Composition of E. coli (dry weight): 55% protein, 20% RNA, 10% lipid, 15% other
Protein concentration is about 100 mg/ml or 3 mM. From the size of an E. coli cell, 1 nM is about 1 molecule/cell. This is ~1000 molecules/cell for HeLa cells.
Diffusion coefficient for an "average" protein: D ~ 5-15 microns^2/s, or ~10 ms to traverse an E. coli. For reference, a small metabolite in water diffuses about 30-100x faster.
Reference: Cell 141:1262, Key Numbers in Biology
This question has no particular answer. There are several families of DNA binding proteins, some of them bind specifically (e.g. restriction enzymes like EcoRI which binds to and cuts GAATTC or transcription factors like lac repressor which binds a particular point of the e coli genome about 25 base pairs long) and some of them bind semi-specifically (e.g. zinc fingers which bind GC rich regions), others non specifically (e.g. the sliding DNA clamp).
For all of these proteins, they will have a tendency to have positively charged amino acids facing the DNA because the DNA's phosphate backbone is negatively charged. There are lots of protein motifs (like the helix turn helix motif) that fits into the major or minor groove of the DNA. The lysine and argenine are important because they are the positively charged amino acids. Histidine is also positively charged, but it is not as long and flexible, and doesn't seem to fit as often or as well.
The ribosome moves relative to the mRNA by, in effect, pulling itself along it. If both the ribosome and the mRNA are freely floating and not attached to anything else (as in jp89's answer), the relative amount of movement should depend on their relative masses.
(Actually, it also depends on how much drag each of them experiences with respect to the surrounding liquid medium, but since I have no idea how much that is, and since it's probably highly conformation-dependent anyway, I'm going to just ignore that and just assume that the drag is also more or less proportional to mass, at least to first order.)
As it happens, a quick Google search and some back of the envelope calculation suggests that the mass of a ribosome and the average mass of an mRNA are both around a megadalton. Of course, the length (and thus the mass) of an mRNA varies quite a lot, so it would seem likely that sometimes it's the ribosome that moves mostly, sometimes it's the mRNA, and sometimes it's both.
Also, as shigeta and others have pointed out, there can be more than one ribosome attached to the same mRNA strand. That's going to make the mRNA move more (and, correspondingly, the ribosomes move less), since there are more ribosomes pulling it along.
Then there's also the protein being transcribed, which is attached to the ribosome but also being moved with respect to it. And I really have no idea how negligible the interactions with the tRNAs and so on are. It's a mess, but my guess would be that, usually, it's mostly the mRNA that moves, but that the ribosomes aren't completely stationary either (unless they're attached to something, of course).
Ps. Here's an exercise for you, which you may try out if you happen to have a friend who works at a public swimming pool. Otherwise consider it a gedankenexperiment. You know those floating ropes that separate the lanes in the pool? Try getting your friend to let you into the pool when it's not in use and to release one of the ropes from the walls. Then get in, grab the rope with your arms and legs and try pulling yourself along it. While doing so, try to decide whether it's you or the rope who moves more. (Also, to more closely approximate the Reynolds numbers involved inside a cell, imagine doing this in treacle instead of water.)
By programmable, I suppose you mean that it contains information or can be altered in response to some input or stimulus. The answer is "no" for both. Well, sort of.
Does noncoding DNA contain information? By definition, no. There are probably many regions of the genome that appear to have no information, only later to be found to contain introns, regulatory elements such as enhancers, boundary element, MAR/SARs, targeting sites, etc. Even functional tests (such as removing the region) may not reveal anything because the effects could be minor, or only evident under special conditions. But arguably, if you remove a region and it has an effect on the organism, then it's not really a noncoding DNA, it's just you didn't see the coding before hand.
As for the latter, can it altered, the answer is again "no," or at least "apparently not." Intergenic regions (those stretches of DNA that do not contain obvious or characterized transcribed regions or their control elements) are very stable between organisms and even between species. They seem to have a mutation rate expected for having no information, and thus free to mutate slowly without being swept away. There is no evidence (as far as I know) of any region of the genome being purposefully altered, with the exception of a handful of specific genes whose regulation is controlled by DNA nicking or some such.
Perhaps I am missing your question, being a biologist and not really knowing what a "Turing Machine" is. If I misunderstood, please clarify.
Pigliucci gives a good review of some aspects of this topic in "Is evolvability evolvable?" (2008). He sees what you're asking about, which he calls "evolvability", as one of the key topics for the future of the study of evolution.
It's very conceptually dense evo-devo-theory, so I'll probably do a poor job trying to explain it, but he tries to set up a framework that deals not just with things like life-history (per kmm's answer) and mutation/recombination rate (low fidelity in HIV per GWW's answer, and, I suppose, the evolution of sex itself), but also with constraints that evolve at various levels to "positively channel" mutation (that is, the understanding that while mutations are effectively random, the phenotypes that emerge, and are acted upon by natural selection, are not random, but are channelled by the developmental system of the organism).
He also includes the role of development in opening up "phenotypic space" into which a lineage may evolve. For instance, single-celled organisms have a limit on size and complexity, the evolution of multicellularity opens up this huge zone of evolvability. In a sense, this is also the "evolution of evolution".
My understanding is that gene expression, in response to some stimulus, generally occurs on the order of minutes. I'm curious about the extremes...the quickest and the slowest cases.
What is(are) the fastest time(s) recorded for genes being expressed in response to a stimulus? What are the slowest times?
I like your question!
Low surface pressure on Mars (averaging 600 Pa or about 1/170 of Earth's at sea level) is only one difficulty that an organism would have to contend with. In addition, mean surface temperatures are ~210 K (-63 C), the surface ultraviolet flux is extremely high (no ozone layer) and an aridity comparable to the Atacama desert. On the plus side, a 95% CO2 atmosphere might promote photosynthesis.
So, higher plants are extremely unlikely to prosper on Mars. Purely in terms of pressure, experiments suggest that at 1/10 Earth atmospheric pressure vascular plant transpiration increases significantly. So much so that they enter into a drought response which often leads to plant death.
However, lichens may be another matter. These are often adapted to low precipitation/pressure environments such as high mountains. Indeed, this article addresses exactly your question (sadly it is not open access). The authors suggest that the lichen Xanthoria elegans experiences no loss in vitality after 22 days exposure to laboratory Mars-like conditions (low pressure, low temperature etc.)!
Having skimmed this article I am frankly amazed (and slightly dubious) at the result. However, it should be noted that they only ran the experiment for 22 days, applied no ionising radiation (to simulate the high UV flux) and make little mention of the precise metabolic state of the lichen. If it has entered into cryptobiosis (cessation of metabolic processes) then it can't exactly be regarded as prospering.
Of course the sphincter muscle is at the exit point. To use a toothpaste tube analogy, if I want to squeeze out some toothpaste, it does me little to no good to jostle the nozzle; I need to squeeze the tube (which is analogous to the colon) to get the paste (payload) to come out.
So when a human is sitting on the toilet squeezing, is that squeezing flexing of the sphincter, or squeezing muscles along the sides of the colon pushing on it as one's fingers push on the tube to get toothpaste to come out.
If it's the sphincter that's getting flexed, how is that helping get a big log out?
Really good questions. As the guy who brought up LTP/LTD in the question you referenced, I thought I would weigh in.
There is the traditional definition of LTP/LTD as an increased/decreased synaptic efficacy at a single synapse or in a single cell. As you've noted, this is unlikely to be the only phenomena underlying memory and sometimes it's hard to see how some of these mechanisms can result in memory on behavioral timescales.
Let me propose, therefore, that the term long-term plasticity is more relevant these days, as it can refer to a variety of mechanisms that relate to the ability of the nervous system to change in stable ways over time. Physiological mechanisms involving changes in protein expression include traditional LTP/LTD at single synapses, but also homeostatic plasticity and long-term changes in intrinsic excitability where the tendency of the cell to fire changes independent of changes in synaptic weighting. Some structural mechanisms include the growth of new synapses, new spines, and new neurons--synaptogenesis, spinogenesis, and neurogenesis.
