Is there any proof of beneficial mutations?

I'm with Wounded King, this is an example of colonial behaviour emerging in a unicellular organism not the emergence of a multicellular organism. Boraas et al do suggest that it's a possible starting point for multicellularity in a later paper* but there's no cellular differentiation, and the colony reproduces as individuals, not as a collective. In fact pretty much the only difference is in cell adhesion.* - Boraas M.E., Seale, D.B.,Boxhorn, J.E. (1998) Phagotrophy by a flagellate selects for colonial prey: A possible origin of multicellularity Evolution Ecology 12(2), pp.153-164Edited by Mr Jack, : No reason given.

I can think of four reasons off the top of my head:1. The repair of DNA is an extremely energy intensive, and on-going, process. At times of stress organisms may divert some of the energy invested in maintaining the health of DNA into more immediately vital functions.2. Many stressors will themselves directly damage DNA. This is often why they're stressors at all.3. Stressors that occur during mitosis can disrupt the process, resulting in copy errors, replication slippage (causing duplication or deletion errors) or the misseperation of plasmids, and proteins into the two daughter cells.4. Organisms will often respond to stress by commencing the synthesis of many new proteins. In order for genes to be expressed, the DNA coding them has to be unwound, and the strands separated so that the antisense strand can be accessed for transcription. During these processes the DNA is more vulnerable to damage than usual.Although, I'll note my disagreement with AZPaul3 when he says "a colony of bacteria will often quicken their individual mutation rates in hopes of hitting on some useful mutation before the colony dies out completely". I do not think there is any particularly credible reason to think the increase in mutation rates is adaptive rather than simply a consequence of the circumstances.

Also, using negative plating, you can specifically choose a founder population that you know, for a fact, is not resistant. Doing it this was you can be quite sure that any resistant bacteria found later must have emerged by mutation.

Wounded King has alluded to the CCR5 Δ32 variant in his reply. I am not sure whether this is the mutation that Greyseal referred to, but having just finished a course on how genetic variation effects HIV susceptibility and performed lab experiments specifically into the Δ32 mutation in human cell lines it's one I happen to know quite a bit about.The HIV-1 virus enters human immune cells by binding to two surface receptors, one is called CD4, the other is either CCR5 or CXCR4. CCR5 binding is usually involved in the initial infection and early stages of the disease, CXCR4 binding in the late stages. CCR5 is a cell surface receptor involved in immune system signalling, and part of a family of receptors referred to as 7TMs because the protein crosses the plasma membrane that forms the cell surface seven times.In the CCR5 Δ32 variant a 32 base pair section of the CCR5 gene has been deleted. As you'll doubtless be aware, DNA is "read" in codons of 3 base pairs at a time, each coding for an amino acid. Because 32 is not a multiple of 3, this deletion produces what is called a frame shift meaning that the codons after the deletion are read in a different fashion. In the particular case of the CCR5 Δ32 variant this frame shift produces a stop codon shortly after the deletion. A stop codon being, of course, one of the three codons that does not code for an amino acid but instead triggers translation of the protein to stop.Now, human cells (like other eukaryotic cells) have a mechanism for detecting damaged protein transcripts and genes called nonsense-mediated decay in which gene transcripts that contain multiple stop codons are marked for destruction before they can be converted into proteins. It is thought that this mechanism means the CCR5 Δ32 protein is never produced (certainly none has been found). Even if it were produced, and transferred to the cell surface it would not bind HIV-1 because it lacks the section to which the virus binds since this occurs after the stop codon.So, without the CCR5 protein on the surface, the HIV virus is unable to enter the cell, and thus unable to infect the person carrying the mutation. In people who are heterozygous for the wild type and Δ32 variants, they merely have fewer CCR5 receptors on the cell surface and are approximately 25% less likely to catch HIV than wild type homozygotes. Δ32 homozygotes are, while not quite totally immune (because it is just possible for the virus to enter via interaction with CXCR4) they are about a thousand times less likely to catch the disease.(Oh, and BTW, whether the CCR5 Δ32 variant is actually a beneficial mutation depends on context because while it protects against AIDS, it makes the carrier more susceptible to West Nile Virus) This is quite wrong. AIDS is well understood in terms of what it is, and what causes it. In fact, compared to most diseases, it is extremely well studied. Edited by Mr Jack, : + bit about West Nile VirusEdited by Mr Jack, : No reason given.

While West Nile is typically harmless, or only produces mild symptoms, it can also cause fatal encephalitis, so it's not as harmless as all that. I'm personally sceptical that the variant is as completely harmless as thought because organisms don't usually carry around functional but pointless genes. However, if the Δ32 variant is as harmless as currently suspected, I'd point out that the incidence rate is within that explicable simply by genetic drift and other neutral factors. Especially as the trait is largely recessive.I don't know specifically of any work done in this area, though.

I don't think they are lying; I think they are wrong - as do the vast majority of the scientists with working knowledge of the area.You'll note that like many other scientists with what could kindly be described as unconventional views she's not a specialist in the area she's holding forth her views on - she's a PhD in Mathematics, not biology, not epidemiology, not viriology, not medicine, etc., etc.

We agree with you. That's exactly how mainstream evolutionary theory describes matters. New features, almost without exception, are simply modifications of old features. Often after duplication freed up one copy for modification. This is where you are wrong. Functions are not discrete entities. Take a feather for example. A feather is a modified scale (we know this because of the proteins involved in its formation, the proteins involved in its structure, homologies with other organisms, and the developmental processes through which it goes). A scale's primary function is protection. Simple feathers, similar to those found today on many birds, and in the fossil record on many dinosaurs, are a small modification of a scale. A small shift in the timing of various development signals causes the production of a small branched structure. These "downy" feathers provide insulation.A few further small modifications turn these downy feathers into stiffer, straight structures similar to those that appear to be present on pre-avian running dinosaurs. These were probably primarily used for signalling, but may have also had an aerodynamic role. And then, finally, you have the true flight feathers, capable of directing the flow of air, and providing a light, stiff-but-flexible, large flight area. A new function, but no abrupt change, just modification of existing function.The same with the wing bones themselves (in bats, birds and pterosaurs, in fact); no new bones, no new muscle groups, just modification of the proportions of existing bones leading, eventually, to a new function.Edited by Mr Jack, : No reason given.

Huh? What do retroviruses have to do with this?There are a great many genes involved in feather formation, including many regulatory genes. It is rare for regulatory genes to be uniquely involved in any particular feature so it is likely that many of the genes involved are active elsewhere.