Aging in lower metazoans
My dissertation research concentrated on several aspects of aging in asexual metazoans. I did studies with the marine oligochaete Paranais litoralis to address the claim, commonly found in the literature, that asexual organisms should not senesce because they lack a clear distinction between germ line and soma. In a paper published in PNAS, I present evidence that Paranais undergoes senescence, discuss the inadequacy of the cited claim, and advance the view that the evolution of somatic differentiation was the necessary condition for the evolution of senescence.
I also showed that the lifespan of Paranais can be experimentally extended by repeated injury. Bisected worms regenerate their lost parts and resume budding. Worms bisected only once in their lifespan exhibited the same longevity as untreated control worms. Worms bisected three times during their lifespans lived significantly longer than untreated control worms. I suggest that repeated injury enhanced the normal level of somatic repair of the worms thus resulting in a rejuvenation of the soma.
My dissertation work included a study of aging in Hydra addressing the controversy regarding the immortality of this creature. I have continued this work at UC Irvine. Individual hydra have been kept alive for almost four years now. Only a few animals have died during this period and there has been no apparent decline in budding rates. This suggests that hydra seems to escape aging, a process known to affect all other metazoans.
This work has lead to an interest in investigating the presence of telomerase in hydra. Telomeres are nucleoprotein complexes at the end of chromosomes which protect chromosomes from degradation and fusion. Unless they are maintained, telomeres shorten with multiple cell divisions. Shortening of chromosomes might be responsible for "replicative aging", i.e., the finite proliferative capacity of somatic cells. Germline cells of most eukaryotes maintain their chromosomal ends by the action of telomerase, a ribonucleoprotein enzyme. Somatic cells appear to lack mechanisms to prevent the shortening of telomeres; perhaps an evolved trait to limit the proliferative potential of somatic cells in multicellular organisms. The epithelial cells of hydra, however, have retained their proliferative capacity. This results in the constant renewal of hydra's body and might explain hydra's immortality. The mechanism for preserving telomere integrity in the somatic cells of hydra is not known. I plan to investigate the presence of telomerases in the somatic cells of hydra in the future. This work could include cnidarians that undergo aging, e.g. several colonial hydroids, to investigate whether or not the evolution of aging is related to the loss of telomerase activity in somatic cells.
Martínez, D.E., 1997. Mortality patterns suggest lack of senescence in hydra. Experimental Gerontology, 33: 217-225.
Martínez, D. E., 1996. Rejuvenation of the disposable soma: Repeated injury extends lifespan in an asexual annelid. Experimental Gerontology 31: 699-704.
Martínez, D. E. & J. S. Levinton, 1992. Asexual metazoans undergo senescence. Proc. Natl. Acad. Sci. USA. 89: 9920-9923.