In the end, it is all of these mechanisms (and probably more) at play. Note, for instance, that the plasticity may move through structural changes in the system. This means that the lifetime of LTP in one cell or at one synapse does not necessarily have to be the same as the lifetime of the memory itself. All that said, I think all plasticity mechanisms ultimately reduce down to a change in the ability of an input to elicit an action potential somewhere in the brain (known as EPSP-spike coupling). This is likely to be the basic underlying mechanism of memory.
I regularly encounter students who believe humans came from amoebas and when asked why they often say Macro-Evolution has been scientifically proven.
Macro-evolution is defined as evolution at or above the species level, which leads to the problem: Scientific evidence does exist for speciation at the Biological Species Concept (BSC) level, but not for all species concepts and only if a helpful definition is employed. Lions and tigers are considered different species and have been know to reproduce--sometimes with fertile offspring. Therefore, what benefits are there to such a broad category as macro-evolution?
The distinction between lions and tigers is so much smaller than feathered vs. scaled creatures! Surely the current definition of macro-evolution is overly broad and confusing to newcomers. Only the fuzzy edge of the macro-evolution definition has been proven. Proving that 1 inch of a yardstick exists does not prove that the rest does. There is a distinct lack of rigor to the statement that "macro-evolution has been scientifically proven."
Surely the definition of macro-evolution could be chopped in half with the goal of distinguishing between relatively trivial changes (Lion vs. Tiger, but beyond micro-evolution) and relatively non-trivial distinctions (either at and above the genus or the family level). The "trivial" changes could be termed "Middle Evolution" and work something like this:
1.) Middle evolution: evolution at or above the species level, but below the family level.
2.) Macro evolution: evolution at or above the family level.
Substitute the word genus for family in the above definitions if that seems better. I admit that line would be somewhat arbitrary, but would not the term "Middle Evolution" be informative?
I was given an explanation that birds and reptiles are polyspermic because they have an abundant yolk sac. But how does it explain the thing?
Chicken as an adult is not using in my opinion yolk as an energy source.
Yolk is used during embryogenesis as the primary energy source with blastula and gastrula -stages and during organogenesis, since the embryo needs proteins and energy somewhere.
How does abundant yolk sac make birds and reptiles polyspermic?
There have been some studies regarding the use of intensive UV light installations in surgical wards or other settings as a anti-microbial tool. Generally speaking, these are part of a general interest in non-cleaning based anti-microbials in hospitals, such as UV light, O3-based machines, and copper/silver coated surfaces.
The answer to your question will depend on what you consider "lasting" and "significant". They're a relatively new technology, and haven't had a huge penetration into the market yet, so the only evidence you're likely to find is hospital-sized non-randomized trials.
So basically, the answer to your question, as I read it, is "No, but..."
There hasn't been an opportunity for these technologies to show any sort of lasting, significant reduction in hospital acquired infections. But there is some promise that these types of technologies, and those like them, may help reduce the burden of infections when they're used appropriately. The current state of research is figuring out just how workable they are, how to best use them, and what they can and cannot be expected to do. That kind of evaluation is actually what I'm doing as part of my dissertation work, though my focus is on the general concept, rather than a specific device.
Not sure if generalized plasmid taxonomy is going to be relevant any longer. A lot of these old names were created before the exact sequence and function of the various DNA sequences were known. This is becoming especially true as synthetic biology allows us to mix and match parts of plasmids at will. If you want to dig through a lot of the old plasmid classification papers, a lot of them are published before 1980.
Back then I'd imagine conversations went more: "oh look, I found an R plasmid conferring ampicillin resistance", instead our more modern understanding: "oh, I have a plasmid conferring ampR via bla "
That being said, I think the more specific / specialized plasmid classifications will stick around for a while as they confer a lot of domain specific meaning. Check out Ti and Ri plamids which have very specific meanings in plant pathogens and are used in the genetic engineering of them. You'll notice that the classification for these plasmids comes from a lot more than a single gene.
There have been some modern attempts to classify plasmids, but rely a lot more on the structure / lineage of the plasmid rather than the payload genes (replication origin, size, etc.). Check out [1] for an example.
This is basically the same that happens after pruning and involves a basic hormonal regulation mechanism in the plants.
What happens is that the cut piece of the wood forms a new meristem which allows the growth of new organs. What’s important is that there is no other growth happening nearby, since that would hormonally inhibit any further growth. This is why such growths happen once you’ve cut the wood, not before (on the healthy stem). This inhibitory effect is known as apical dominance, which has now been disabled.
As to where the energy and water comes from, to some extent it is stored within the branches themselves. That’s why you need to dry them before being able to use them in a fire. However, this growth is pretty limited. Further water is probably collected by condensation of water vapour in the air.
Intrinsic termination (rho-independent) relies on a stable hairpin with a subsequent uridine repeat. The common explanation on how these sequences cause the termination of the transcription are based on the thermodynamic stability of the sequence. The GC-rich stable hairpin together with the destabilizing U-repeat supposedly destabilize the binding of the polymerase enough to cause it to disassociate from the template.
What I'm looking for are specific requirements on the termination sequences that are not based on thermodynamics.
The typical requirements I read are 5-14bp and GC-rich, and I'd like to know if there are any more specific requirements, especially ones related to the structure and not the stability of the hairpin.
There is some evidence to support the idea that sodium benzoate may be detrimental to the development of the foetus:
TERATOGENIC EFFECTS: Classified POSSIBLE for human.
DEVELOPMENTAL TOXICITY: Classified Reproductive system/toxin/female, Reproductive system/ toxin/male [SUSPECTED].
This has been shown experimentally in rats by Minor & Becker in 1971. They introduced high doses of up to 1000 mgkg-1 intraperitoneally and recorded reduction in foetal weight and "gross anomalies". Whilst I struggled to find a copy of their original paper, it is referenced in the Catalog of Teratogenic Agents1 (Thomas H. Shepard).
There is some evidence to refute this, however. The Acceptable Daily Intake limits on sodium benzoate is a maximum of 5mgkg-1, at this dose there is no noticeable effect of exposure. (2,3) The latter paper by EC food safety standards goes further:
There appear to be sufficient studies to conclude absence of teratogenic potential, with an overall NOAEL* for developmental toxicity of 500 mg/kg bw/day, based on effects on fetal weight.
*(No observed adverse effect level)
So the consensus from the food safety bodies suggests that E211 should not pose harm to an unborn child in the quantities allowed to be present as an additive.
1 Emire, Ronald J. "306: Benzoate, Sodium." Catalog of Teratogenic Agents. By Thomas H. Shepherd. JHU, 2004. 44-45. Google Books. Google. Web. 10 Feb. 2012.
2 Nair, B. "Final Report on the Safety Assessment of Benzyl Alcohol, Benzoic Acid, and Sodium Benzoate." International Journal of Toxicology 20.3 (2001). International Journal of Toxicology. Web. 10 Feb. 2012.
3 Scientific Committee on Food. Opinion of the Scientific Committee on Food on Benzoic acid and its salts. Rep. 24 Sept. 2002. EUROPEAN COMMISSION HEALTH & CONSUMER PROTECTION DIRECTORATE-GENERAL. 10 Feb. 2012
I can't give a definite answer, and there's nothing in the literature about this specifically, but perhaps some relevant information and a suggested behavioural experiment will help.
Background
Firstly, I assume you are talking about sodium hypochlorite (which is usually what people mean by bleach)? If so, there are several compounds your cat could be reacting to. Chlorine is an obvious candidate, which is released as sodium hypochlorite decomposes in solution. Additionally, bleach can react with various organic materials to release a variety of volatile organic compounds (VOCs), which your cat might be able to smell. In addition to also releasing chlorine gas, the same suite of VOCs are released when the chlorine in chlorinated tap water reacts with organic contaminants (Odabasi, 2008). The VOCs include chloroform and carbon tetrachloride.
Next, cats are known to exhibit modified behaviour in response to a variety of compounds. Some are suspected pheromone components of cat urine, such as felinine (Hendriks et al, 1995) and its breakdown products, such as MMB (Miyazaki et. al, 2006).
