Only a handful of gene families regulate aging

[Guest guest]

Very interesting new research featured in "PLoS Genetics", which is free to anyone with an open mind. They basically found that most of the genes that influence "true aging" have to do with the IGF-1 signalling pathway, or mitochondrial respiration, or "CR" itself. Interestingly, they found that if you interfered with the IGF-1 pathway, *or* with mitochondrial respiration, you got increases in lifespan.

What is particularly interesting is that you can inhibit the mitochondria and get lifespan extension. Most people think you want to "help" mitochondria, but I am not so sure that "babying" them is such a good idea. When you mess around with them a little bit, the cell gets tougher.

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Research Article

New Genes Tied to Endocrine, Metabolic, and Dietary Regulation of Lifespan from a Caenorhabditis elegans Genomic RNAi Screen

Malene Hansen☯, Ao-Lin Hsu¤a☯, Dillin¤b, Kenyon*

1 Department of Biochemistry and Biophysics, University of California, San Francisco, California, United States of America

"In this study, we identified many interesting new genes whose normal function is predicted to inhibit longevity. Although our screen did not reach saturation, an interesting picture emerged. Most of the genes we identified fell into one of three classes: genes that influence lifespan through DAF-16/FOXO (8/29), genes that influence respiration (12/29), and genes that appear to affect the response to DR (4/29). Two more genes affected integrin signaling, which was known to influence lifespan in flies. Like the insulin/IGF-1/FOXO system and the respiratory chain, most biological pathways and systems consist of many genes, and we failed to identify even one component of many such systems (e.g., the TGF-â signaling system). In fact, of the genes that had conserved sequence motifs, only one, the rha-2 RNA helicase homolog, could not be linked to a known pathway. These findings are thought-provoking because until now, we have had no way of knowing whether the longevity

pathways we know about represent only the tip of the iceberg. Our findings suggest that, in contrast, at most only one or a few other large multigenic systems influence lifespan in C. elegans. In other words, we may now be aware of most of the major biological pathways in C. elegans that, when inhibited, can produce large extensions in lifespan."

http://genetics.plosjournals.org/perlserv/?request=get-document & doi=10.1371/journal.pgen.0010017

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T.

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