Strongyloides ratti A Nematode with Extraordinary Plasticity in Aging

Michael P. Gardner, Mark E. Viney and David Gems

Aging has been characterized in detail in relatively few animal species. Here we describe the aging process of a nematode with an unusual life cycle, Strongyloides ratti. This organism has distinct parasitic and free-living reproductive adult forms, which are genetically identical. S. ratti exhibits a remarkably high degree of pheno-typic plasticity of aging: the maximum lifespan of parasitic adults is 80 times greater than that of free-living adults (403 and 5 days, respectively). Free-living S. ratti adults are short-lived even by terrestrial nematode standards; their lifespan is approximately only 30% of that of the short-lived free-living nematode model species C. elegans. Phenomenologically, aging appears similar in S. ratti free-living adults and C. elegans, except that it unfolds much more rapidly in S. ratti. Demographic senescence (a hallmark of aging) occurs in free-living S. ratti, with a mortality rate doubling time (MRDT) of 0.8 ± 0.1 days (females), compared with 2.0 ± 0.3 in C. elegans. Likewise, parasitic S. ratti undergo senescence, but have an MRDT approximately 30 times greater than that of free-living adults of S. ratti. Among nematodes, parasitic species are generally longer-lived than free-living species. This presumably reflects the evolutionary consequences of differences in levels extrinsic mortality experienced in their respective niches. Here, we describe in detail the aging process in the two adult forms of S. ratti and explore how these different lifespans might have evolved, despite sharing the same genome. In this species, an evolved and vast difference in the rate of aging appears to be determined by gene expression alone. This implies that, at least in this one species, ''late-acting deleterious mutations'' correspond to regulated differences in gene expression that generate a shorter lifespan. Potentially, differences in lifespan between species might evolve via similar mechanisms, involving mutationally driven alterations in gene expression.

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