CharonY

If you are really interested interested in long-term preservation better do not use bleach. While it will not harm it immediately but after a while (which actually can take months) the skull will actually look old and brittle. If the specimen was still fresh one of the standard techniques is to boil it gently or to let it macerate in warm water. This is probably not really necessary anymore, if your specimen lost most of its meat anyway. Best fist wash it thoroughly (use gloves and old clothes). The best way to proceed then is, as mentioned above, using biological washing powder (essentially enzymatic detergent). Ideally keep the water temp at 50-60 C, though it depends a bit on what you use. You may even use a detergent that does have antibacterial substances (but not bleach). Though most of the time it is probably not strictly necessary, if it has been cleaned thoroughly. Finally, if you want to have the the skull have a bleached look, hydrogen peroxide is the way to go.

Essentially no. Some of the details between eu- and prokaryotic translation intitiation are different, requiring additional factors in eukaryotes. A simple transplantation of the ribosomes alone would thus render them dysfunctional. And as mentioned by GDG the code itself is essentially not ribsomally enforced.

Well there are single celled organisms that do phototaxis, mostly positive as they are photosynthetic. But it is not normally linked to predator avoidance as most organisms predating on anything of that size do not cast noteworthy shadows.

Well, they are bigmouths, then. A few years older than you means that they are still undergrad or maybe just grad students. Very few will be able to really run a lab (as opposed to go in lab and do what they are being told to) and no one knows everything within a given field. If they believe that, they are in for a nosedive. That being said, you are still just starting off. At your level almost no one will already have a real inkling what science really is about and how it is conducted in a research setting. Do not be distracted by others or thoughts how you think things should be. The most important bit: build your own knowledge foundation. This is what undergrad studies are all about. You are not (yet) being trained being a scientist, but you are there to learn the basics. The more solid you can make the knowledge, the easier the transition from learning science to doing science will be. Do not overestimate things like "talent" or being "naturally good" at something. This is way overrated. Working hard and learning how to learn beats the crap out of talent (but being lazy) every time.

Off topic, but are there real-life examples for this? While technically not impossible and apparently logical I cannot recall any single-cell organisms off-hand that do that (active predator avoidance, that is). The only mechanism I am aware of are more passive in nature and inhibit the predatory mechanisms (e.g. by means of reducing accessibility of inhibition of lytic activities, etc).

OK, so in summary different states have different prerequisites and even in the "hardest" case it does not go above a bachelor's degree? That is... surprising. (Unless I misunderstood something).

What, btw. are the required qualifications before one is allowed to teach in highschool? I have one or two things to say regarding uni education sometime later, too.

You mean whether these are specific to pathogenicity? Well, maybe one should consider some definitions at this point. Pathogenicity factors are generally used to describe elements that cause the disease, whereas virulence factors attenuate the severity of the diseases (e.g. success rate of infections). Regarding the list in the link: for instance pili are a common feature of bacteria and it is mostly involved in adhesion and/or motility. Pathogens as well as non-pathogenic bacteria possess them aplenty. Same goes for flagella. Toxins are a special case, though depending on the nature of the toxin several cases are imaginable. Some toxins are secreted and may e.g. accumulate in food, while the bacterium itself does not infect the body. Still, it will cause harm. Bottom line is that characteristics of pathogens usually involve a relative large number of factors, some of them readily identifiable (as e.g. toxins) some are more obscure or involved in general pathways.

This is depends largely on the context of the talk. In lectures it is ok, in short presentations (as indicated above) it is a waste of time and generally frowned upon. Unless you have a brilliant hook of sorts. But even then a rhetorical question may be more appropriate.

Well, again, contagious and pathogenic are two different aspects. Almost all bacteria (except extreme specialists) can spread to a given extent, and are therefore by definitionem contagious. Yet they do not necessarily cause harm. If your hand is sterile and you touch any surface you will get bacteria on it. There, transmittance happened. You won't usually get sick, though. The bacteria just has to be able to grow on the given surface (in this case, skin). And also again, there is hardly anything that can be considered a pathogenicity factor that is shared by all pathogens (if we want to limit it to diseases). The routes of infection and persistence that bacteria employ are simply too varied. Of course one can have a bit of a circular argument instead. Pathogenic bacteria share traits that enable them to infect, overcome immune response, and cause disease . I think one of the few common things I can think of are toxins of some sorts, though they are very diverse in nature (and are just commonly labeled toxins due to their ability to cause harm) and not all pathogens are known to produce any of them.

