineages and their relationships.

With a quick google search it is easy to find this type of tree

A perfect online resource would...

Contain a lot of lineages going to the most detailed lineages
Contain links to wikipedia or other source of information that could help someone to:

identify a group
have an overview of their culture

Contain visualization of their current (or past) geographic range.
Contain visualization of migration patterns
As mtDNA and Y chromosome may typically show different story, it'd be great if the resource would differentiate these and highlights specific cases where the two tree differ.

Can you recommend some online resources?

A review paper with nice graphs would also be welcome.

Related:

The post The best free and most up to date phylogenetic tree on the internet? recommend resources for visualizing the tree of life.
This webite offers a pretty amazing tree of religions.

Trees for haplogroups

See

https://www.eupedia.com/genetics/phylogenetic_trees_Y-DNA_haplogroups.shtml
https://www.eupedia.com/genetics/
focus on Europe: https://www.eupedia.com/europe/origins_haplogroups_europe.shtml

and many pages linked therein such as https://www.eupedia.com/europe/Haplogroup_J2_Y-DNA.shtml#subclades

and so on.

More detailed for mtDNA (female lineage):

https://en.wikipedia.org/wiki/Human_mitochondrial_DNA_haplogroup

and many links therein

More detailed for the Y chromosome (male lineage):

https://en.wikipedia.org/wiki/Human_Y-chromosome_DNA_haplogroup

and many links therein

https://en.wikipedia.org/wiki/List_of_Y-chromosome_haplogroups_in_populations_of_the_world and links therein
https://isogg.org/tree/index.html
and the Google Sheets linked therein
https://www.yfull.com/tree/

"Trees" for populations

Note that the trees are for genes/haplogroups, whereas such a "tree" for populations actually also has gene flow across branches. Imagine overlaying the tree for mtDNA (female lineage) with the slightly different tree for Y-DNA (male lineage).

Geography of migration

Migration and geographical distance played a key role in the emergence of distinct populations. See

maps of migration by haplogroups: Human migration by haplogroups, World map of Y-DNA haplogroups, Early human migrations, Simplified interactive map, And so on.
maps of distribution of haplogroups: mtDNA in Europe, Y-DNA in Europe, many of the links listed here, and so on

Also check out how theories about migration are changing. For example about mutation M174: theory around the year 2010 vs. theory since at least 2016.


How does the body really react to exposure to the vacuum of space? I've seen sci-fi movies where the effects the body being unprotected in outer space are wildly different. In one movie, a guy radios for someone who's been ejected into space to breath all the air from his lungs immediately. In some movies, eyes are pulled from sockets. In others, ice crystals form, and the eyes begin to look a bit red... Sometimes the exposed person is a goner right away, sometimes they're shown to last for a minute or more. The Hollywood portrayals of space exposure just vary tremendously.

So I'm curious, what really happens to the human body in the vacuum of outer space?

With regard to the vacuum - Apparently nothing happens as long as you don't hold your breath, just like you shouldn't hold your breath when ascending after scuba diving and the pressure drops. See NASA's answer to the same question. Of course there's the radiation that does other funny things in space, see the NASA link.


Do RNA modification proteins bind to specific repeats on the RNA polymerase II CTD? The C-terminal domain (CTD) of human RNA polymerase II has 52 repeats of a similar heptapeptide sequence.
Will the RNA modification proteins only bind to some repeats at specific locations on this (e.g. the 1st repeat/the 10th repeat/the last repeat, etc), or will they bind randomly to any of the repeats?
If they bind to specific repeats, how can this specificity achieved?
If they bind to any of the repeats, then it would seem to me that several molecules of an RNA modification protein could be bound to a single RNA polymerase II CTD. Does this happen?

In attempting to answer questions about protein structure, the first port of call (which one might expect the questioner to have also visited) is the Protein Data Bank — the global repository of such structures. There one can search for RNA Polymerase II CTD, look for complexes with other proteins, find recent publications in which they are reported, and consult them to find the state of knowledge of a topic.
Knowing nothing of the protein in question, I adopted this approach, and after looking at a few proteins and a few papers the following points seemed to emerge.

The CTD has a series of 7-amino acid (heptad) repeats — in mammals 21 of these are consensus(YSPTSPS), and 31 non-consensus (K7, rather than S7).
Further heterogeneity is afforded by phosphorylation (especially) and also glycosylation and proline isomerization, together with modification of the lysine of the non-consensus repeats.
It is thought that different post-transcriptional modifications are responsible for differential activation of 5′-capping or 3′-processing enzyme activities.
The CTD is disordered (unresolved) in the crystal structure of RNA Polymerase II, indicating that in the protein itself it does not adopt a fixed structure.
There are no structures of the CTD complexed to proteins it activates, so the question cannot be answered definitively.
There are structures of proteins complexed to short peptides (10- to 19-mers) based on the repeating sequence. These suggest that the structure of CTD in the complexes may be a spiral bound by specific interactions in a groove. The spiral formation may involve hydrogen-bonded β-turn motifs. A deduced structure from one such study with a 10mer is shown, together with indications of specific protein–protein interactions.

