CharonY

I would go to the nearest university library.

It could be helpful to break out some specific mechanisms and discuss their implementation in the US. Oftentimes terms like universal health care, European/socialist system etc. are thrown around without specifically defining what is meant. This is especially troublesome if quite different models are discussed under the same term.

One thing that one should note is that there is no European systems. Each country has a different model ranging with the NHS sytem in the UK being the most centralized (I believe) to mixed models (e.g. Germany). They are compulsory, however, and all receive at least some degree of public funding, ranging from almost 100% in the UK to about 50% as in Italy, I believe.

It will depend on your application and the type of your sample. For trace analysis, for example use of strong acids is pretty much standard for a variety of reasons. However, if your sample is a liquid, the use of ion exchange and/or chelators can be an alternative. Same goes for deproteinization. If you want to remove it e.g. from body fluids, precipitation using a variety of techniques (TCA, acetone etc.) are often used.

What is this "English" everyone is talking about?

Typically, both will compete for the available nutrients until it becomes limited at which point nitrogen fixation may start to occur. If nitrogen is provided in excess, both will happily utilize it. As chadn737 explained, just because the plant has the potential to symbiotically fix nitrogen, it will not initiate it until it senses nitrogen limitation.

Describing the context or the protocol would be helpful.

I am not sure who the someone is, but this here is a science forum and unless that someone has published something pertaining to this his/her opinion or the depiction of in a movie is immaterial. If you really want to use the analogy with the alphabet, the mutation create new words. Recombinations just changes the order of existing words. If you eliminate mutation from this we are stuck with a limited vocabulary. Just to make it clear, assuming that mutation only plays a minor role in evolution directly contradicts existing knowledge. It is strange that you want to replace one misconception with another. Also: -especially in animals, plants or other organisms with larger genomes mutations are more likely to be neutral rather than under positive or negative selection -life started about 3.6 billion years ago so roughly a billion after Earth was formed Let us flip things around. The importance of mutations for evolution is well established in a vast body of literature. Do you have anything (e.g. literature) to provide except random thoughts that provide evidence to the contrary? If not I would advise you to actually take a look at the literature and, if something is unclear, ask question to improve your knowledge.

Just in case that there was a misunderstanding, a straw man argument is essentially building up an argument that no one made and then tearing it down. As has been mentioned, no one is arguing that evolution is driven by mutation alone (this is the straw man), and therefore trying to refute this point is moot. As already mentioned mutations are a crucial element (but obviously Darwin was not aware of details, but then there was quite some progress since his days). Also, many, if not most organisms are haploid, so dominance plays basically no role here. Take prokaryotes, for example. Important variations arise by mutations and some of them have the ability to increase their mutations rate once being severely stressed. They do engage in horizontal gene transfer but obviously that accelerates spread of genes but does not create allelic variations per se. The whole argument is based on limited understanding (which is fine) but I recommend reading up a bit more before trying to propose a model that flies in the face of current knowledge. The main threads are there to discuss mainstream science, which generally requires a bit understanding of the same (or willingness to learn about it).

That OP is a bit of a straw man, as evolution is not clearly driven by mutations alone. Nor is it mainly driven by recombination (quite obviously, considering the vast abundance of asexually reproducing organisms). Both are but aspects of the larger pictures. It should be repeated that evolution is in essence the change of allele frequency in a population. Mutations and recombination affect the available diversity, selection and stochastic events change the frequency. As such obviously mutations are still will continue to be an important aspect.

Well it is not the first to conclude this. It just has a larger data set. The issue is that unfortunately it does not really matter. Anti-vacciners have ignored all the other evidences and it is unlikely that an additional data set is going to sway their minds. Those that follow the data should be pretty much already be aware that the link is bogus, anyway.

The situation you describe is pretty close to what happens (there are some extra caveats, but I will it ignore it for now). The way to test this is simply by looking at a population of, say hundreds of cells and simply count whether the mutations are somewhat equally distributed. If they are, it indicates that under the given condition none of them are being selected. Put the same cells into a selective condition, you will see a massive change in frequencies (i.e. the beneficial ones will be suddenly dominant). For the horse example it would require that its own DNA changes during its lifetime while eating from high leaves as opposed to eating low leaves (which can also be easily tested). As for the plos paper, here the population of flies is kept under a given selective condition (i.e. dark) and again, the mechanism is that during these conditions there will be a shift towards beneficial traits. What may confuse you is that these changes have to be viewed from a population perspective and results in changes of overall frequencies over several generations. If a horse feeds from a taller tree, its DNA does not change and its offspring will not have significant longer necks. However, if in a population of horses there are a few with longer necks, they will likely have more offspring and after a few generation you might see horses with longer necks. However, you can trace them back to those parents who originally had longer necks, as opposed to those with shorter necks but who fed on taller trees more frequently.

The bacteria are grown under non-selective conditions. I.e. the auxotrophy or sensitivity has no bearing on their survivability. As such the mutations would be neutral under the given circumstances, but turn beneficial under selective conditions. They the molecular mechanisms would have no way to peak into the future there cannot be any specific changes. One should also add that outside of mathematics science does not work with proofs. As a general rule we eliminate hypotheses. For example one could assume that once faced with a give selective situation cells somehow respond in a Lamarckian way. However, as the actual mechanism (gene mutation) are happening before they face the selective situation it can be seen as highly unlikely. Moreover, we have quite a deep understanding of the biochemistry behind mutations and also the specific changes resulting in certain revertants (in case of auxotrophs) or resistances (and it is an almost trivial matter to sequence the DNA of mutants now to validate it). In other words, the body of evidence strongly points towards unspecific mutations rather than adaptive responses. Note that there are also developmental effects in multicellular organisms, in which phenotypic variation is the result of complex signaling (internal and external) rather than on mutation.