OK, that makes more sense. Note that I am not an expert in this field, but assuming that he/she meant an antibody staining after fixation, there is no real way to confirm origin as (afaik) the recycled proteins do not undergo any specific and detectable modifications. Additional experiments are needed and may either include disruption of recycling pathways or tracking the internalization of (labeled) surface proteins. For instance, if the protein in question is not stably localized in the membrane, one could label it shortly (e.g. with an antibody), wait until it vanishes and check for the re-appearance of the antibody on the surface after re-incubation.

Yupp, precisely.

Well, in a way by trying to be vague you inadvertently made a false statement. Ie "combining" molecules usually would be a reference to anabolic pathways, which is the opposite to what is happening with glucose. It would be more correct if you had worded it as "breaking down"- both are not normally used, but for a layman they make somehow sense and are not really wrong. I just had to point that out as I was unable to pass up the irony in your post

Actually I prefer to have everything on a slide, but it has to be very short so I can skim through it in a few seconds and then concentrate on the talk (as part of the audience) or to remind me what I am going to talk about and in which context (as speaker). Personally I dislike things popping up. I prefer a slide to be static (with very few exceptions). Talk to the audience and do not stare on your screen, notes, whatever. Rather use the points on the slide to remind you what you want to talk about. Practice your talk! Stay in time and allow some for discussion. As a student or sometimes even postdoc showing nerves is expected, just do not overdo it.

Well, if we talk about proper wording, glucose does not yield ATP by combining it with other molecules... To be precise, the yield varies with how the complete oxidation is conducted and how the created reduction equivalents are used for oxidative phosphorylation. The substrate level gain is easy to assess, however the oxidative phosphorylation is based on estimates as the ATP generation is based on the creation of a proton gradient to power the ATP synthetase. The often cited 36 (or even 38) ATP is likely a bit of an overestimation.

Also the context of the question is important. It sounds like a highschool question, which expect a dumbed down answer. Even for that the question is pretty lousy, though. Contagious just means transmissible (and not, as iNow correctly mentioned, the means of transmission). Essentially all bacteria that are able to live on a given vector are transmissible. This includes non-pathogenic bacteria. Just think about it. How do you get your normal bacterial flora? Now if the question is what are common characteristics of contagious pathogenic bacteria, things are complicated. Short answer is that there is likely no common trait exclusively shared by all pathogens that are not present in non-pathogenic one. Many pathogens are specialists in one way or another and quite often pathogenicity factors are elements that are also found in non-pathogenic bacteria, but it makes them pathogenic in conjunctions with yet another factor.

Sorry, maybe it is just the lack of caffeine in my blood system, but you are not making terrible sense to me right now. First you started off with (my bold) and now it is not based on microscopic observation but based on... what? Also the main question is still not clear to me. Evidence for e.g. localization can be based on different techniques, of which some are considered more definite than others. Thus the actual technique in question is significant.

It is true, though.

First, how did you detect the protein in the first place? Fluorescence tagging? Antibodies? Second, what precisely is your question? Whether it is a membrane associated or integral membrane protein versus co-purified membrane fraction?

You would only get around a third of all characters in an average newspaper, though.

Uh Pangloss? Being literate usually requires the knowledge of 3 to 4000 characters.

Use the BLAST programs. Generally searching for 100% matches has only limited value in real analyzes, hence alignment programs as BLAST are used.

Well essentially the answer is there, a virus is a mobile genetic element requiring a cell to propagate. Hence, it cannot predate cells.

Actually it is always the complementary base. That is A pairs with T (or U) and G with C (and vice versa). So if the DNA sequence on the strand to be transcribed ist ACTG the RNA sequence would read UGAC. The whole system works unidirectional (5' to 3') so towards the 5' is considered up and the reverse downstream. Also in addition to the actual start codon the mRNA also contains more sequences that are not transcribed into a protein but are necessary for transcription (i.e. ribosomal binding site).

The first thing you need to get is that RNA is just transcribed DNA. Ie the sequence is complementary to the DNA strand getting transcribed. Now, the promoter is a specific DNA sequence upstream of the actual part of the DNA that gets transcribed into RNA. Essentially it is a regulatory element to which an enzyme, the DNA dependent RNA polymerase, together with certain other factors, bind in order to create the complex that does the actual transcription from DNA to RNA. It is often also the target for regulatory elements that enhance or reduce the binding efficiency of the complex and thus regulate the transcription rate.