Aye. Looking at the Giardia genome is like looking at MicroSoft Windows code...lots of unused subroutines hidden in both.
Posted on 02/07/2005 1:15:22 PM PST by js1138
Giardia Bares All: Parasite genes reveal long sexual history
Christen Brownlee
While it hasn't yet been caught in the act, a single-celled parasite has been ready for sex for billions of years. A new research finding provides evidence that sexual reproduction started as soon as life forms that have nuclei and organelles within their cells branched off from their structurally simpler ancestors.
The parasite Giardia intestinalis is well known for causing a diarrheal disease that animals and people contract after drinking contaminated water. Many researchers consider this species to be one of the most ancient living members of the eukaryote, or true nucleus, lineage. However, unlike most eukaryotes, G. intestinalis and its relatives have been long considered to reproduce only asexually—by division into two identical cells.
To determine when reproduction via sperm and eggs originated, John Logsdon of the University of Iowa in Iowa City and his colleagues took a close look at G. intestinalis' mysterious reproductive life. They focused on the hallmark of sexual reproduction known as meiosis, the process that halves the number of an organism's chromosomes to make gametes such as sperm and eggs. Among available data on the G. intestinalis genome, the researchers searched for genes similar to those that control meiosis in other eukaryotes, including plants, animals, and fungi.
The researchers' analysis revealed that G. intestinalis possesses genes similar to those used for meiosis by other eukaryotes. At least 5 of those genes function only in meiosis, and 10 others have roles both in meiosis and other functions, Logsdon's team noted in the Jan. 26 Current Biology.
Although the researchers didn't establish that G. intestinalis reproduces sexually, Logsdon notes that a discreet sex life might turn up after further study. "Lack of evidence is not evidence of lack," he says.
On the other hand, the findings suggest that meiosis was established early in eukaryotic evolution, making sexual reproduction "a very central feature of being a eukaryote," says Logsdon. Bacteria and other simple-celled life forms, or prokaryotes, don't make eggs and sperm.
All living eukaryotes, including G. intestinalis, share numerous cellular features and processes that aren't seen in prokaryotes. According to Andrew Roger of Dalhousie University in Halifax, Nova Scotia, establishing that all eukaryotes are capable of meiosis could "make the evolutionary transition from prokaryote to eukaryote even more difficult to sort out.
"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.
Logsdon says that he and his team plan to continue their research by looking for meiosis genes in other eukaryotes thought to be asexual.
References:
Ramesh, M.A., S.-B. Malik, and J.M. Logsdon Jr. 2005. A phylogenomic inventory of meiotic genes: Evidence for sex in Giardia and an early eukaryotic origin of meiosis. Current Biology 15(Jan. 26):185-191. Abstract available at
http://dx.doi.org/10.1016/j.cub.2005.01.003.
Sources:
John M. Logsdon Jr. University of Iowa Department of Biological Sciences 310 Biology Building Iowa City, IA 52242-1324
Andrew Roger Department of Biochemistry and Molecular Biology Dalhousie University Halifax, NS B3H 1X5 Canada
http://www.sciencenews.org/articles/20050129/fob1.asp
From Science News, Vol. 167, No. 5, Jan. 29, 2005, p. 67.
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 VRSA—strains of SA that are fully resistant to vancomycin—do 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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