(Phosphorylated 10mer based on CTD complexed to the conserved CTD-interacting domain of mRNA processing factors RPRD1 and 2 — Adapted from Ni et al., Nature Structural and Molecular Biology (2014) 21, 686–695)
Concluding Remarks
The question contains two invalid assumptions — that proteins that interact with the CTD should interact with a single repeat, and that repeat should have a compact structure. Nevertheless, the functionality of the repeats and whether there are multiple interactions are valid questions. It appears from discussion in the paper by Ni et al. that the interacting unit is a 24-mer that binds to a dimer of the interacting protein (CID), and they propose that for phosphatases (and I presume protein kinases)15 molecules interact with the CTD at once.
What the situation is with 5′-capping or 3′-processing enzymes is another matter. There will only be one mRNA emerging from the RNA polymerase, so multiple binding would appear to make no sense. How much of the CTD is needed as rope to attach the processing enzyme soap? Does the soap slide along the rope? One would hope that eventually such questions would be answerable by molecular visualization techniques (see e.g. this BioRxiv preprint).


Help Identifying Tree I live in the upper southeastern region of Arizona in U.S. There's a type of tree growing in my back yard that I can't seem to identify. Its growing in an arrangement very similar to an ocotillo plant.  It has single spiny stems coming up out of the ground.  They don't branch out but have large sharp spines with leafs growing out of them.  It doesn't look anything at all like any of the native desert plants in the area.  There's mesquite and sage and various types of cactus.

At the moment the stems are about five feet tall.  I took clippings about two feet in length and photographed them.  It seems I'm only able to post two links so I've chosen the clearest images that I have.  I'm very curious as to what this is and any help would be greatly appreciated.

It looks like this could be Lotebush, Ziziphus obtusifolia. The thorny branchlets and blue-green color (at least, as it appears in the photos) suggest Ziziphus to me, although you could compare it with the photos or description here. If it is in the buckthorn family, it does seem to key out to Ziziphus using the Christie et al. key.

If you wanted to be sure, you could follow up with the ASU herbarium (see citation).

Christie, K., M. Currie, L.S. Davis, M.-E. Hill, S. Neal and T. Ayers (2006). Vascular Plants of Arizona: Rhamnaceae. Canotia 2(1): 23-46. Open access


chaperone protein names I am studying chaperon proteins DnaK, DnaJ etc. This question sounds trivial but I would like to know what the acronym stands for. I have looked on google/google scholar. My best guess is that the name comes from the fact that these are genes whose products are necessary for bacteriophage DNA replication. Can this be confirmed? The full name of GroES and GroEL may also be helpful. Thanks!

DnaK: the recommended name is Chaperone protein DnaK; the alternative names are HSP70, Heat shock 70 kDa protein, and Heat shock protein 70 (source: UniProtKB); the name of the protein, DnaK, is derived from the name of the gene, dnaK (Yochem et al., 1978, Mol Gen Genet. 164: 9-14):

  We show that a collection of 93 E. coli mutations which map between
  thr and leu and which block phage lambda DNA replication define two
  closely linked cistrons. Work published in the accompanying paper
  shows that these mutations also affect host DNA replication, so we
  designate them dnaJ and dnaK; the gene order is thr--dnaK--dnaJ--leu.

To find the recommended and alternative names of GroS and GroL, search UniProtKB . . .


What Kind of Bug is This I found this bug in southern Florida in February. It was approximately 1cm long or less, fully extended.  What type of bug is this?

It's probably the larval state of a tortoise beetle, or a closely related beetle. They are known to build a "faecal shield" at the end of their tail, sometimes including shed exoskeleton and any debris that sticks to it. They hold this shield over their bodies for defensive purposes that aren't fully  understood.
Lacewing larva look somewhat similar and also cover themselves with debris, but their legs are longer and their head and mandibles look quite different.
Here's an image of a thistle tortoise beetle larva:


Is it possible to still grow taller after growth plates have been closed? In addition, when do we know we stop growing taller? Or we keep growing taller?
To the first question:
Recently, I went to a doctor to have a check up, he said that my growth plates are closed and cannot grow taller anymore. True or false? Is it possible to have a second growth spurt. I am about 16.

No, because growth only occurs at the epiphyseal plate or growth plate. In the picture here, the epiphyseal plates are the two horizontal lines in the tibia and fibula, and bone growth occurs in the upward direction, or toward the middle (shaft) of the bone. Once the epiphyseal plates close, the bones can no longer elongate.

It's possible to have a second "growth spurt," but it's only because the epiphyseal plates haven't closed. David Robinson, the basketball player, was 6'7" as a senior in high school, but ended up being 7'1". The "growth spurt" is caused by the sex hormones, which is why a significant amount of growth occurs during puberty.