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Genetic coregulation of longevity and antioxienzymes in Neurospora crassa.

作者信息

Munkres K D

机构信息

Department of Genetics, University of Wisconsin, Madison 53706.

出版信息

Free Radic Biol Med. 1990;8(4):355-61. doi: 10.1016/0891-5849(90)90101-n.

Abstract

Further analysis of a model of the biochemical genetics of cellular longevity in Neurospora crassa confirms and amplifies the hypothesis that antioxienzymes and lifespans are genetically co-regulated. The model consists of seven classes of closely related strains with genetically determined median lifespans ranging from 7 to 90 days and differing by about 15-day intervals. The nuclear gene mutations Age- and age+ respectively decrease and increase both lifespans and the constitutive enzyme activities relative to the wild-type parent. Here the number of such enzymes correlated with lifespans is extended from 6 to 12. Four of these enzymes have not been previously noted in Neurospora. Statistical analysis indicates that the genes may coordinate the 12 enzymes' activities with respect to one another to facilitate their "collaborative" function. The genes probably perform a regulatory role in the synthesis of the antioxienzymes. Neurospora may have a global unit of genetic function, an oxy-regulon, analogous to that of enteric bacteria.

摘要

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