Punching the timeclock of life

Has anyone read the full paper from the following abstract?

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Superoxide is a mediator of an altruistic aging program in Saccharomyces cerevisiae.

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Aging is believed to be a nonadaptive process that escapes the force of natural selection. Here, we challenge this dogma by showing that yeast laboratory strains and strains isolated from grapes undergo an age- and pH-dependent death with features of mammalian programmed cell death (apoptosis). After 90-99% of the population dies, a small mutant subpopulation uses the nutrients released by dead cells to grow. This adaptive regrowth is inversely correlated with protection against superoxide toxicity and life span and is associated with elevated age-dependent release of nutrients and increased mutation frequency. Computational simulations confirm that premature aging together with a relatively high mutation frequency can result in a major advantage in adaptation to changing environments. These results suggest that under conditions that model natural environments, yeast organisms undergo an altruistic and premature aging and death program, mediated in part by superoxide. The role of similar pathways in the regulation of longevity in organisms ranging from yeast to mice raises the possibility that mammals may also undergo programmed aging.

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Superoxide is a mediator of an altruistic aging program in Saccharomyces cerevisiae | Journal of Cell Biology | Rockefeller University PressIf so any comments?
Is the following article a good assessment of the work?http://www.sciencedaily.com/...ases/2004/09/040928123106.htm

Judge copies this obviously extremely complicated excerpt from some link and pastes it under the assumption that he understands it.IOW, you are just showing off and daring someone to call you on it.If someone accuses you of this then you and others will laugh at them for being ignorant.My point:Stanford professors in the 1950's coined a word for this nonsense, they called it logidemic/"logidemicizing", which is communication only understood between experts.Only few experts understand the nonsense you pasted. You are insulting ordinary persons to be in need of intellectuals to feed them the truth which is too complicated so trust us and our interpretations = fascism.What you don't know can and will be used against you.This is the problem with evolution. It is so complicated a person must trust another to interpret the research.The atheist bias is craftily interwoven in the translation, and if it isn't then the worldview of the scientist is silently validated.The beauty of theism is that anyone can pick up the Bible and read a verse and hear the voice of God and get saved.With evolution, ordinary persons must take a God hating evos word on it.

Uh, Judge's excerpt made perfect sense to me. It's complicated and techical, yes, but nothing exceeding my biologu education, which constitutes one single semester.If you didn't understand it, wasn't the appropriate, mature response to ask for clarification, not rant? I'll try and explain it to you, if you like. Again, I understood it just fine, and I'm far from being an expert. Would you like me to explain it to you?

Correct me if I'm mistaken, but didn't we establish immediately after your arrival here that Dr Gene Scott coined that word? Was he at Stanford? Does he have multiple personality syndrome?There's nothing difficult or obscure in that paragraph, anyway!This message has been edited by Coragyps, 10-08-2004 05:36 PM

Lol. Hey WT - Is this your attempt to say you don't understand any of that post? I like ur style, lol - but to be honest if it helps I couldn't understand a fu**ing word of message one, but I doubt it's against God - any more than that mitosis program I watched.You were a bit offensive of innocent scientists here. But if you're just playing the "mike provoker" game. .......

If you are serious - go ahead, but remember I am a ordinary person.Also, you evaded the point of my post but I am now used to this.

Yes, he taught me it.Then after this I also learned from him that he learned it from his profs at Stanford.Dr. Scott has a Ph.D. from Stanford - cross departmental in philosophy and religion.

Well, since you made it pretty clear that you didn't understand the abstract, any statements you made about its content were entirely without merit. That's why I didn't address them. Ok, I'll go line by line. If you don't understand something, ask a question.

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Superoxide is a mediator of an altruistic aging program in Saccharomyces cerevisiae.

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Superoxide is ionic oxygen gas (O2), one example of what are known as "free radicals." Maybe you've heard of these on TV, like on Neutrogena ads? They react strongly with organic compounds and cause damage, and are believed to be related to the aging process in humans and other mammals."Altruistic" means a behavior that is detrimental to an organism but advantageous to its "kin", that is, other organisms that share its genes."Saccharomyces cerevisiae" is the species name of the organism you know as regular brewing/baking yeast. It's the most common eukaryotic model organism in cell biology experiments like these, and was the first organism to have its genome entirely sequenced.So, in other words, the title says it all - There's an aging program in common yeast, and its controlled at least in part by O2 free radicals, and this aging program is not simply a maladaption that has escaped selection; rather, it's advantageous to the population as a whole for yeast to die this way.

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Aging is believed to be a nonadaptive process that escapes the force of natural selection.

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Here they specify the biological "conventional wisdom" about the aging process, that it's simply a detrimental process that has escaped natural selection because it only takes effect, generally, after an organism has already been successful in reproducing.

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Here, we challenge this dogma by showing that yeast laboratory strains and strains isolated from grapes undergo an age- and pH-dependent death with features of mammalian programmed cell death (apoptosis).

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You should know all about challenging dogma. They specify that they used both lab strains and naturally-occuring strains of yeast to eliminate ideosyncracies which might have existed in one or the other population. They state that, like mammallian cells, yeast experience programmed cell death, or "apoptosis." This is a well-known phenomenon in mammal cells; in fact, cancer is a result of cells refusing to undergo apoptosis at the proper time. In yeast, they say, this cell death is dependant on age and pH.

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After 90-99% of the population dies, a small mutant subpopulation uses the nutrients released by dead cells to grow.