Some cats also react to externally-produced compounds with a particular response called the 'catnip response', which involves rubbing the face on the ground or other objects, shaking the head, rolling, etc. (Tucker & Tucker, 1988). Not all cats exhibit the response, around 50-50% do, and susceptibility is genetic and heritable. Some sources eliciting the catnip response include:
In general all the catnip response elicitors share a two-ring structure, which is not to my knowledge shared by any of the volatiles given off by bleach.
A possible experiment
So, two obvious possibilities (regarding what type of behavioural response is being elicited) are that either:
As a first experiment, you could check whether your cat (and any others you can get hold of - in an ethical way) respond to bleach and/or to catnip. If the cats do not exhibit the catnip response to catnip, they aren't exhibiting it in response to bleach, and thus some other explanation is more likely.
As a second experiment, you could make a detailed observation of the precise behaviour shown in response to bleach. Compare it to that exhibited when the cats encounter catnip (depending on the outcome of the first experiment) and when they are oestrous (if female) or encounter an oestrous female (if male). You could also compare to the response to the urine of other (male and female, familiar and unfamiliar) cats.
An experiment you shouldn't do
If you wanted to find out which chemical your cat is responding to, you could allow your cat to sniff pure chlorine which hasn't encountered organic contaminants, as well as chloroform, and carbon tetrachloride. However, all three of those compounds are extremely dangerous and could easily kill you or your cat, so please don't.
I general, I would caution against exposing your cat to bleach, because it can induce serious health effects depending on dose and mode of exposure, ranging from asthma to third-degree burns to carcinogenesis. If they are attracted to it, that is a good reason to keep it away from them to prevent them ingesting it, which is more harmful than inhaling the fumes.
I can't comment on whether the behaviour is acquired as result of domestication, but that too could be tested by comparing the reaction of a large sample of wild cats (!).
References
Well, if we look in very basic detail at how muscle contraction works within a myofibril of the sarcomere:
N.b. this isn't on a loop and only plays through seven times
The red lines represent actin filaments whilst the blue lines represent myosin filaments. During muscle contraction the filaments move over each other:
As shown in the above diagrams the "more contracted" a muscle is then the smaller the size of the H zone (the area where there are just myosin filaments).
So if we consider a penetrating impact that went through a plethora of identically aligned sarcomeres (obviously this is not the case in nature) then we could presume that (et ceteris paribus) the object would not penetrate as deeply into a contracted muscle as it will hit more tissue on its route than in a relaxed muscle.
It really depends on what you consume, how much of it you consume, and the state of your immune system. Let me give you some examples. Yogourt is full of bacteria, and yet we can eat it without issue. The bacteria likely don't survive digestion, but if they do, they will quite happily live in our intestines contributing to the already existing population of good bacteria.
Streptococcus is a genus of bacteria that contains some species that live all over us. They are on our skin, in our upper respiratory tract and intestine. If the species, S. pneumoniae makes it into our lungs, this can cause a bacterial pneumonia. There are likely few bacteria making it into our lungs on a regular basis, and normally our immune system can fight this off without concern. If we some how become immune depressed or compromised (for a number of medical reasons) then that's when we become symptomatic and ill.
On a more extreme side, if we have a bacteremia it is called a bacteremia. There are benign cases of this every time your brush your teeth and bacteria are able to enter tiny cuts in your gums from the brushing action. A healthy person fights this off. If a bacteremia is left unchecked, because of a lack of immune response or trauma, this can develop into a sepetcemia, a toxic infection of the blood. This can be very life threatening and is quite serious.
In general, we always have bacteria all over our hands which we likely transmit to our food or otherwise ingest. This is normally not a problem, but there is an appreciable risk of getting some kinds of viral or bacterial infection (eg, strep throat or a cold). Washing with soap (and to a lesser degree, using hand sanitizers) minimizes this risk.
I have had a little time to look over this paper.
They do overexpress a native sir2 clone in high doses, called sir2.1 OE. Which seems to be native and also appears in high copy numbers. This strain was found in previous publication to have a high lifespan... that is old news.
This paper sees sir2.1 expression levels as an oversimplification of the causes of longevity. When they create crosses of the sir2.1 OE strain with wildtype, you can see the Outcross, which is verified to have a high level of sir2 expressed no longer has an extraordinary lifespan.
This can be seen in Figure 1. http://www.nature.com/nature/journal/v477/n7365/fig_tab/nature10296_F1.html
So this paper is now asking, if sir2 levels do not convey the information that creates an extended lifespan, then what does? It must be some modulation of some protein that sir2 affects. They implies that the actual cause of the lifespan increase may have been a mutation somewhere else in the organism.
"However, longevity was not suppressed by sir-2.1 RNA interference (RNAi) ... indicating causation by factors other than sir-2.1, either on mDp4 or elsewhere in the genome."
"This implies that lifespan extension is due to transgene-linked genetic effects other than the overexpression of dSir2."
In the second half of the paper (figure2) the investigators have moved on to drosophila work, where they look at how expressing constructs or inhibiting sir2 protein levels might affect lifespan. Although the dSir(EP2300) / + construct (drosophila sir2) with a wild type gene promoter did not live quite as long as dSir2(EP2300) with a fancy promoter (dSir2(EP2300) / tub-GAL4), the promoter construct (tub-GAL4/+) alone also had just as long a lifespan. How can this be? Not sure, but the expression of sir2 is clearly not the panacea we had hoped. Note however that the reduced power gene still gave the same boost to lifetime. This shows dramatically that sir2 activity alone does not drive the longer lifetime.
Lastly, deletion constructs (dSir4.5/1.7) , which should have lower than wild type protein levels for sir2 had completely normal lifetimes.
So the answer to your question; you need to test a hypothesis going in both directions - does increase of the protein really create a strong effect? Does decreasing it have a negative effect then? There are lots of other reasons to use knockouts and non functional genes in such an experiment, but those are the broad strokes.
Various people in our lab will prepare a liter or so of LB, add kanamycin to 25-37 mg/L for selection, and store it at 4 °C for minipreps or other small cultures (where dosing straight LB with a 1000X stock is troublesome). Some think using it after more than a week is dubious, but we routinely use kan plates that are 1-2 months old with no ill effect.
How long can LB with antibiotic such as kanamycin, chloramphenicol, or ampicillin be stored at 4 °C and maintain selection?
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 problem you are looking for is called the "Nature vs nurture" debate. Lots of scientists have written lots of books and papers and done lots of studies on the subject. As you can see, the title of the debate already includes the two main concerning factors: nature (genes) and nurture (environment).
These of course each include a variety of ways in which they influence personality. Genes provide the biological basis for your personality, they determine how everything in your body works1. At the same time, these genes build a system that has a life of its own - your brain.
It consists of neurons, and nobody knows how personalitites comes about from them exactly but somehow they do. Neurons reshape all the time in ways that no other cells do. The connections between them, synapses, are formed, destroyed, reinforced or weakened all the time - in response to things that take effect on them, for example the things that you see and hear, smell, taste and feel. A very interesting subject in this field is the study of neuronal networks, giving some insight into how memory and learning may work.
But while this may seem like external factors must then be more important for personality, it depends on the setup provided by your genes how your neurons respond to certain influences - what concentrations of neurotransmitters they produce and secrete etc.
As you can see, the only thing that is really safe to say is that it is not "either or", both definitely play a role.
1But even the biological development of the body has non-genetic influences - at the moment I can think of epigenetic inheritance though this seems to be disputed (see comments). Apart from that as far as I know there are uterine influences on embryonic development. And then there are the more or less obvious external influences such as cutting things off before they develop.
One of the important pigments that the earlier answer hinted at is melanin. Melanin is a brown pigment with photoprotectant properties.
As you correctly identified in your question, exposure to EM radiation (particularly UV and shorter λ waves) is damaging (indirectly) to DNA, which can cause mutations and therefore possibly cancer. Melanin production is one of the defence mechanisms the body has evolved to deal with this threat.
