You do it by measuring the incidence of spontaneous genetic diseases.
For example, you're talking about mitochondrial DNA. Now, there are some genetic diseases which affect mitochondrial DNA. So if a child has them, and the mother doesn't, then that represents a mutation. Now given that mutations are random, there's no particular reason why that harmful mutation should be of higher frequency than neutral mutations. So you can use the incidence of such mutations to measure the mutation rate generally.
I'm too lazy to find a reference right now about mitochondria, but here's a paper where the guy does the same thing for dominant diseases in non-mitochondrial DNA.
Following the logic of the argument that Adam and Eve were created with perfect genes 6,500 years ago I'm wondering if that doesn't necessarily predict that we should be able to take a look at dna from people three thousand years ago and see a pretty huge difference between it and our dna today in that it should be "half as perfect". Anyone know of an example of this? Or does this pretty much not make sense at all.
Note: By "this" I'm referring to what this argument would predict, not the argument itself which is, of course, absolutely retarded.
I want to find a book in the library. Long time ago, I heard someone give me a brief description of it. It's about a spaceship carrying a group of vampires through space looking for a new home. Earth is suppose to be destroyed or something.
Space vampires? I have not heard of this book, but am now intrigued. If you ever find out the title and give it a read, I'd love to hear your thoughts on whether I should likewise try it out.
"Ignorance more frequently begets confidence than does knowledge: it is those who know little, not those who know much, who so positively assert that this or that problem will never be solved by science." - Charles Darwin.
A more recently discovered and less well-known aspect of genome evolution in bacteria is gene loss, in which entire chunks of the genome are deleted. "A region of a hundred genes or ten genes may have been lost [at a time]... these big deletions occur all the time," Ochman states.
Whereas gene acquisition can be beneficial, gene loss is usually catastrophic. However, in host-inhabiting bacteria, the protection of the host environment may allow the bacteria to survive such a loss.
"If you're a free-living organism, you lose a certain gene, if it's essential, you're dead. But if it's something that's not essential," for example a gene for the production of a nutrient you can get from your host, bacteria can keep living and reproducing after the loss, but they can never perform that function again. Further, because they are imprisoned within the host, they may have little opportunity to gain the genes back from other bacteria by swapping genes.
Again: Google is your friend.
"Ignorance more frequently begets confidence than does knowledge: it is those who know little, not those who know much, who so positively assert that this or that problem will never be solved by science." - Charles Darwin.
You're misunderstanding me. It's not about space vampires coming to earth. It's about a group of vampires leaving earth to look for a new home. Earth has been destroyed or something like that.
I don't know. The exact words he used were a group of vampires wandering through space after Earth is gone. At the time, I really wanted to find the book to read it. But then something traumatic came up in my life and I forgot about it until now.
Re: Bacteria Evolving Loss Of Function --- Example Please?
This also isn't exactly what you were looking for ...
Bizzarri et al. 2008 writes:
Four strains of B. thuringiensis, which had been isolated in vegetative form from leaf surfaces, were grown for 500 generations in batch culture in a rich medium. One of the strains, S4g, differed from the parent in the following respects: greater cell width; changed plasmid profile; complete loss of ability to produce delta-endotoxins; loss of ability to produce beta-exotoxin and disruption of vip3 gene; radically different fatty acid composition; and altered metabolic activity. Two of the other evolved strains (S1g and S6g) showed differences in fatty acid profiles compared with the parents. Genetic finger-printing showed that there were also mutations in the cry genes of two of the evolved strains (S1g and S2g). The delta-endotoxins of strain S6g were significantly less toxic to the larvae of Pieris brassica compared with those of the parent and it also differed in the plasmid content.
In this paper (Bizzarri et al, 2008) what the bacteria lose is not metabolic functions associated with vital function as much as those associated with toxicity to insects which eat the bacterias normal hosts.
One of the Lenski lab's long term evolution papers was on this topic (Cooper and Lenski, 2000) and may be more along the lines you were looking for.
Cooper and Lenski writes:
We analysed the decay of unused catabolic functions in 12 lines of Escherichia coli propagated on glucose for 20,000 generations. During that time, several lines evolved high mutation rates11. If mutation accumulation is important, their unused functions should decay more than the other lines, but no significant difference was observed. Moreover, most catabolic losses occurred early in the experiment when beneficial mutations were being rapidly fixed, a pattern predicted by antagonistic pleiotropy. Thus, antagonistic pleiotropy appears more important than mutation accumulation for the decay of unused catabolic functions in these populations.
Unfortunately they don't identify the specific mutations involved in this paper. Another paper however does go into the molecular genetic details of the loss of ribose catabolism (Cooper et al., 2001). Interestingly they find this loss associated with increased fitness.
Cooper et al. writes:
At the molecular level, the loss of ribose catabolic function involved the deletion of part or all of the ribose operon (rbs genes). The physical extent of the deletion varied between mutants, but each deletion was associated with an IS150 element located immediately upstream of the rbs operon. The deletions apparently involved transposition into various locations within the rbs operon; recombination between the new IS150 copy and the one upstream of the rbs operon then led to the deletion of the intervening sequence. To confirm that the beneficial fitness effect was caused by deletion of the rbs operon (and not some undetected mutation elsewhere), we used P1 transduction to restore the functional rbs operon to two Rbs(-) mutants, and we constructed another Rbs(-) strain by gene replacement with a deletion not involving IS150. All three of these new constructs confirmed that Rbs(-) mutants have a competitive advantage relative to their Rbs(+) counterparts in glucose minimal medium.
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