CharonY

One with a lot of function is the Staden package (probably more than you need). I think there is a built for Mac around now (OSX that is).

Wait a tick. What precisely are you doing with them? Seqman is normally used for sequence assemblies. So do you sequence your putative mutated area and use Seqman to assemble it? Or do you actually need a sequence alignment programm? Or in other words, what parts of Seqman do you really need? Sequence editors are around aplenty. I have to check whether there are Mac compatibles, though (I normally run them on a solaris or linux system)

In that case the documentary is clearly faulty. Especially because it has both been shown in humans and mice not to be the case.

AFAIK the indy gene was primarily analysed as a potentially life expanding gene in Drosophila (which has been challenged recently). Given the fact that the transporter itself has been identified not so long ago, I doubt that there are very deep analyses regarding the regulation yet. Much less specific tissue-dependent regulatory networks.

I think there was similar thread somewhere already, but anyway. I would like to discuss it in some more depth when I got more time (maybe around next wee or so). But I would like to state that it is clear that the modern synthesis clearly needs an update. This has been apparent at least the last decade or so. The modern synthesis has never been as concise as, say, the darwinistic theory, simply due to the problem of summarizing all the available, very different type of data into one single theoretical work. As such the modern synthesis grew over time, without a real complete update. In my opinion the real need for a new theory is not the fact that new data is available, as these can be integrated rather easily, but rather because some of basic assumptions of the modern synthesis are now generally regarded as wrong. These include: -that genomes are well ordered libraries of genes (partially true for prokaryotes, not that much for most eukaryotes) - genes have usually have single functions honed by natural selection -Species are finely adjusted to their ecological circumstances due to efficient adaptive adjustment of biochemical functions. (well due to the fact that species concepts are arbitrary, especially within the realm of prokaryotes this does not make any sense anymore) -The durable units of evolution are species, and within them the organisms, organs, cells, and molecules, which are characteristic of the species. (see above) -Given the adaptive nature of each organism and cell, their machinery can be modeled using principles of efficient design. (newer modeling approaches showed that this usually does not work for eukaryotes. Though sometimes it has limited uses in prokaryotes). In any case there has been a rather large discussion to what has to be added into a new synthesis and how it should be called. EES is by no means the only call for an update, though we could use the given paper as a basis and compare it to other similar papers. I do recall that someone here (sorry, forgot who) actually had a nice idea of starting to call it alpha, beta... synthesis.

You may have misunderstood my point. It was talking not about the modification of one or two bases, but those throughout the whole tRNA. You may want read up on Dalluge et al. 1997 (one of the few papers I remmeber on this subject). Journal of Bacteriology (so it should be long free by now). IIRC it dealt with the high abundance of pseudouridine in psychrophiles. However, giving that structural RNAs are single stranded molecules, it is not that much surprising that even single nucleotide modifcations can have profound effects on their local structure. For more info on this you should read up on models for RNA folding (papers from Michael Zuker's group might be a good starting point). More specifically, the modifications in the T-arm contribute to stabilizing the (L-shaped) tertiary structure of the tRNA. However, as always, things are a bit more complicated. As tRNA are the structural element of the genetic code modification not only are involved in maintaining a certain tertiary structure, but are also involved in the actual translation process, most notably in wobble pariring.

So you drink more beer then?

Well there is smart and there is smart... There are kids that are good at school but not socially savvy. Either they do not manage to get into a group, or refuse to do so and thus get easily targeted. It is often not enough to be simply intelligent, but one also has to be able to sense group dynamics and be a part of it. Which kind of of requires different kind of intelligence.

The sperm is staying outside the body all the time.

Perception of time is a funny thing. It is not directly related to cellular function per se, that is, an increase of APs per time does not translate into a slower perception of time. A classic experiment by Libet showed that a stimulus requires around 500 ms to enter the brain, however subjectively you experience it in half the time. The reason is that your brain backdates this sensation, giving you the illusion that you can feel a stimulus 250 ms before it actually reached your brain. This is the reason, why we feel stimuli subjectively as almost immediate (e.g. upon touch) rather than with a half-second or so delay, which we actually do. Drugs that fiddle with this type of perception can easily mess up your sense of timing. I should add that Libets findings came under some serious discussion around 2000, but I think the gist of it still holds true.

It really depends on what level you define "senses". On the cellular level you require receptors for signalling molecules, nutrients etc. to sustain life.

I also fail to see any controversies, and was therefore not able to address the question. The follow-up post makes it clearer what is meant, but as already mentioned, the tRNA is post-transcriptionally modified in several areas, especially the uridine. Again, that is basic textbook, no controversies here. These modifications influence the structural integrity of the tRNA. For instance, the composition of modified bases is markedly different in thermophilic as compared to psychrophilic organisms in order to ensure a functional tRNA despite extreme high/low temperatures. It could be that the misunderstanding was just the result of maybe slightly awkward wording in the OP. In any case, a number of enzymes

Introducing proteins directly sounds interesting. However I am not sure if it is a good measure of DNA transfection. But then I assume that the authors will have made comparisons. In any case, I would be interested to hear what worked for you.

