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Author Topic:   What exactly is ID?
Meddle
Member (Idle past 1379 days)
Posts: 179
From: Scotland
Joined: 05-08-2006


Message 407 of 1273 (540889)
12-29-2009 10:26 PM
Reply to: Message 402 by Smooth Operator
12-29-2009 6:46 PM


Re: l
Smooth Operator writes:
Did you know there are people resistant to HIV? Yup! It's true. And guess what? Obviously, that's a beneficial mutation, right! But the best part is, it's reduces the amount of genetic information, by a deletion, thus making the receptor that HIV uses to enter the cell, inactive! Therefore, it's increaseing the genetic entropy, yet it's a beneficial mutation!
The same thing as sickle cell. I told you that beneficial mutations also cause genetic entropy by degrading biological functions, yet you didn't want to believe it, well now you have it. Enjoy.
The problem is you are referring to genes which apply to disease resistance. The diseases in question rely on the target cells to be functioning normally, so by necessity any resistance mechanism is going to affect normal function.
However, I read of an example recently posted by PZ myers in his blog on the evolution of alpha-actinin which anchors the actin cytoskeleton of cells. To describe it briefly, invertebrates have one of these genes whereas vertebrates have four. These extra genes resulted from a duplication event 200-300 million years ago. In that time these duplicated genes have undergone mutations, adapting to subtly different roles, in particular alpha-actinin 2 and 3 which are expressed almost exclusively in skeletal muscle tissue. So how does this fit into your hypothetical genetic entropy?

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 Message 402 by Smooth Operator, posted 12-29-2009 6:46 PM Smooth Operator has replied

Replies to this message:
 Message 442 by Smooth Operator, posted 12-30-2009 7:36 PM Meddle has not replied

Meddle
Member (Idle past 1379 days)
Posts: 179
From: Scotland
Joined: 05-08-2006


Message 684 of 1273 (542928)
01-13-2010 7:52 PM
Reply to: Message 668 by Smooth Operator
01-13-2010 11:56 AM


Re: Nonsensical creationist notions
It doesn't matter if it lost affinity specifically to streptomycin. It probably can bind to something else too. The original structure is the original information content. Now, if it loses the affinity, to anything, it got degraded, and it lost information.
Of course the ribosome binds to something else. It binds to mRNA and the anti-codons of tRNA carrying amino acids, in it's role of protein synthesis. Streptomycin interferes with the normal role of the ribosome by irreversibly binding to it. This is why streptomycin is an antibiotic, since without protein synthesis the bacterial cell dies, and why it is ridiculous to describe the failure to bind streptomycin as a loss of function. The relevant mutation allows the ribosome to continue functioning in protein synthesis even in the presence of streptomycin, which can be described as a gain in function.

This message is a reply to:
 Message 668 by Smooth Operator, posted 01-13-2010 11:56 AM Smooth Operator has replied

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