Weindruch R H, Doerder F P
Mech Ageing Dev. 1975 May-Aug;4(3-4):263-79. doi: 10.1016/0047-6374(75)90028-7.
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 senscent 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 rejevenated 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 of course of aging is regulated through the accumulation of unrepaired damage to the micronuclear genetic material.
在梨形四膜虫同宗配合系1中,衰老的特征是小核(生殖核)有丝分裂和减数分裂的细胞遗传学异常以及细胞死亡频率增加。通过基因组排除这一依赖年龄的过程可以恢复完全活力,在过早衰老的克隆C、A III和A V中,这会导致有缺陷的小核被替换,但不会产生新的大核(体细胞核)。在经历一段正常行为期后,克隆C中持续约40次分裂,A III和A V中持续约100次分裂,与旧大核处于同一细胞质中的新小核再次变得有缺陷, rejuvenated克隆再次出现衰老迹象。这些有缺陷小核的起源可追溯到旧大核的作用。有人提出,衰老进程的时间是通过对小核遗传物质未修复损伤的积累来调节的。