Posted on 02/07/2005 1:15:22 PM PST by js1138
Aye. Looking at the Giardia genome is like looking at MicroSoft Windows code...lots of unused subroutines hidden in both.
" Is this all they have to do? LOL Like who really cares about the sexual activities of Giardia? :)"
They probably have lots of taxpayer dollars to burn.
Yes, it does make one wonder, but I kinda think Geraldo would fall into the category of "sexual escapades." LOL
Proof that you don't lose it just because you don't use it.
"LOL Like who really cares about the sexual activities of Giardia? :)"
If you ever get it, YOU will.
"Proof that you don't lose it just because you don't use it.'
Just sittin' around pickin' and grinnin' and waiting til the time is ripe.
Did all the intermediate forms go extinct, and why?" Roger asks.
Cause they didn't have gay marriage and couldn't reproduce,
Oh, wait....
"A lot had to happen when eukaryotes evolved. Why aren't there any intermediate stages of this process alive today? Did all the intermediate forms go extinct, and why?" Roger asks."
Very simple, they are in extinction's dustbin.
The way many protozoans handle their genes and chromosomes is quite complicated. As a bugologist, this means that a lot of duplication and unnecessary intervening DNA can easily creep in.
Perhaps they aren't interested in sex because they are too happy where they are (retreat into an ecological niche - doesn't explain the retention of the sexual DNA code, though, unless it has been very recent). Then again many protozoa have "mating types" (think of them as bug sexes). They don't like their brothers (or sisters, depending). Just lookin' for the right stud.
Related flagellates have no problems finding partners.
Please excuse this microbe ramble.
Oversimplification often fails to answer the questions asked...
Indeed!
Yet technically, an organism would be genetically superior if it had all of its functionality without also having unused genetic code as baggage. Natural Selection *should* favor those without the unused code...
On what basis?
Completely unused code requires more energy for genetic copying, yet delivers, by definition, no benefit to the organism.
Sort of like these recessive genes...
Vancomycin Immunity
This antibiotic binds to the cell wall of a microbe and prevents it from forming successfully. Like the opposite of penicillin (which breaks the completed wall down), this one acts as a sabotaged building block and doesn't let it form in the first place.Bacterial populations usually respond to penicillin by developing beta-lactamases, enzymes that destroy the chemical before it takes effect. Vancomycin, however, becomes highly toxic to germ organelles when broken down--an apparent catch-22! If the germ doesn't break it down, it incorporates poison into its cell wall and dies; if it does break it down, it creates poisonous by-products and dies anyway.
So, we have a "damned if you do, damned if you don't" drug on our hands, something that should be able to take out any nasties we aim it at. So, we aimed and we fired, and time passed, this new selective pressure had been introduced into the microbial world in Doctors' surgeries and hospitals across the western world.
This tale, however, would have a sting in it's tail, it showed us that we were in a chemical arms race with foes much much smaller and much much dumber than us.
A mere 30 years after vancomycin had started being used, a bizarre, multi-part anti-vancomycin system sprung forth in enterococci and other bacteria.
No less than 5 genes are involved in this contrived monstrosity of a defense. VanR and VanS produce enzymes that detect the presence of the antibiotic in the bacterium. Once activated, those enzymes activate VanA, which activates, in turn, several genes with subfunctions that (A) prevent vancomycin from being incorporated in the cell wall, (B) break it down, and (C) catalyze its toxic byproducts into harmless remnants.
This by no means stopped with vancomycin, several antibiotics have now become innefective in the hospitals against many infectious bacteria.
A particularly nasty one is MRSA, or methicillin-resistant Staphylococcus aureus, which luckily for us at the moment, is still vulnerable to the above vancomycin. MRSA strains first appeared in the late 1970s and currently 40-50 percent of SA isolated from U.S. hospitals are resistant to methicillin. These infections are treated with the powerful antibiotic vancomycin. Scientists hypothesize that the strains of SA most likely to evolve resistance to vancomycin are the MRSA.
Scientists expect strains of the bacterium Staphylococcus aureus (SA) that are fully resistant to the antibiotic vancomycin to evolve soon. Vancomycin-resistant Staphylococcus aureus (VRSA) is the term used to describe these strains. The expected emergence of VRSA is alarming because vancomycin is the only antibiotic that is effective against MRSA, strains of SA that are resistant to the antibiotic methicillin (MRSA).
Although VRSAstrains of SA that are fully resistant to vancomycindo not currently exist, medical workers have recently isolated strains of SA that are four times more resistant to vancomycin than SA strains found previously. Because infections due to these strains do not respond to the usual doses of vancomycin, many physicians and other experts incorrectly refer to them as VRSA. They should be described as SA strains with intermediate resistance to vancomycin. Infections due to these strains can be cured using higher doses of vancomycin.
Lets rephrase that to be relevant for our discussions: "No less than 5 [EXISTING] genes are involved in this contrived monstrosity of a defense."
... And then lets mention: it appears as though genes not only interact with each other, but also that they have multiple functions rather than the old perception (true or not) that each gene did only one thing.
Interestingly enough, this is also *precisely* what we find when we analyze the subroutines in large computer programs and operating systems...
Do you know the dofference between a gene and an allele?
Do you?
Yes he does.
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