CharonY

This is off-topic, but why would you think so? Per definitionem most of us will be average (well, depending on the distribution, as well as the kind of average, given variance etc.). If everyone tries to be exceptional, well that would just shift the average, no? Reminds me a bit of something a student wrote on an evaluation (not mine): "This lecturer makes it really hard to get an average of A"...

The charge of DNA is primarily due to the phosphate groups in the sugar backbone. But first for the definitions. What does melting of DNA mean (or using your words, what should dissociate?). And what is the bond that holds it together?

I am not familiar with psychology databases (with the exception of those that are also present in pubmed). With regards to keywords it is usually helpful to look if there is a specific term describing what you need. As I am not familiar with the subject I would start with "feedback intervention" get a couple of reviews and try to work backwards from there.

In vertebrates it is TAP/NXF1. The homologue with the same function in yeast is Mex67p.

Some shops want to minimize the risk of selling alcohol to minors. Many (especially chains) therefore have implemented the rule that if the buyer looks younger than 35-40 (varies from shop to shop) the driver's license has to be shown. But of course other info including zip code are also often picked up. I have no idea at why you would assume that the government has a hand in it, as this info is mostly used for marketing purposes (or sold for the same reason). If the the government (e.g. police) wanted to know what you are buying they usually just get your credit card info (which probably is also somehow sold by the credit card company). In fact it is more likely that the private sector is toying around with your private information as they have more direct interest in it.

Just a short note: I messed up on a point The wait time is of course [math]\omega[/math]. That is what you get when posting in a rush. Geez.

First of all, most health related issues due to dampness are afaik more due to fungi (i.e. mold) rather than bacteria. Most that are pathogenic are not that competitive outside the body. Also the counts themselves are not helpful by itself if there is no quantitative reference to what is expected. That being said, starting with the bottom, Rhizobium is a root nodule bacterium that forms symbioses with legumes. It is absolutely harmless. Corynebacterium these are ubiquitous bacteria, often associated with soil samples, but also commonly found on the body. Most are harmless, but there are a few pathogenic strains. However the mere presence is usually not cause to alarm as they are expected to be there. Bacilllus same as with corynebacteria. Chances are that they are harmless. Staphylococcus are also found in soil and on your body. Most are harmless and are expected to be presence in a house. Micrococcus species are also found in skin and afaik there are no reports strains pathogenic for healthy humans. Kocuria kristinae (finally something on the species level) are also known to be part of the skin flora (they were initially classified as Micrococus and similar to those only cases where the immune system was already compromised infections were reported. Do not take this as a medical advice, as I am not qualified to give any, however the list of bacteria is not uncommon to be found in a house. Most of them are part of the normal skin flora and are the likely source. Also many are found in soil, which provides an additional way of getting them in. Unless the titers are unnaturally high they are not by themselves a matter of concern. It should also be noted that most of the pathogenic species are less competitive than their soil living counterparts so that if they are found on some surface it is more likely to have the non-pathogenic ones than the others.

Ok continuing the post: So keep in mind that the authors took a look at fitness increase and mutation rate (=genomic changes). One question is what the expected relationship between those two is. To summarize what I said in the earlier post the time until a beneficial mutation escapes extinction is [math]\omega[/math] [math]\approx[/math] 1/(2SN[math]\nu[/math]) And the time for the beneficial mutation to spread to 50% of the population (and assuming a Poisson distribution of offspring) is [math]\tau[/math] [math]\approx[/math] log2(0.5N)/S With S being the selection coefficient (high values indicate higher selective advantage), N being population size and [math]\nu[/math] the rate of beneficial mutations. The important bit is only to keep the relation of the parameters in mind. So assume the following scenarios: 1) no effect on the selective advantage or beneficial mutation rate due to substitutions of beneficial mutations. In this case both, the rate of genomic changes as well a increase in fitness should remain constant. 2) assume that the number of beneficial mutation sites is finite. The more beneficial mutations it already has, the less likely it is, to gain a new one. Hence [math]\nu[/math] declines over time. Thus, the wait time [math]\tau[/math] becomes longer and both, the fitness increase, as well as the genomic change rate will decelerate over time. 3) assume that the selective advantages decline as more beneficial mutations arise. I.e. the first mutations gives a large boost in selective advantages, but the second one only adds a little bit more to it, etc. With a decline of S both [math]\omega[/math] and [math]\tau[/math] increase. And the effect would be a deceleration of fitness increase and genomic change rate. Note that in all scenarios fitness increase as well as genomic change rates either decline or remain constant, without the need of changing the mechanisms that lead to mutation. In scenario 2, for instance the deceleration is merely due to the constraints on targets that may mutate (i.e. due to the limited beneficial sites). Now take a look at the abstract again. . Here they state that the fitness increase decelerated, whereas the genomic change rate was constant. This does not fit any of the simple models stated above. How do the authors explain this? Stay tuned for more after a short break.

Yeah nomenclature is quite a bit messed up with regards to amoeaba. Essentially it is a catch-all name for anything that does not appear to have a rigid structure. Naegleria for instance are (as pointed out) called amoeba, but they belong to a completely different phylum (Percolozoa, I think). But my knowledge is pretty dated and I may find myself wrong in a number of details.

Read up on gluconeogenesis.