When DNA is damaged by the UV-B radiation, melanogenesis (the increased production of melanin pigment) is induced.(1) Therefore, people often exposed to more UVB (i.e. in sunnier climates) are likely to have more melanin in their skin, which makes it appear darker in colour. It is likely to be the increased incidence of melanin proteins in your skin which leads to the formation of a tan.
Melanin and its derivatives work as photo-protectors (protecting the body from the damaging effects of ultra-violet exposure) by absorbing UV-B photons and converting them into much less damaging infra-red wavelengths (heat energy). It does this extremely rapidly by internal conversion and extremely efficiently - efficiency in excess of 99.9% has been reported.
As the melanin removes the danger posed by the UV within a few femtoseconds (x10-15 s), the more melanin that is present in skin tissues (and consequently the darker the skin), the lesser the chance of the UV damaging molecules in the skin so the lesser the risk of developing skin cancer.
I found the link to a commercial product by Evrogen to normalise cDNA samples for gene discovery projects here:
http://www.evrogen.com/technologies/normalization.shtml
The most up-to-date reference seems to be this Curr Protoc Mol Biol. paper by Bogdanova et al.:
http://www.ncbi.nlm.nih.gov/pubmed/20373503
They claim their method is compatible with nextgen sequencing platforms:
cDNA normalization using duplex-specific nuclease (DSN) is a highly
efficient approach that can be applied for normalization of
full-length-enriched cDNA (Zhulidov et al., 2004; Zhulidov et al.,
2005). The resulting cDNA contains equalized abundance of different
transcripts and can be used for construction of cDNA libraries and for
direct sequencing, including high-throughput sequencing on the next
generation sequencing platforms (Roche/454, ABI/SOLiD or
Illumina/Solexa).
Has anybody successfully used it for next-gen gene discovery projects?
It's a spatial constraint. As the DNA is replicated, the two resulting chromatids are kept stuck together by cohesin proteins. The DNA sequence that corresponds to the centromere then coalesces the kinetochore. It seems that the DNA-protein interactions at the centromeres creates a particular structure along the chromosome. Since the two chromatids have their kinetochores pointing in opposite directions, when a spindle microtubule attaches to the kinetochore, it is nearly impossible for another microtubule from the same spindle to attach to the opposing kinetochore.
Having read this article on tool use in Chimpanzees in full, I am inclined to say that if such a term existed then either the article itself or the titles of any of the 30 articles referenced would have included it.
Searching a couple of online biological dictionaries and ethology sites hasn't yielded anything either, therefore until someone else points out that I'm missing the obvious I'd say you're free to coin the term yourself!
To answer this question in its entirety we have to split it into two questions:
What are the underlying mechanisms of carcinogenity?
One of the main mechanism behind carcinogenity is the mutagenity of the cancerogens, i.e. the ability to cause mutations, that are abberations of the cell DNA leading to uncontrolled proliferation. This classical paper investigates the relation between cancerogenity and mutagenity.
One should mention here that there are many types of mutations possible, mutations are not equally dangerous for cells and some mutations can be successfully repaired using the intact strain.
Therefore the following parameters of the source substances need to be measured to estimate the cancerogenity:
How can we measure the carcinogenity of different substances?
The most general approach here is to introduce certain amount of cancerogen into the animal body or to the cultured cell and to see the effect. The effect is calculated as the percentage of cells that undergo the transformation from normal into cancer cells. Two metrics are available here:
DT = Tumorigenic Dose (the amount of substance causing certain
percentage of cancer in treated animals, all treated animals are taken
for 100%)
CT = Tumorigenic Concentration (same, but adjusted for
concentration and used in cell cultures).
(They are written CT and DT because in science people tend to used Latin abbreviations where the adjective actually follows the noune).
The common metrics are DT5/CT5 (5% cells/animals get cancer) and DT50/CT50 (50% of the animals). Those are similar to other common metrics, the most common is LC50/LD50 -- lethal dose for 50% of the animals/cells.
Unfortunately I couldn't not find any pre-compiled list with most known cancerogens and their TD/TC values. These seem to be interesting primarily for scientists. But going back to your question: you are absolutely right: some cancerogens are much more potent in causing cancer than the others!
I can't speak to the causes of hypotension, but you are indeed correct, caffeine is a stimulant. As a stimulant, there is a well documented acute period of hypertension that lasts for up to 4 hours. Interestingly, there is no causal link established between caffiene consumption and chronic hypertension leading to cardiovascular disease (see here and here).
Having said that, caffeine is also a diuretic, which could cause someone who is already fairly dehydrated to exacerbate that state. It's possible to faint from a result of severe dehydration but I think it would have to be pretty severe.
It's possible someone is prone to fainting for non-medical, purely physiological reasons, such as standing for long periods, standing up too quickly, hypoglycemia, or some other predisposition.
I found a book chapter for you here
Quick summary:
3 hypotheses to Origin of viruses
Drawbacks:
Because of these drawbacks, the problem of virus origin was for a
long time considered untractable and not worth serious consideration
The rest of the chapter looks more in-depth into the 3 hypotheses
From this source,
We answered this question on the show...
We posed this question to Dr David williams from the Veterinary School
at the University of Cambridge... David - First of all, what actually
makes something smell? Molecules have to leave the smelly objects
and get to your nose through the air and that means that these
molecules must be very small and volatile. That's to say they must be
easily evaporated. The chemicals that make dogs smell are mostly what
we call volatile organic acids and they are produced by bacteria from
the fats that are breaking down from sweat; and that's maybe why we
find these body odours unpleasant. They signal a presence of bacteria
and decay and death to us.
Their [dogs] skins mostly have
Staphylococcal bacteria, which don't produce much in the way of a
smell at all, but they've also got some yeasts too which are really
pongy. But why does the smell seem worse when the dog is wet? Here,
I think we have to go into some physics. The amount of evaporation of
a substance is related to the concentration of the compound on a
surface it’s evaporating from and the amount of compound that's in the
air, just above the surface.
So how might that change when it’s wet?
Well, if the organic acids are dissolved in water on the fur of the
wet dog, as the water evaporates, the concentration of those smelly
acids increases, so they'll evaporate more, so there are more
molecules in the air for us to smell. Diana - A bit of evaporation
can effectively amplify the amount of volatile chemicals that emanate
from a dog’s skin, and Dr. Williams thinks it’s the same effect that
causes that damp earth smell when it rains. It may also alter how
dogs interact with each other when they're wet. So, if you have a
dog, watch to see if it sniffs differently at other dogs on a dry day
versus a wet one...
There's a start, sounds legitimate to me...
I don't have a definitive answer, but I suspect Hymenoptera is "just a name," albeit a name that has lasted through the phylogenetic nomenclature revolution.
Hymenoptera was erected by Linnaeus in the 10th edition of Systema Naturae (1758). The description of Hymenoptera (membrane wing; p. 553 [hope your Latin is better than mine]) follows that of Lepidoptera (scale wing) and Neuroptera (net wing) and precedes Diptera (two wing).
Classical taxonomy, which Linnaeus was more or less inventing at the time, was based on shared similarities. Those insects which Linnaeus thought more similar to each other than to other insects (e.g., ants, wasps, bees) all shared the characteristic of having a membrane based wing. The scaly wings of moths and butterflies made them more similar to each other.
He needed names for these groups, so he chose logical ones based on outward appearance of the wings: scaly, netted, membranous, or paired. That fact that these major groupings have more or less stood the test of time suggests that Linnaeus picked a good characteristic on which to name his classification of the major groups of insects.
Ah, what a classic biophysics problem.
One first needs to understand how a membrane gets a potential. The lipid bilayer is a large sea of hydrophobic interactions that essentially prevents any ion from crossing. As a result, Na+ and K+ concentrations remain constant and different on the cytoplasmic side and the extracellular side. However, ions can pass through ion channels like the K+ channel. It is important to understand that in K+ channels, only K+ can pass and these channels are actually selective against Na+ (answer to question 1).