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This should be self-explanitory.

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This adaptive regrowth is inversely correlated with protection against superoxide toxicity and life span and is associated with elevated age-dependent release of nutrients and increased mutation frequency.

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In yeast who are protected against free radicals, or in yeast who live longer, this rebound effect is lessened. The new subpopulation benefits from freed nutrients and mutates faster than the original population.

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Computational simulations confirm that premature aging together with a relatively high mutation frequency can result in a major advantage in adaptation to changing environments.

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In computer models, populations with a reduced generation time due to premature aging combined with increased mutation rates adapt much faster to new environments than those populations with longer generation times and slower mutation rates.

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These results suggest that under conditions that model natural environments, yeast organisms undergo an altruistic and premature aging and death program, mediated in part by superoxide.

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They made sure that the environment that the yeast was in was as close as possible to the natural environments of the yeast. Under these conditions, superoxides can regulate a process that decreases the time between generations of yeast and increases the mutation rate, which is bad for each individual yeast, but really great for the population, which can adapt to new environments faster as a result.

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The role of similar pathways in the regulation of longevity in organisms ranging from yeast to mice raises the possibility that mammals may also undergo programmed aging.

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Many different organisms, including mammals like mice, etc., have the same chemical pathways for apoptosis that yeast do, which raises the possibility that aging in mammals does the same thing in aging in yeast; that is, increases the rate of adaptation to new environments under certain conditions.Clear enough, to me. What really blew my mind and brought it all together for me was this, from Wikipedia (I had to look up "superoxide" because I wasn't entirely sure which free radical they meant):

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Superoxide is scavenged by the enzyme superoxide dismutase, or SOD. Although the rate of reaction of SOD is close to the spontaneous diffusion rate, the genetic inactivation or "knockout" of SOD produces deleterious phenotypes in organsims ranging from bacteria to mice (the later species dies around 21 days after birth if the mitochondrial variant of SOD is inactivated).

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So, in other words, superoxide levels are kept down by an enzyme called SOD, and when genetic change prevents SOD synthesis, superoxide levels rise - triggering the response discovered by the researchers above. In other words, mammals may be programmed to die faster and mutate more in response to a change in environment; a process that would allow them to adapt quickly to new environments but also keep mutation levels slowed down in stable environments.Cool!

I appreciate the work you did in responding.Is there a "big picture" message and if so what is it ?I presume the paragraph which you de-logidemicized has a message - what is it ?Is it anti-ID or is it just explaining how something behaves/works ? I see ID in that blue box.A program evidences ID.That which leads to order is the product of an ID system because chance cannot always luck out. And if it appears to be the product of random chance then what is to say that the said process is not the product of ID seeing how it produces a complicated working system ?It took intelligence to create the paragraph you explained, and it took intelligence to explain, but the subject of the paragraph is not the product of intelligence ?I would like to read a response by Loudmouth to my post also (this one).Once again, thanks for the work you put into the post.WTThis message has been edited by WILLOWTREE, 10-08-2004 09:49 PM

That, under certain circumstances, yeast populations reconfigure themselves to experience greater mutations and shorter life spans, which speeds adaptation to new environments.That's as big as the picture in that article gets. They do suggest that because mammals have the same or similar biochemical pathways for apoptosis, they might experience the same age accelleration effects. But that's just speculation on their part. It's up to others to design and perform experiments to see. It's just an explanation of the results of an experiment on yeast.You don't read a lot of scientific literature, do you? Almost none of it is anything but extremely dry results of experiment, just like this article. If you say so. You're free to interpret it that way. Me, I see the amazing power of random mutation and natural selection. No, but chance plus selection always does. That's what we're seeing here - a response to a biochemical situation by the yeast that increases the amount of random mutation and natural selection that occurs on their population.If those forces didn't have substiantial power to stimulate adaptation and change, then why would the yeast employ them in times of stress? No problem. If it made it clear for you, then I've done myself a favor for when we debate. Plus, laying it out for you made it clearer to me. It is said that you do not truly understand something until you teach it to someone else.

I completely agree on this. I found this out while giving calculus to other students.

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Ponlo todo en las manos de Dios y que se joda el mundo. El principio de la sabiduria es el temor a Jehova

Willowtree wrote:

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Judge copies this obviously extremely complicated excerpt from some link and pastes it under the assumption that he understands it.

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Actually I don't really understand the technical side of it. I first read the news story on it that I posted a link to. This gave me the gist of it.
Then I was able to understand the paper (a bit). I am actually a creationist but I have posted here in the past and found the regulars here very helpful, when I try to learn what sceice actually does.You will notice in the news article that there is a suggestion that certain Darwinian principles were challenged by this work, so I wanted to get the the perspective of some more learned than myself.This is stuff actually being observed so why be afarid to examine it and ask what it means.

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This is stuff actually being observed so why be afarid to examine it and ask what it means.

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A VERY refreshing sentiment from a creationist...wish you would post more often.

Not exactly. The Darwinian principle of natural selection pressures isn't challenged by this; rather, a potential selection benefit is found for age-related apoptosis. The previous, prevailing view was that age-related apoptosis was a non-adaptive trait that escaped selection by virtue of not occuring until well after the organism had reproduced.This doesn't really challenge Darwinism in any way.

What like, physics, geology, medical research, airplane design, semiconductors, chip design, car design and, well, pretty much every other area of modern knowledge?Evolution is hard because the world is complicated.