Abstract

In the ciliate Tetrahymena pyriformis, syngen 1, senescence is marked both by mitotic and meiotic cytogenetic irregularities of the micronucleus (germinal nucleus) and by an increased frequency of cell death. Full vigor can be restored through the age-dependent process of genomic exclusion, which in prematurely senescent clones C ★, A ★III and A ★V results in the replacement of defective micronuclei but not in the development of new macronuclei (somatic nuclei). After a period of normal behavior, which lasts about 40 fissions in C ★ and 100 fissions in A ★III and A ★V, the new micronucleus placed in the same cytoplasm as the old macronucleus again becomes defective and the rejuvenated clone again shows signs of senescence. The origin of these defective micronuclei is traced to action of the old macronucleus. It is suggested that the time course of aging is regulated through the accumulation of unrepaired damage to the micronuclear genetic material.

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