I guess they all ran away.
Run away! Run away! It's Precambrian RABBIT!!
Close enough anyway.
Posted on 07/04/2006 8:42:50 AM PDT by DouglasKC
Now that's interesting. Would you please define these a little more precisely, please?
I.e. within each family (parents to child), each individual member of the next generation has on average 4 mutations?
...and could you give examples of specific human alleles, in which changes qualify as a "mutation" ?
...that'd be helpful in resolving disputes in this and similar threads concerning mutation rates in T-rex or elephants, or changes in that experiment with microorganisms whose holding tank was systematically heated over several weeks.
Cheers!
Err ... Sorry about that. I was late mailing the bill.
They'll hook it back up as soon as the check clears.
Fish will forcefully spit out food to break it into smaller pieces.
"...and could you give examples of specific human alleles, in which changes qualify as a "mutation" ?
"...that'd be helpful in resolving disputes in this and similar threads concerning mutation rates in T-rex or elephants, or changes in that experiment with microorganisms whose holding tank was systematically heated over several weeks.
This questions seems to be a little difficult to answer. The number I have is ~7 mutations per person. The problem lies with the type of mutation and where on the genome it occurs. A mutation in the genome is not the type of mutation commonly imagined, that of a horrible twisted monster, but of simple copy errors during meiosis. (Evolution is only concerned with changes to the germ line cells) During meiosis, single nucleotides are frequently switched from one base to another without affecting the shape of the resulting protein. When you look at a codon you will see that changing the third codon does not change the amino acid so of the single nucleotide mutations, mathematically, at least 1/3 will be effectively neutral.
Just a note here, a neutral mutation is not necessarily a mutation that does not affect the phenotype, it is a mutation that is invisible to selection.
Of the remaining single nucleotide polymorphisms, the vast majority will affect the non-conserved non-coding regions of the genome. Roughly 97% of the human genome is non-coding and non-regulatory, most of it made up of transposons, psuedogenes and repeat segments. A SNP occurring in these areas will likely not produce a phenotypic change.
Of those that do affect the phenotype and produce morphology that is subject to selection very few will be deleterious and even fewer beneficial. Most dramatically deleterious mutations will be selected out before they can get close fixing in the population. Just defining a mutation as beneficial or deleterious can be a problem since a change in environment can change the 'state' of the mutation. (Think malaria resistance).
Of course there are also many mutations that are not just SNPs, everything from chromosomal duplication to reading frame offset.
There is a short list of beneficial mutations here. (There is also a mutation that appears to protect against heart attack and one that increases bone density but I couldn't find links for them in my pile of links)
(I have not even touched on the ability to repair mutations in certain areas of the genome.)
I suspect you already knew all of this, I just took the opportunity to explain a bit to the lurkers. :-)
Well they do. So do centipedes
You forget to consider the possibility of the exaptation of structures that were evolved for a completely different purpose.
Very fascinating. Wrong conclusion but fascinating fish - just because we don't understand something doesn't mean we conclude there is a supernatural explanation.
I guess they all ran away.
Close enough anyway.
I had a couple of other follow on questions / comments concern ing your posts, if you wouldn't mind.
The number I have is ~7 mutations per person...(Evolution is only concerned with changes to the germ line cells)
What with the human genome project, it'd be interesting to do longitudinal studies (if not in humans, then in other species) to map out the approximate number and distribution of the mutations.
a) Is it true that the original single-codon mistranscriptions, etc., are 'uniformly distributed' within the germ cells, or are they "already" clustered in areas in which a screw-up would be minor instead of fatal? (thinking of your line later in the post "haven't touched on"...) This needn't posit intelligent design, just that the error checking mechanisms within DNA replication work a little harder on some regions than on others...
b) How many of the mutations are in the 'junk DNA'?
c) You know, this experiment would be even more compelling in a reproduction of that experiment with the microorganism in the tank whose temperature was raised systematically. When the experiment was repeated, the same mutations came up. Right Wing Professor correctly pointed out that this was due to "saturation" of the genome--there were enough daughter cells created that every point mutation *was* exercised. What would be interesting would be to look at the distribution of *all* the mutations in the presence and the absence of the heating, and see if the distribution of the mutations differed. This is not an exact analogy since the unicellular critters in this experiment reproduced by fission, without gametes...but still kinda cool.
There is a short list of beneficial mutations here. (There is also a mutation that appears to protect against heart attack and one that increases bone density but I couldn't find links for them in my pile of links)
Another interesting point is that a mutation need not confer survival advantage, but survival advantage during breeding years, when genes will be passed on. But carrying this further, since propagation is all that matters, this would imply that marginal changes in attractiveness or being chosen as a mate would also be selected for rather quickly. But that begs the question, what is so "hot" about a brightly colored baboon's ass or a peacock's tail anyway? Why were THOSE particular hues the ones which (socially?) were chosen as desirable?
Cheers!
How do you know it isn't going to happen?
The Wiki article said that the fish seem to learn by trial-and-error. That's observation.
Yes, develop. You can start with a clone of a single non-resistant bacterium and find some that resist a particular antibiotic.
Same or different?
teacup poodle and wolf
horse and donkey
horse and zebra
lion and tiger
lesser black-backed gull and herring gull
camel and llama
Selection selects; it doesn't generate anything new. Mutation does.
A good counter example to your claim here is sickle-cell. This is caused by a single point mutation. Since people with sickle cell trait have two kinds of hemoglobin, rather than just one, new information is present.
Selection (in this case by malaria) has incresed the frequency of the sickle-cell trait in some populations.
So, here we have new information generated by a mutation, and selection making it spread.
FairWitness: Well that seems to cover the bases ... When it can be put into an equation it can't be argued with.
OK, why don't you tell us what the environment (including viruses and bacteria) will be for the next 500,000 years, then we'll give a more precise prediction.
sobieski: Again, this is in the eye of the beholder. You can't use DNA to confirm something unless the DNA matches...
Interesting how there are exact matches in the genomes of us primates. (I'm thinking of the ERVs specifically, but the facts are true for any genetic marker) It's also interesting how they are distributed amongst us and our relatives: for example, if an ERV is found in gorillas and orangutans, it is also found in people and chimps. There are several hundred examples of this phenomenon, and no known exceptions.
Study frame shift mutations.
So, let's say you're a newly-minted baleen whale. How do you keep from swallowing any zooplankton?
There were no whales in the Garden, because there was no ocean in the Garden, just a river (Gen 2:10).
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