Yes mutation rates vary, but adaptive mutation is not a point in the paper there was no selective pressure involved. In fact the increase in mutation rate is based on a frame shift mutation in the mutT gene. This gene is known to be involved in base transversions. Also it was only a minor element of the whole article and I am a bit surprised that SA highlighted it as much. The original article is this here, btw. Genome evolution and adaptation in a long-term experiment with Escherichia coli. Barrick JE, Yu DS, Yoon SH, Jeong H, Oh TK, Schneider D, Lenski RE, Kim JF. Nature. 2009 Oct 18 In which Lenski and Kim are the corresponding authors. Take a look at the abstract: The authors investigated two elements. The rate of genomic changes (=observable mutations) as well as the relative fitness increase of the new strains compared to the original parent strain. What is important to keep in mind that even a mutation that gives a selective advantage may be lost due to stochastic events (drift). The larger the selective advantage the larger the chance that the mutation persists. Thus, in order for a mutation to spread through a population it first takes time for it to escape extinction. This time is inversely proportionate to the selective advantage it confers and the mutation rate with which this particular mutation occurs. And then the mutant spreads by selection. The required time for t to become the majority is again dependent on the selective advantage it confers. --------Just running out of time, if interest exists I will continue when I get a break sometime----------------------- Just btw. increasing mutation rate is for most multicellular organisms a bad idea. Think cancer. Asexually reproducing organisms can do it, as even if a lot of sister cells die, almost complete copies of their gene sets will survive (in those that adapt). This strategy obviously does not work with other organisms as well...

Could you point out the context in which they used it? I do not have the article with me right now. But it is likely that you are on the right track.

Weird, I could have sworn that we had a thread about it already, but I cannot find it. The key paper is this here, btw. Proc Natl Acad Sci U S A. 2008 June 10; 105(23): 7899–7906. Published online 2008 June 4. doi: 10.1073/pnas.0803151105. Historical contingency and the evolution of a key innovation in an experimental population of Escherichia coli Zachary D. Blount, Christina Z. Borland, and Richard E. Lenski

Dictyostelium is a slime mold. It also belongs to the amoebozoa. The ones that are more commonly called amoeba (e.g. the Enatamoeba and Amoeba) belong to the Tubulinea, whereas slime molds belong to the Mycetozoa. The latter are the ones that form macrocysts, which represents a form of sexual reproduction (as indicated by GDG). I am pretty sure this has not been shown in the non-social amoeba.

You forgot the most important one. Personal protection. S. aureus are biosafety level 2. Before thinking of handling them get a formal training. At minimum a biosafety hood is required (certified for BSL2 and up, which most are). All work that may create aerosols (including pipetting) or involves handling of cultures in significant amounts have to be conducted under the hood. In addition appropriate personal protection gear has to be worn. Finally the details of cultivation depend on volume and type (e.g. batch cultures, plate cultures, etc.). There is quite an assortment of techniques that are regularly used. Depending on the hood, burners may be inappropriate, for instance (as they may interfere with the laminar stream and hence reduce the protection).

The transfer between pro- and eukaryotes often depends on type four secretion systems. The actual transfer is somewhat different between eu- and prokaryotes, though. The transfer of the ti-plasmid between bacteria, for instance relies on different mechanisms than the transfer to the plant host cell. As such I would assign different names to the underlying mechanisms. Though I think around 2000 there was a high-ranking paper that described the acquisition of plasmid DNA from bacteria by a hamster cell. I believe the author ( I cannot recall the name right now) also referred to this mechanism as conjugation, although the actual transfer was not observable. As I originally came from the prokaryotic side may definition may be a bit more stringent. It is an interesting topic, though and I would be happy if anyone would like to discuss anything in that regard

Conjugation relies on a specific machinery in either pro- or eukaryotes. They are unable to conjugate with each other. Horizontal gene transfer between the kingdoms is dependent on other mechanisms. However, is there anything specific that you want to understand or discuss?

It is cooling to 38° C here. Yey. Bleh.

I was replying to the OP. This is not what is happening (usually). Once the genetic information has entered the genome it will copied over to the daughter cell. This also includes plasmids (or more likely a few copies of the plasmid end up in the daughter cell during cell division).

It appears there is some confusion here. Exchange of genetic material is not reproduction as no offspring is created. What you are thinking of is horizontal gene transfer. Amoeba may be able to conjugate, but to be honest I do not know how common this may be. However, the genome of Entamoeba histolytica for instance showed extensive horizontal gene transfer from bacteria, quite possible from those that have been consumed.

What do you mean with only one plate? One Ouchterlony plate? In any case it depends whether the difference due to the modification is sufficient to raise specific antibodies against it. Or at least distinguish between native and modified insulin. In other words, it depends on the type of mdification.

There are a number of possibilities. Paraquat is often used to generate oxygen radicals in tissue tests. You should just keep in mind that different radicals affect tissue differently and are protected by different mechanisms (with major players being SOD and catalase). As a side note, every aerobic organism possesses mechanisms to defend against oxidative stress (that is why they can be aerobic to begin with). But it does not mean that it oxidative stress does not influence the organisms. It only means that they can survive a higher amount of it.

Sterile techniques in general? They are almost universally the same, regardless of organism. Or do you mean cultivation, or manipulation?

Precisely. Differences in reproductive success is the main point. Death is but only of the possibilities that can affect it. Immortality (as defined as immune to age effects) is basically a trait of relatively simple organisms. The mechanisms necessary for that (e.g. rapid cell proliferation) is probably unsustainable in more complex (in terms of cellular complexity) organisms. For instance, cancer cells are essentially immortalized cell lines. And they clearly do not promote reproductive success....

There are organisms that in their unicellular lifestyle are sometimes called amoebae, like e.g slime molds that form macrocysts. But amoebae in the stringent sense generally do not proliferate sexually.