Sunday, October 24, 2010

Comment on TEs

From Madlung and Comai:

To summarize, abiotic stress can result not only in well-programmed
physiological stress responses but also in
genome-wide changes. Stress-induced genomic responses
include transposon activation, transposition, and structural
genome changes. Like other stress responses transposon-mediated
alterations in transcriptional activity of affected
genes might lead to avoidance or tolerance of the stress.
Unlike many other stress responses, however, transpositional
activation appears to be a reaction not directly targeting
an evolutionarily developed physiological pathway but
is a hit-or-miss approach to finding an appropriate way of
handling an unusual challenge.


This is more or less what I was trying to say. It seems like it has already been said and much more eloquently. However, I disagree with his conclusion. They say that "transpositional activation appears to be a reaction not directly targeting..." Whereas I believe that while transposition could be a 'random' and disorganized process, perhaps it has evolved a complex regulatory pathway, and that certain parts of the 'junk' DNA (all 98% of it) somehow contain the information necessary to create an appropriate way of handling an unusual challenge. Considering that human life has been around for many hundreds of thousands of years, not to mention all the inherited genetic history, I believe that the human body has faced many of the same challenges that it is faced with today (even in the face of such new, xenobiotic chemicals and anthropogenic pollution). With this "experience" in our genetic "memory", the cellular machinery "knows" how to respond in a way that is at least a little better than hit-or-miss.

Here's a story: metabolites are accumulating in the cell because the protein that is supposed to process them is more affected than average to the stress. The increasing levels of the metabolite increase the expression of the affected protein (by some feedback loop). The high concentration of the metabolite in the cell and/or the stressor molecule induce the activation of DNA-affecting systems (e.g. - TEs), which have as a target regions the places where high levels of transcription are taking place. RTs have been shown to use the machinery of cellular division to insert themselves into the genome. Would it be to far of a leap to assume that they (or mutating, inserting elements) could utilize the machinery of transcription, as well?

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