There are two potentials at work here. First is a chemical potential created by the flux of K+ from high K+ to low K+. The second is a counteracting membrane potential created by a charge imbalance. Note, that the swapping of a few ions will a) result in a negligible change in the concentration ie. the chemical potential, b) result in a large change in the membrane potential. At some point, the flux out due to the chemical potential and the flux in due to the membrane potential will be equilvant and the cell will reach a resting potential otherwise known at the Nernst potential or equilibrium potential (technically a steady state).
When a cell depolarizes by closing these channels, the local charge will quickly go back to an equilibrium or a non-charged state.
So why K+ rather than Na+? For typical cells, the extracellular concentration of Na+ is 145 mM and cytoplasmic is 12 mM. For K+, it is 4 mM and 155 mM respectively. Doing the appropriate calculations of the Nerst potential, for Na+ it is +67 mV and for K+ it is -98 mV. Qualitatively we can see that this would result in vastly different things.
Most of this information can be found from Pollard and Earnshaw's Cell Biology
I have recently been doing a lot of research into the interplay between the innate and adaptive immune systems in humans, and mammalian laboratory models. This has led to my reading some interesting information on the immune response in insects;
Insects have a highly efficient immune system. In response to a bacterial attack, their fat body (the equivalent of the liver in mammals) synthesizes a whole range of peptides with an antibacterial and antifungal effect.
This fascinated me, as the clear inference is that there are no ‘dedicated’ immune cells, but that adipose tissue has far more diverse functions that I had realized.
I have done a little more reading, and also looked at plant immune systems, which seems far more analogous to those in insects than mammals;
Plants, unlike mammals, lack mobile defender cells and a somatic adaptive immune system. Instead, they rely on the innate immunity of each cell and on systemic signals emanating from infection sites.
(Jones, 2006)
My questions relates to the need of an adaptive immune response in mammals. The immune systems in insects and plants - a more 'systemic' immunity due to the lack of dedicated/mobile immune cells - seems much simpler.
Given that evolution works incrementally (there are no 'jumps' - for instance, going from a non-dedicated immune system, to a dedicated immune system), I would hypothesise that organisms less distantly related to insects and plants may have tissues with duel functions (similar to insects?), but that specialize further as immune cells until gradually (down the evolutionary tree) a complex and specific immune system emerges. (This is complicated by the fact that our immune systems do have multiple roles - e.g. tissue remodelling, but I wasn't going to go into that here. Feel free in your answers if it is necessary!).
My overall curiosity can be summarized as 2 questions;
Let's say you accidentally walk into a room pressurized with pure nitrogen (or you're jettisoned into space). Within a couple of seconds, the partial pressure of oxygen within your lungs drops to 0. But there's still a (small?) reserve within your bloodstream.
Now, will the oxygenated blood travel to your lungs? If so, will the usual gas exchange reverse, with oxygen going from your blood to the oxygen-poor environment?
Probably not many side effects except in specific instances, but no benefits either. My guess is that there are potential side effects because these glasses reduce the amount of light that the eye receives and restrict the visual field. Therefore, the restricted visual field would be bad for activities such as driving, in which you need your peripheral vision. And the reduced light makes objects appear dimmer, so it is harder to see with them at night. I also imagine (just a guess) that they would be bad for very young infants, who are almost always born without perfect vision and require some visual stimulation to correct.
There are probably many reasons why optometrists use a pinhole occluder for diagnostic purposes, but never prescribe it as treatment...
There are always exceptions but you can consider some general rules.
A is 1 i.e the sequence that is perfectly complementary (2 is complementary but direction is parallel — cannot base-pair), then B would be 1 (siRNA). Reasons (some are just based on general rules of siRNA design):
See here for guidelines for siRNA design.
We suspect a bi-directional transcription event is happening at a locus in our organism where two genes are directly adjacent to each other. The annotation data is not well established. The intergenic distance is probably less than 200 base pairs.
The two genes are expressed in opposite directions towards each other. Base on the preliminary transcriptomics data, it seems like one gene is over transcribing (3' UTR perhaps?) into the adjacent gene, possibly resulting in some kind of transcriptional regulation of the adjacent gene.
Here is a rough diagram of what we think might be happening:
------------------------==========gene A================>----------------------
----------------------------------------<====gene B=====-----------------------
Of course we need to first confirm this by designing primers to see if this over transcription is actually happening.
If this is happening, we intend to do some knock down experiments. We have no transgenesis available in our organism, only RNAi by dsRNA. It is possible to specifically knock down geneA by introducing dsRNA to the 5' region of geneA that does not overlap with geneB. Perhaps this will lead to ectopic/over expression of geneB.
Is there anyway to knock down geneB specifically without knocking down geneA? It looks like designing dsRNA for geneB would knock down both A and B.
If you are talking about sound damaging the sound sensing organs in the ear, analogous to an ultrasonic heavy metal concert, I've found an interesting report just on this topic.
For ultrasonic components above 20 kHz, the limits were set to avoid hearing damage in the audible (lower) frequencies. One-third-octave band levels of 105-115 dB were observed to produce no temporary hearing loss, and were therefore judged non-hazardous in respect of permanent hearing damage.
If you are talking about high frequency sound from a explosion, or some sort of sonic cutter with intensities of such a level of compression or a high decibel range that conveys enough energy to physically damage something of course the answer would be 'yes this would damage your ears and the rest of the body too.
Operators of ultrasonic equipment with levels above 60 dB complained of headaches and fatigue, even nausea below 60 dB they felt no effect (reference table 7 in paper). But they did not seem to have any hearing loss.
One soviet experiment is both informative and maybe also entertaining to read about:
An unspecified number of subjects were exposed for an hour to a tone of 20 kHz at 110 dB. Tests were made to examine shift of hearing threshold over the frequency range 250 Hz to 10 kHz. Pulse rate, body temperature and skin temperature were also monitored. These tests showed no appreciable effect, even when the Sound Pressure Level was increased to 115 dB. These same subjects were given a one hour exposure to a 5 kHz tone at 90 dB: a considerable TTS was found. The 5 kHz tone at 110 dB produced a powerful vascular response.
...
It seems safe to infer an underlying concept: A sound which does not produce temporary
dullness of hearing cannot produce a permanent noise-induced hearing loss.
The bowel movements are influenced by a lot of factors. For example, when you eat a meal it induces a movement in your large intestines, to defecate and clear up space for new food.
Also, there is MMC, migrating motor complex, which is responsible for the bowel movements when you are fasting. It causes a flushing effect, which prevents bacteria to overproduce in intestines.
So, the daily bowel movements are mainly influenced by the timing and content of the food that you eat. But as I said there are many other factors. The gastrointestinal system has a very complex nervous system. Even psychological factors can effect the bowel movements greatly, for example extreme physical pain may induce the symphatetic system and cause constipation.
Also caffeine may affect it, like many drugs do.
Your approach to translate the AA sequence, codon by codon, was correct. This was a bit of a trick question because to recognize it, you had to read the sequence backwards.
UGG-CAA-GGT-CAC etc is read directly off of the 3'->5' strand of the circled answer, reading from right to left.
The bottom left is a red herring because it starts with a start codon, ATG, but reading beyond the start codon, the sequence wouldn't match.
The answer to this could be that there are many factors contributing to the length of the life of tree species.
Climate: You can see that trees that have a reputation of becoming really old live in environments that have low moisture levels and much sunlight over the course of the year.
For example, you can see that the most long-lived trees in America are located in California, where the temperatures are relatively high, while moisture levels are low. If you have one without the other trees don't tend to live that long. Cold climates make growth
harder for each individual, yet hot and moist climates tend to help trees grow easier, but also die easier. Think of the amazon. It is one of the richest forests in the world, yet the growth of bacteria and high competition in the areas of the equator make life a lot harder for the longest living and slowest growing species.
As you can see, the vast majority of the longest-living trees are located in California, or other regions of the same latitude!
http://en.wikipedia.org/wiki/List_of_oldest_trees
Other species and the life around it/Its Ecosystem: Individual trees tend to be less likely to be destroyed by a fire, as they are less likely to catch fire. At some instances, forest trees or dried-out grass can catch fire and pass it on to other individuals.
