"The new perspective reveals DNA to be not just a string of biological code but a dauntingly complex operating system that processes many more kinds of information than previously appreciated."
John
"The new perspective reveals DNA to be not just a string of biological code but a dauntingly complex operating system that processes many more kinds of information than previously appreciated."
John
Hopefully this will be used to head off the insurance companies before they get too carried away with discriminating against people for having "bad" genes. At least for a while anyway.
We got invitations from our HMO to participate in some kind of gene study. Went straight into the bin, of course. I mean, who in their right mind would do that? From there to Orwell is only one small step.
-- Regards, Joerg http://www.analogconsultants.com
I commend your interest in this subject given your limited intellectual capabilities, but please stop posting *old* news. If you want to read something really interesting do a search on epigenetics, then turn yourself into a caveman...
The sciencists are in denial of Sentience, is all.
Cheers! Rich
-- For more information, please feel free to visit http://www.godchannel.com
The next issue is: is DNA alive?
John
Design anything fun lately, Fred?
John
He did, but Roto-Rooter finally fixed it.
-- Service to my country? Been there, Done that, and I\'ve got my DD214 to prove it.
Of course. Everyone knows humans (and other live things) are just DNA's way of making more DNA. ;-)
Cheers! Rich
As Fred Bloggs says, this isn't news. You might like to read up on "gene expression" and the various mechanisms that regulate the activity of individual genes and bits of individual genes. My younger brother's genetics text - published in the 1970s - has a lot of information on the subject.
Genes and gene expression are more complicated than you and the Washington Post reporters may have thought, but what genes can do is still strictly limited by the information they can access and process.
In particularly, there is no way in which they can try out or simulate a mutation in advance - all they can do is generate various sorts of random errors in the amino acid sequences and launch the consequent phenome into the real world. The new organism has no way of knowing it is a mutant, so it can't even undo unhelpful errors.
Unless - of course - you see the human genome project as a gene's way of evolving a better mechanism of genetic evolution. It seems to be a clumsy way of generating a reference data base, but that's evolution for you.
-- Bill Sloman, Nijmegen
Don't be too hard on John. He's doing the best he can, and is probably a whiz at learning tone languages.
-- Bill Sloman, Nijmegen
sounds like Windoze ...
definitely sounds like Windoze ...
yup, sounds like Windoze ...
On Jun 19, 4:06 am, snipped-for-privacy@ieee.org wrote: [.. DNA ..]
That isn't completely true. Genes come in pairs. Many of the mutations are only fully expressed if you have both genes in the same offspring. In this way, a mutated gene can be passed down through generations and either gradually increase or decrease in numbers. It may hang around in low numbers until either a new mutation or a new situation makes the mutant an advantage.
The case of sickle cell anemia is sort of an example of the case. If a child gets just one gene for the disease they don't have the anemia. However that child also won't get malaria. In an environment where malaria doesn't exist, the gene is a disadvantage but in a lot of the tropics, it improves survival. We don't know where the mutation first happened but it need not be where malaria was a major problem.
Sure, but the cell doesn't have any way of working out which of the paired genes is the mutant.
Gene frequencies change because more or less of the bearers of the gene survive long enough to get and raise children to carry more copies of the gene on for suceeding generations.
True - there is an formula for working out how fast neutral genes are lost from the population by random fluctuations in their frequency (essentially a drunkard's walk) and for all but very small populations, the rate is pretty slow. Recessive lethal genes aren't lost much faster, once the frequency has droopped to the point where there is very little chance of a kid getting two copies of the lethal recessive ( a 1% frequency makes this a 0.01% chance).
We all carry a few.
-- Bill Sloman, Nijmegen
How can you possibly know this?
Have you published your thesis yet, describing the operations inside a cell, with enough detail to show that the cell "doesn't have any way"?
If you can say that with certainty, then you either have a deeper understanding of the inner workings of cells than anyone on Earth has ever had before, or you're fantasizing.
Cheers! Rich
Are you sure that there is no way? There may be a checksum in the telomere. There has to be reasons why the mutant gene is less likely to be expressed.
Yes in most cases this is true. There are some genes that are carried in plasmids that can spread in spite of causing a disadvantage. They are passed to all offspring and thus must make serious trouble before they get removed.
The formula doesn't work for small populations. It the random walk hits either wall it sticks to it. The formula ends up only saying the odds of the gene going away in that case.
Hey, sloman is the final authority on what cells can't do. DNA repair enzymes must be pure myth.
John
You've got two almost identical sequences of amino acids along two strings of DNA. Say they differ at one point - a single point mutation. How would you work out which one was the mutant?
You have to sequence both strings of DNA, work out where they were on their particular chromosome, then go into the human genome data base to find out which amino acid normally appears at this point.
The cell does have machinery to sequence DNA, but it doesn't have access to the human genome data base, or anything like it. If we - or any other intelligent designer - had desinged the system, we might have put error detection and error correction hardware into the cells DNA processing machinery, and extra data into the sequences, but then we have stopped evolution, or a least slowed it down a lot.
In short, I'm not fantasising, but thinking like a system designer. You should try it sometime.
-- Bill Sloman, Nijmegen
Kind of you, but there are people on this user group who know as least as much as I do, and loads of people who know a great deal more.
The kind of DNA repair enzymes that you would need for that kind of job are impossible rather than mythical.
You could usefully read up on what real DNA repair enzymes do
The most powerful of the enzymes uses the other half of a paired chromosome as a template to rebuild an extended area of damage on the other half of the pair .... rough on your kids if the template included a lethal recessive.
-- Bill Sloman, Nijmegen
It seems extraordinarily unlikely that there is a checksum on the telomere. Any single point nuclear polymorphism would invalidate the checksum, and the only error correction mechanism would be apoptosis.
Why not?
saying the
That *is* the mechanism for neutral gene loss,
-- Bill Sloman, Nijmegen
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