Well, evidence is pretty much ubiquitous. But if you are thinking in terms of controlled lab experiment, one typical undergrad experiment is to take bacteria that are not able to grow under a given condition (e.g. auxotrophic mutants that require feeding with amino acids, or antibiotic sensitive strains) and expose them to a mutagen (not strictly necessary, but it increases mutation rate and accelerates the experiment). Then plate them onto restrictive media (i.e. either lacking the necessary nutrient or with a low amount of antibiotics). Usually there are a few colonies growing indicating that they had mutations that allow them to grow on the respective media before they actually ever encountered that situation. The experiments by Lenski are somewhat similar only on a much longer scale and with larger phenotypic changes.

One interesting bit that was cited is: One of the reservations that I have with powerful companies controlling food supplies (though is basically already the case for a long time and not specific to bioengineered food), is that normally small scale farmers see little benefit and/or they may become financially tied to a given corporation (and again, other companies are also already doing that). Due to the business models involved I am skeptical that under the given circumstances some of the benefits (such as alleviating hunger) is really going to fly. The Gates Foundation backed model seems to specifically benefit those vulnerable farmers, which is quite a positive change.

Electrolytes are formed when dissolved in water. Cells on the other hand have a lot of stuff attached to them (produced by the cells) that serve a number of functions such as proteins that can act as sensors or transporters etc. While they do affect the overall surface charge of the cell it they are not electrolytes. The latter is almost exclusively reserved to characterize small ions.

It is going slightly off-topic here, but there are mechanisms that are even stronger than our feeling loyalty. Social insects die for their hive, for example. Vampire bats would sacrifice valuable nutrients to feed non-related individuals, each act at the potential loss of their life (as blood does not hold much nutritional value) and so on. I think it is fair to say that if we look much closer at social behavior of animals (and honestly our knowledge of behavior in the wild is really limited) I am quite confident that we will see behavior that at least rival our own. We do have the ability of empathy, which appears to be an important element and so do many other social mammals. What I am saying is that what we perceive as social behavior arising from intelligence, is most likely rooted in a similar mechanistic context as other organisms. We do express it differently, but then it is also because or living conditions affect the way we express it. For example, if we were organized in communities with food limitation, I am pretty sure that we would detect much more evidence of altruism based on kin selection.

I think that needs a bit of a qualifier . As a whole plants and animals are generally aerobic, of course, but individual cells do not necessarily full access to oxygen and still survive. For example in many animal bodies there are steep oxygen gradients as not all cells have equal access to blood and quite a bit are functioning at or close to hypoxic levels for quite some time. Somewhat similar effects are also observed in plants e.g. during seed germination or certain very compact tissues. In fact in plants hypoxic (posttranslational) signaling has been relatively recently discovered that regulate anaerobic respiration. This does not invalidate the point that for proper cell proliferation oxygen is required and that at you cannot cultivate cells endlessly under anerobic conditions, but I think one should point out that there quite a few shades of grey to think about (or I am just nit-picking).

I assume with proof you mean evidence. Except you only provided anecdotes, which qualifies as neither. The only thing you offer are a stream of thoughts while bypassing any literature that may address the points you mention. Overall, not a terrible successful way to conduct yourself on a science board. The OP is no better than other speculations claiming to have found the secrets of the cosmos. For now, I am moving it to speculations.

Pretty similar things happen during normal maturation. You start off as a single cell and it grows into a large multicellular being. It is an interplay of a lot of signals and cellular reactions. The whole scientific field of developmental biology is devoted to this. If you expect a simple two-paragraph answer I must disappoint. The whole thing is quite complicated and would require significant background to understand. Suffice to say that the process is far from perfect and there are a lot of mishaps that occur fairly often.

I would rather say "than some other animals". Social behavior can be found in many species and I am pretty sure we share some basic mechanics that make us want to be social (as opposed to primarily solitary animals).

Moved to homework.

By activating transcriptionally I presume you mean activates transcription? If the starting protein amount (after the pulse) is very different, it may skew the results in unexpected ways. Generally pulse-chase is sensitive to quite a number of factors (with time being a critical one) as many steps such as starvation prior to pulse or use of inhibitors can alter the physiological response of a cell (which in turn affects half life e.g. by activation the proteasomal degradation pathways). If it has dual functions you would probably really have to look at the result before one could figure out what to do. For example, if A is produced in larger amounts than the degradation system can cope with, the half-time shifts to a higher value even without actual stabilization. On the other hand it is possible that stabilization by B is crucial but it is not similarly induced then a smaller fraction of A is going to be stabilized and the calculated half-life would appear lower (just to give some crude ideas off the top of my head). In the end it would probably depend whether you actually can see a change in half-life and then you may have to alter experimental design, maybe using inhibitors to eliminate other sources of stabilization effects.

If the mode of interaction is not clear you may open up a giant can of worms. For example, another possibility to affect protein stability is post-translational modification. For example, by preventing or enabling ubiquitination degradation by proteasomes are initiated. The half-life of a protein is the sum of these and many other factors and it would be very tricky to elucidate the mode of interaction based on this property. But the first thing I would do is to figure out whether B has any domains that indicate any of these roles (such as DNA-binding).

How about hippos?