Microbes and bugs found in some parts of the world are known to their abilities to destroy trees!
Current size of the tree: Larger trees are generally less likely to die of causes like drought or damage to their trunks, as they have greatly extensive nets of roots and thick trunks and thus are able to, even partly, recover these incidences.
If a rockfall for example causes damage to one side of the tree, some of the brunches will probably die, but the rest of them, that have their own network to the roots, will probably survive.
This means that luck is involved and if the tree is lucky enough to avoid dying for a certain amount of time, regular fluctuations in the environment do not kill it as they would kill a younger, less robust tree.
Biology of tree species: Debate is held as to whether tree cells have telomeres working the same way as they do in animals. Research published in 2001 suggests that telomeres don't work the same way, as plants developed without telomeres after six generations continue living and growing without problems. But even if they do use telomeres, they may use them in a different way. This is an area where research is still being conducted, though, and you may find controversies in the bibliography!
For example in the paper "Analysis of telomere length and telomerase activity in tree species of various life-spans, and with age in the bristlecone pine Pinus longaeva"
Barry E. Flanary & Gunther Kletetschka which can be found in the rep
we can see that sometimes, short lived trees have longer telomeres than long lived ones!
(Look in the second paragraph of the section "Results"). This means that actually, nobody really knows!! It may be the telomeres, it may be something else, it may be a combination of factors.
http://www.madsci.org/posts/archives/2002-04/1019349924.Bt.r.html
(notice that this post has links to pages that are no longer available).
Distillation and the most important point: The way that the tree is adapted to its environment determines its longevity in it. Planting an olive tree in the amazon is a great way of making sure it will not survive! Some trees are better at surviving in a certain climate (even if it is at your own garden) simply because they have evolved to live there.
That means that the trees probably don't have a defined lifetime in general, but the life expectancy is defined in each environment, depending on the circumstances!
This means that species we currently think of as short-lived can reach get really old:
http://www.ncbi.nlm.nih.gov/pubmed/11295506
What some companies may have done is try to combine characteristics of individuals through selective breeding - and yes, it works for trees as well!- to match the climate and terrain characteristics found in the certain country or region! Or they may have selected for resistance against the most common pests in your area!
I hope I answered you question adequately!
The biological environment in every cell and tissue of your body is an extremely complex, tightly controlled system. There are tens of thousands of genes in a typical eukaryotic genome, and depending on tissue types and environmental conditions, these genes are turned on and off in a very controlled manner. There is regulation at every point in the flow of genetic information: nucleosome disruption to expose DNA; RNA transcription from the DNA; protein translation from the RNA; and in some cases, additional modifications of proteins or intermediate mRNAs. At early stages in development, regulation of RNA and protein levels is even more crucial than, say, when an organism is fully developed and healthy.
All living organisms share some basic building blocks--DNA, RNA, and proteins work pretty much the same in all of life (there are a few rare variations of the genetic code but the basic premise is identical). However, the way that specific genes, transcripts, and proteins work together to sustain life varies widely between different organisms.
For a very rough analogy, imagine you want to bake a batch of cookies. Then consider the three following scenarios.
The first example we can relate to two individuals of the same species mating. Of course there is natural variation in the population, but this doesn't typically lead to lethality during development. The second example we can relate to individuals of two related species (such as a horse and a donkey). Sometimes these matings can produce viable offspring, although these offspring are often sterile. The third example we can relate to individuals of two very divergent species (such as donkey and dog in your original question). The biological systems inside donkeys are just so different from those inside dogs that this mating cannot produce a viable offspring.
Admittedly this is a rough analogy, but hopefully is sheds some light on the issue.
Free radicals are damaging because their unpaired electrons (or not fully filled valence shell) makes them highly reactive species. They are often considered together with highly oxidizing "reactive oxygen species" (ROS) such as peroxides. They are especially problematic for cell membranes and DNA. In the latter they can react with (oxidize) heterocyclic bases.
As suggested first by Gerschmann et al. (1954), since oxidative damage to cells and cell structures is seen to accumulate with age, the corollary of this could be that aging is a result of oxidative damage. The very fact that cells have antoxidant enzymes such as superoxide dismutase (SOD) suggests that suppression of these species is important in the cell.
Many (but not all) ROS originate from mitochondria during cell metabolism. Therefore, it has been suggested that by regulating metabolism (that is, reducing the metabolic rate) the "rate of living theory" (Harman 1981) the rate of oxidative damage can be reduced. One way to do this may be calorie restriction.
This idea seems to fallen out of favour though. Another possibility is that the rate of mitochondrial ROS has nothing to do with metabolic rate per se; rather it might simply be a longevity determinant.
However, having said all this there is evidence that ROS are actually crucial in a number cellular pathways. It may be that it is the deregulation of pathways managing ROS that can contribute to aging rather than simply damage accumulation with age.
Gerschman, R., Gilbert, D. L., Nye, S. W., Dwyer, P., and Fenn, W. O. (1954). "Oxygen poisoning and x-irradiation: a mechanism in common." Science 119(3097):623-626.
Harman, D. (1981). "The aging process." Proc Natl Acad Sci U S A 78(11):7124-7128.
Yes it is possible, and as far as I can see, there should not be any plant which would be impossible to grow in a such an environment, just more or less difficult, although this is just my speculation.
I have myself grown tomatoes from only a liquid solution of minerals and nutrients, but you have to change the solution from time to time to prevent bacteria and fungi growing starting to grow in it. The reason why this is not a method used in industrious growing is because it is a lot more expensive than using soil and fertilisers, and more work.
TL;DR:
There is a dearth of actual experimental evidence. However:
there is at least one study that confirmed the process ([STUDY #7] - Myxococcus xanthus; by Fiegna and Velicer, 2003).
Another study experimentally confirmed higher extinction risk as well ([STUDY #8] - Paul F. Doherty's study of dimorphic bird species an [STUDY #9] - Denson K. McLain).
Theoretical studies produce somewhat unsettled results - some models support the evolutionary suicide and some models do not - the major difference seems to be variability of environmental pressures.
Also, if you include human predation based solely on sexually selected trait, examples definitely exist, e.g. Arabian Oryx
First of all, this may be cheating but one example is the extinction because a predator species specifically selects the species because of selected-for feature.
The most obvious case is when the predator species is human. As a random example, Arabian Oryx was nearly hunted to extinction specifically because of their horns.
Please note that this is NOT a simple question - for example, the often-cited in unscientific literature example of Irish Elk that supposedly went extinct due to its antler size may not be a good crystal-clear example. For a very thorough analysis, see: "Sexy to die for? Sexual selection and risk of extinction" by Hanna Kokko and Robert Brooks, Ann. Zool. Fennici 40: 207-219. [STUDY #1]
They specifically find that evolutionary "suicide" is unlikely in deterministic environments, at least if the costs of the feature are borne by the individual organism itself.
Another study resulting in a negative result was "Sexual selection and the risk of extinction in mammals", Edward H. Morrow and Claudia Fricke; The Royal Society Proceedings: Biological Sciences, Published online 4 November 2004, pp 2395-2401 [STUDY #2]
The aim of this study was therefore to examine whether the level of
sexual selection (measured as residual testes mass and sexual size dimorphism) was related to the risk of extinction that mammals are currently experiencing. We found no evidence for a relationship between these factors, although our analyses may have been confounded by the possible dominating effect of contemporary anthropogenic factors.
However, if one takes into consideration changes in the environment, the extinction becomes theoretically possible. From "Runaway Evolution to Self-Extinction Under Asymmetrical Competition" - Hiroyuki Matsuda and Peter A. Abrams; Evolution Vol. 48, No. 6 (Dec., 1994), pp. 1764-1772: [STUDY #3]
We show that purely intraspecific competition can cause evolution of extreme competitive abilities that ultimately result in extinction, without any influence from other species. The only change in the model required for this outcome is the assumption of a nonnormal distribution of resources of different sizes measured on a logarithmic scale. This suggests that taxon cycles, if they exist, may be driven by within- rather than between-species competition. Self-extinction does not occur when the advantage conferred by a large value of the competitive trait (e.g., size) is relatively small, or when the carrying capacity decreases at a comparatively rapid rate with increases in trait value. The evidence regarding these assumptions is discussed. The results suggest a need for more data on resource distributions and size-advantage in order to understand the evolution of competitive traits such as body size.
