Studies on Caenorhabditis elegans have demonstrated that worms with mutations in the insulin/insulin-like growth factor-1 receptor homologue DAF-2 gene remain youthful and active longer and can live more than twice as long. This appears to be mediated through DAF-16 (a transcription factor); phosphorylation of this factor through Akt signaling appears to shorten lifespan. DAF-2 prevents DAF-16 accumulation in nuclei. Both sensory neurons and germline activity regulate DAF-16 accumulation and lifespan can be extended by modulating the sensory neurons or germ cells.
Reference:Nature Genetics 28, 139 - 145 (2001)
This produces an interesting line of thought; is our lifespan modulated by our reproductive capacity? Are we programmed for shorter lifespans if we reproduce, so we don't compete with our progeny for resources?
What do you think?
Reference:Nature Genetics 28, 139 - 145 (2001)
This produces an interesting line of thought; is our lifespan modulated by our reproductive capacity? Are we programmed for shorter lifespans if we reproduce, so we don't compete with our progeny for resources?
What do you think?