Bell (21) established the deep connection between the two invariants of life—birth and death—by demonstrating that protozoan lineages grow old as the result of an accumulated load of mutations. The senescence can be arrested by recombination of micronuclear DNA with that of another protozoan through conjugation. Conjugation (sex) results in new DNA and in the apoptotic-like destruction of old operational DNA in the macronucleus (Fig. 1). Thus, rejuvenation in the replicative DNA, and senescence of operational DNA are promoted by sexual reproduction. When this concept is extended to multicellular organisms, sex and somatic senescence are inextricably linked (22). In multicellular, sexually reproducing organisms, the function of somatic cells (i.e., all cells constituting the individual, except the germ cells) is survival of the replicative DNA—the germ cells (or gametes, either of two mature cells which, when they unite, form a new individual). Prior to bacteria, the somatic DNA was the germ line DNA; prior to multicellular animals, the somatic cell was the germ cell. Like the macronuclei in the paramecia, the somatic cells senesce and die as a function of their mitotic task of ensuring the survival and development of the germ cells. The advent of sex in reproduction allowed exogenous repair of replicative DNA (22); in multicellular organisms, the replication errors of somatic growth and maintenance are segregated from the DNA passed on to daughter cells and these errors are discarded at the end of each generation. Senescence is built into the life history concept of all sexually reproducing organisms. Thus, modifying senescence can alter death rate but death itself can never be eliminated. This evolutionary argument concerning senescence can be regarded not only as one of the most basic principles of biogerontology but also as one of the fundamental canons in the emergence of all sexually reproducing organisms.
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