As far as supporting evidence, some studies are listed in "Can adaptation lead to extinction?" by Daniel J. Rankin and Andre´s Lo´pez-Sepulcre, OICOS 111:3 (2005). [STUDY #4]
They cite 3:
The first example is a study on the Japanese medaka
fish Oryzias latipes (Muir and Howard 1999 - [STUDY #5]). Transgenic males which had been modified to include a salmon growth-hormone gene are larger than their wild-type counterparts, although their offspring have a lower fecundity (Muir and Howard 1999). Females
prefer to mate with larger males, giving the larger
transgenic males a fitness advantage over wild-type
males. However, offspring produced with transgenic
males have a lower fecundity, and hence average female
fecundity will decrease. As long as females preferentially
mate with larger males, the population density will
decline. Models of this system have predicted that, if
the transgenic fish were released into a wild-type
population, the transgene would spread due to its mating
advantage over wild-type males, and the population
would become go extinct (Muir and Howard 1999).
A recent extension of the model has shown that
alternative mating tactics by wild-type males could
reduce the rate of transgene spread, but that this is still
not sufficient to prevent population extinction (Howard
et al. 2004). Although evolutionary suicide was predicted
from extrapolation, rather than observed in nature, this
constitutes the first study making such a prediction from
empirical data.
In cod, Gadus morhua, the commercial fishing of large
individuals has resulted in selection towards earlier
maturation and smaller body sizes (Conover and Munch
2002 [STUDY #6]). Under exploitation, high mortality decreases the
benefits of delayed maturation. As a result of this,
smaller adults, which mature faster, have a higher fitness
relative to their larger, slow maturing counterparts
(Olsen et al. 2004). Despite being more successful
relative to slow maturing individuals, the fast-maturing
adults produce fewer offspring, on average. This adaptation,
driven by the selective pressure imposed by
harvesting, seems to have pre-empted a fishery collapse
off the Atlantic coast of Canada (Olsen et al. 2004). As
the cod evolved to be fast-maturing, population size was
gradually reduced until it became inviable and vulnerable
to stochastic processes.
The only strictly experimental evidence for evolutionary
suicide comes from microbiology. In the social
bacterium Myxococcus xanthus individuals can develop
cooperatively into complex fruiting structures (Fiegna
and Velicer 2003 - [STUDY #7]). Individuals in the fruiting body are
then released as spores to form new colonies. Artificially
selected cheater strains produce a higher number of
spores than wild types. These cheaters were found to
invade wild-type strains, eventually causing extinction of
the entire population (Fiegna and Velicer 2003). The
cheaters invade the wild-type population because they
have a higher relative fitness, but as they spread through
the population, they decrease the overall density, thus
driving themselves and the population in which they
reside, to extinction.
Another experimental study was "Sexual selection affects local extinction and turnover
in bird communities" - Paul F. Doherty, Jr., Gabriele Sorci, et al; 5858–5862 PNAS May 13, 2003 vol. 100 no. 10 [STUDY #8]
Populations under strong sexual selection experience
a number of costs ranging from increased predation and
parasitism to enhanced sensitivity to environmental and demographic
stochasticity. These findings have led to the prediction that
local extinction rates should be higher for speciespopulations
with intense sexual selection. We tested this prediction by analyzing
the dynamics of natural bird communities at a continental
scale over a period of 21 years (1975–1996), using relevant statistical
tools. In agreement with the theoretical prediction, we found
that sexual selection increased risks of local extinction (dichromatic
birds had on average a 23% higher local extinction rate than
monochromatic species). However, despite higher local extinction
probabilities, the number of dichromatic species did not decrease
over the period considered in this study. This pattern was caused
by higher local turnover rates of dichromatic species, resulting in
relatively stable communities for both groups of species. Our
results suggest that these communities function as metacommunities,
with frequent local extinctions followed by colonization.
This result is similar to another bird-centered study: Sexual Selection and the Risk of Extinction of Introduced Birds on Oceanic Islands": Denson K. McLain, Michael P. Moulton and Todd P. Redfearn. OICOS Vol. 74, No. 1 (Oct., 1995), pp. 27-34 [STUDY #9]
We test the hypothesis that response to sexual selection increases the risk of extinction by examining the fate of plumage-monomorphic versus plumage-dimorphic bird species introduced to the tropical islands of Oahu and Tahiti. We assume that plumage dimorphism is a response to sexual selection and we assume that the males of plumage-dimorphic species experience stronger sexual selection pressures than males of monomorphic species. On Oahu, the extinction rate for dimorphic species, 59%, is significantly greater than for monomorphic species, 23%. On Tahiti, only 7% of the introduced dimorphic species have persisted compared to 22% for the introduced monomorphic species.
...
Plumage is significantly associated with increased risk of extinction for passerids but insignificantly associated for fringillids. Thus, the hypothesis that response to sexual selection increases the risk of extinction is supported for passerids and for the data set as a whole. The probability of extinction was correlated with the number of species already introduced. Thus, species that have responded to sexual selection may be poorer interspecific competitors when their communities contain many other species.
This seems to be an interesting and ambiguous topic.
On one hand, the collagen as any other protein is cleaved into small-sized chunks (oligopeptides) and single aminoacids before absorption. The chunks of proteins which were not completely digested before absorption are broken up further in the body and cannot be selectively used for collagen re-building in the body. Therefore, there should be no difference between the collagen of different types and, basically, no difference between the supplements containing collagen and just a mixture of aminoacids. This also explains the fact why collagen supplement is in most cases taken in the lysate (pre-cleaved) form.
On the other hand, a quick search in PubMed and I found an interesting article on the topic (source), where the authors claim:
At 6 months, the proportion of clinical responders to the treatment,
according to VAS scores, was significantly higher in the collagen
hydrolysate (CH) group 51.6%, compared to the placebo group 36.5%
(p<0.05).
...
This study suggests that collagen hydrolysate 1200 mg/day could
increase the number of clinical responders (i.e. improvement of at
least 20% on the VAS) compared to placebo. More studies are needed to
confirm the clinical interest of this food supplement.
So, if the article is not a bogus (I failed to get the full version of it and the journal does not seem to belong to the top journal in the field of medicine), there could be some mechanisms yet to be discovered.
"There are antibiotics which contain carbohydrates, such as Gentamycin and Streptomycin (the aminoglycosides). These must be the antibiotics that could account for this phenomenon."
My conjecture that the carbohydrate moities contained within aminoglycosides account for the high energy is incorrect. Aminoglycosides are NEVER metabolized by the body, they are excreted out into the urine UNCHANGED. See here: http://www.ebmedicine.net/topics.php?paction=showTopicSeg&topic_id=43&seg_id=839
And even if it were possible to metabolize the carbohydrate molecules within them, the energy released would be far less than the energy consumed to break their linkages in the first place, thus placing a negative energy balance on the body, and thus, not providing the burst of energy that is apparently observed after taking antibiotics.
Unlike erythrocytes that have a very rigid shape and almost cannot change their size (hence the size distribution is indicative and can be used for diagnostic purposes in medicine), lymphocytes can change their size in a wider range, this is why you see the numbers 6-9 and 10-15 μm.
And they indeed cluster into several different groups: so-called "large granular lymphocytes", also known as NK-cells or "natural killers" (usually >10μm) and "small granular lymphocytes", constituted by a large family of T- and B-lymphocites(usually <10μm). But this clustering is not really distinct, for as I said above, both NK and T/B-cells can shrink (if the osmolarity of the external medium grows due to acidosis, inflammation etc.) and swell (on binding many IgE/IgG complexes, on certain cell factor released etc.). Besides, there are also some intermediate size cells, called NKT-cells, that also flatten the distribution.