Well, that is obvious of course. But then for instance mouse models are sometimes used to explain phenomena in humans that for ethical concerns can not be conducted. And sometimes the pathways are not as conserved. But the real reason of course is that it justifies coffee/tea consumption. The main thing that keeps a lab running

I am not sure I understand you. The modern synthesis has already included more aspects than mere natural selection as the sole driving force of evolution. The call for "newer" evolutionary theories arise at least partly from the fact that a number of the basic tenets of the modern synthesis have been found to be wrong or at least imprecise. At the moment to my knowledge there are mostly publications pointing out these problems and calling for a new synthesis. These are sometimes called extended synthesis, as pointed out, though some other calls for something fancier, like postmodern synthesis. I have not followed this close enough to state whether a consensus will come soon or not.

Actually you can separate according to quite a variety of properties including, but not limited to size, charge and hydrophobicity. Also depending on what you use as the mobile phase or how you derivatize your sample you can change the properties in such a way that allows separation of the substances in question.

Actually the main reason is not to recognize RNA. Or rather it is the other way round. Thymine is formed by methylation of uracil. So in other words, it is additionally modified in the DNA (for stability and fidelity).

Well, generally epigenetics is usually a catch-all-phrase that includes any effects that effect gene expression, are are stable over a cell generation (but not necessarily a generation of the whole organisms) and finally, do not alter the gene sequence itself. A stable trait that is above the level of genes, so to say. Actually the oldest examples (a few decades old) include methylation of DNA, resulting in silencing of specific genes. The results can be very elaborate, like in the case if imprinting (which also require certain acetylation of histones). Chromatin structures are more complicated, though. I have to admit that I am not an expert on this particular area (and there is a bloody large amount of studies in this area), however chromatin structure is heavily directed by a large number of proteins, both structural ones, as regulatory ones, and those in-between. I think in popular science it has become more prominent lately, as some believe that it challenges Darwinian evolution. Which is not really corrects as Darwin did not exclude Lamarckian modes of inheritance. The following neo-Darwinistic theories refuted Lamarck, though. Also the modern synthesis (to my knowledge) assumes that genes are the units of inheritance. However, the modern synthesis is undergoing so many changes in the last decades it only partially resembles its original form anymore. But I digress. To put it short, epigenetics is not a single mode of regulation, but encompasses a number of known and probably more unknown mechanisms of gene regulation. Epigenetic influence on chromatin structure is a bit newer (certainly newer than silencing by methylation), though it clearly still an interplay with a number of TFs and DNA binding elements. To my knowledge in tumour studies a link between Notch signaling and epigenetic silencing has been suggested a while ago, I have not followed that up, though. However, I wonder what the OP means with "easier and more controlled"? More than what? The majority of fast responses will certainly be mediated by TFs, riboswitches and sRNAs, whereas epigenetic modification are certainly a major player in cell differentiation.

I could not find the manufacturer of the bags I was thinking of. I think I left the last package in my old institute. Anyway, those tents are of course not as sturdy as "real" glove boxes, and their main use is often to create an anoxic atmosphere. To see the price you have to register with sigma-aldrich. A selection of glove boxes can also be found at http://www.coleparmer.com/catalog/product_index.asp?cls=2035 If you buy glove bags you also have to buy some cotton gloves to avoid damage to the bag. It is not trivial to completely remove dust completely (I am sometimes doing microfabrication, where dust really hurts) and often the bags and boxes are not that clean to begin with.

Oh, I think it got you now. So you are saying that the beta-galactosidase levels change if the vector of the carrying the regulator, or even if only the regulator changes? Hmm is it possible that the repressors in question have a weak affinity to the promoter of the beta-galactosidase?

Normally beta-galactosidase is fairly stable, hover the viral promoter (in this case CMVp is sometimes not expressed stable and reliable in all types of cells). Maybe this can be a factor. OK I did not quite get that one. Did you observe a change of beta-galactosidase levels if you co-transfect it with a different plasmid than pGL3? Another effect might be dilution. AFAIK the luciferase gene in pGL3 is under the controle of the SV40 promoter. If the beta-galactosidase is, too, then you might get competitive effects.

That is why rhizobia-legume symbiosis rulez

Biologically fixed nitrogen is not a nitrate but ammonium: N2 + 8H+ + 8e− + 16 ATP → 2NH3 + H2 + 16ADP + 16 P The Haber-Bosch process is used industrially to fix nitrogen (again the actual fixation step a catalysed reaction between nitrogen and hydrogen). Legumes cannot fix nitrogen themselves, but root nodule bacteria, collectively called rhizobia, are responsible for it. Actually I do not any plants that are able to fix nitrogen all by themselves.

Essentially you are on the right track. This has more to do with logic than actual genetics (well except knowing what recessive and dominant traits are). So essentially you have just to track down, which possible genotypes correspond to the observed phenotypes. Morganne can only be eebb as noted correctly as her mother, as these are the only genotypes that allow orange with brown nose. However Valor (the father) has four options: EEBB EeBB EEBb EeBb However, only in case can Valor be the father of Morganne. Which is it?

If you cut it with a single restriction enzyme, it depends on the recognition site of the enzyme and how often it appears in the respective plasmids. In the simplest case it is just a function of plasmid size. If there are more than one site in each plasmid, chances are high that the result is not a single fusion of two plasmids but rather (depending on fragments) a number of smaller, circular DNA fragments (which are usually instable in organisms). Also simple recirculization of the respective plasmids will occur with high frequency. Again, dependent on size this will usually occur with higher frequency than a plasmid fusion. Normally type II restriction enzymes always generate compatible ends (either sticky or blunt) as the recognition site is palindromic. There is nothing like a DNA strain, only a DNA molecule. Do you mean a DNA strand instead? Single strand I mean? In that case, just envision how an enzyme cuts and think, how a single strand gets cut.