So, what you can definitely say is that the typical size distribution of lymphocytes has two peaks: around 8 and 12 μm respectively.
The first step in troubleshooting is to run controls - run lanes with your protein input alone, and the conjugate alone (you may need to play with the type/percentage of the gel if the conjugate molecule is much smaller than your target protein - attaching biotin to a 50 kDa protein, for example) to see if the smear shows up. Depending on the type of conjugation you're using, the number of acceptor sites on the substrate, and the time and conditions of the conjugation reaction, you may be adding a highly variable number of conjugate molecules to your substrate. For example, when I first started working with adding fluorophores like Alexa and DyLight dyes to antibodies, the fluor/protein ratio was highly variable from reaction to reaction and between antibodies in the same reaction.
This is most likely what is happening in your case - the number of conjugate molecules being added to each substrate molecule is highly variable. If you haven't already, I'd suggest getting in touch with your conjugation kit vendor's tech support, as they likely encounter this problem all the time. You may need to change the type of conjugation chemistry, get a higher-quality conjugate, or purify the substrate before and/or after the reaction. One of the solutions to my antibody labeling problem I mentioned above was to purify the reaction products through a size-exclusion column. This had the dual effect of separating out the un-reacted antibody and fluorophore, and allowing us to pick different fractions of the conjugated product and decide which were best for our needs.
I am currently reading Richard Dawkins's book 'The Greatest Show On Earth: The proof for evolution' and in the second chapter he talks very much about the evolution of dogs.
He says centuries ago there was only such dog-like creature as the wolf, but in a matter centuries the wolf has evolved into the many breeds of dog we have through artificial selection conducted by man.
This to me seemed very peculiar and quite frankly untrue, and I may be getting the wrong end of the stick and he is in fact being analogous, although I'm pretty sure he's not.
So, did wolves evolve into the many breeds of dog we have through artificial selection conducted by man?
If so, how many centuries did this take?
(Dawkins's point was that if the wolf can evolve into the vast amount of breeds of dog we have at the moment from artificial selection over a matter of centuries, then surely over many millions of years, the evolution we claim to know of through natural selection could definitely have happened).
Absolutely a serious part of research - quantum mechanics defines chemical structure and reactivity. Whenever you see a headline like 'Scientists find quantum effects important in protein activity, weird huh?', read it as 'Scientists find pragmatic classical approximations inadequate in describing protein activity'.
In protein structure, for example, classical molecular dynamics/mechanics are important in generating computationally tractable problems, however they represent a tacit and streamlined parameterisation of underlying quantum mechanics. QM protein structures are usually too gnarly to compute (at least historically speaking), except in regions of interest like an active site, where a model fine-tuned for sequences of amino acids will probably fail badly anyway. As a concrete example, the group that I'm in is in part interested in computationally modelling the active site of plant photosystem II, which contains a cluster of spin-coupled manganese atoms. To glean any useful understanding of how this cluster functions via a computational model, an explicit quantum mechanical level of theory that takes into account electron exchange and correlation must be used. This requirement can probably be extended to any metalloenzyme.
And this isn't touching upon the resonance hole transfer that oxidises the active site, the Davydov solitons that manifest in protein alpha helices, or indeed the quantum electrodynamical origins of the Van der Waals interaction that causes everything to tend to stick to everything else.
Hope this is interesting :D
(note: I am not involved with PetaChem, I just think it's freaking awesome.)
Short answer: yes.
Although clearly the infradian changes in steroid hormones in females are quite "obvious", other changes are less evident, but happen nonetheless in males as well as in females.
Most of the hormones produced by endocrine organs such as the hypothalamus (a region at the base of the brain) or the hypophisis are not secreted in a continuous manner but rather in pulses. The exact frequency/amplitude etc. of these pulses can be different depending on the species considered, but (as fare as we know) the undelying mechanism are fairly conserved.*
In general, you can find circadian (~24 h), ultradian (<24h) and infradian (>24h) rhythms.
For instance these graphs show the concentration of cortisol, aldosteron and renin in a man, showing a strong circadian rhythm.
From: Charloux et al. - Am J Physiol Endocrinol Metab 1999
You can see that on top of the circadian rhythm, an ultradian pulsatility (every ~2-3h) is also quite clear.
Another example is that of GH (growth hormone): here you see secretion of GH in an healthy women (top) and an healthy men (bottom)
From: van den Bergh et al. - J Clin Endocrinol Metab. 1996
Many other hormones show this type of rhythmicity in males, such as testosterone, LH, GnRH, and probably many other.
I am not aware of long term studies on this matter.
* Actually, the mechanisms underlying pulsatility are still poorly understood.
For any kind of frozen cell stock (for cell culture or bacteria) we routinely use freezing vials similar to these: http://www.sigmaaldrich.com/catalog/ProductDetail.do?D7=0&N5=SEARCH_CONCAT_PNO%7CBRAND_KEY&N4=V9255%7CSIGMA&N25=0&QS=ON&F=SPEC
These tubes are internally threaded with a rubber grommet to seal the lid and make the tube air and water tight. I suspect the air tight seal prevents condensation from entering the tube and freezing within the tube, but I've never had a problem with either choice of tube.
The tubes don't really matter at -80 C for a glycerol stab. Freezing cells in liquid nitrogen on the other hand has a huge impact when storing in liquid nitrogen. Some tubes are meant to be stored in the liquid versus the vapour phase of nitrogen and not matching the tube to it's intended storage condition can result in explosion of the tube.
Ligase Independent Cloning is a protocol that allow an insert to be integrated into a vector without ligation. It uses T4 DNA polymerase with only ATP to first chew back from blunt ends to create long sticky ends and then a polymerase treatment with full dNTP compliments to fill in the vector.
While there are several nice articles and resources that describe the procedure, I really would like a protocol with concentrations, temperatures and timing, which I'm having problems finding. OpenWetWare for instance has only stub pages with no details. Can anyone point to a full step by step recipe to make this work, once you have designed the primers?
By default, pymol seems to grab the number of cores on the system for rendering. How can I force it to only use one core?
Motivation:
I have a large collection time-series of of coordinate data from a computational protein folding experiment. I'd like batch render the generated pdb files into a movie in a programmatic way. Pymol however likes to eat up as many cores as it finds available. I'd like to retain some control of the computational burden (required for some computational cluster jobs). How can I force pymol to only use one (or n) core(s)?
Solution:
While the question was closed (as it was decided to not fit into biological criteria of the site) future visitors might find it useful to know the answer:
set max_threads, 1
The solution was found in a Biostars question.
Plants are not a strong suit for me, but in general the answer is yes. What I know mostly comes from animal tissue, so someone may have a better answer than I...
Botanists have been cloning plants from cuttings for thousands of years. More recently, propagation from cell lines around for much longer than for animals. Entire plants can often be grown from a plate of cells. So you can grow roots or an entire plant from cells right now, but I can't find any mention of anyone trying to grow fruit without the rest of the plant, and there might not be any research for this. Let me explain why this may be...
Bioengineering animal tissue and organ growth has been an intensive area of research for the past 15 years or so. In some cases, such as the growth of skin or liver, the technology has proven to be exceptionally valuable and useful.
Using plastics with biological growth factors attached and 3D printing, even more complex organs such as bladders and tracheas can be grown from the patients own cells, which avoids the problems of rejection and the complexities of donor matching.
More recently growing muscle tissue in an animal free culture has been tried, which would relieve some of the environmental and ethical problems of raising meat animals.
All this has been driven by a strong cost-benefit payoff. A transplanted organ is highly valuable and improving that process and making organs more broadly available for patients has a high economic value. The more often the structure is related to the tissue around, the more structurally complex, the more difficult it is to imagine growing that organ independently of the host organism (brain and eyes come to mind). Other transplant worthy tissue cultures look quite promising.
Right now, it seems as if plant fruit like an apple or a kiwi might be difficult/expensive to grow in the lab as opposed to just picking them off the tree. I think that growing a banana pulp or an apple sauce might be possible, though. Who knows what we might be doing in 50 years or more though?