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首页> 外文期刊>Trends in Neurosciences >Relevance of 'adaptive' mutations arising in non-dividing cells of microorganisms to age-related changes in mutant phenotypes of neurons.
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Relevance of 'adaptive' mutations arising in non-dividing cells of microorganisms to age-related changes in mutant phenotypes of neurons.

机译：微生物非分裂细胞中出现的“适应性”突变与神经元突变表型的年龄相关变化的相关性。

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Brattleboro rats do not produce vasopressin (VP) because of a germ-line single-base deletion (di) that causes a frame shift downstream from the VP sequences and a loss of a stop codon. The resulting frame-shifted peptide precursor does not enter the secretory pathway in hypothalamic neurons, thereby blocking the neurosecretion of VP and other peptides. Yet, from birth onwards, a subpopulation of neurons in di/di rats slowly accumulates revertant cells with a hemizygous wild-type phenotype. Because the rate of reversion during aging is slowed by vasopressin infusion, it is of interest to consider these phenomena in relation to recent observations on ?adaptive' mutations in single cell bacteria and yeast that enable reversion of mutations that blocked cell division under conditions of nutrient deficits. In considering mechanisms that could produce revertant phenotypes in non-dividing cells of both pro- and eukaryotes, we note the pertinence of transcription-coupled repair and SOS ?error-prone' repair.
机译：Brattleboro大鼠不产生加压素（VP），因为种系单碱基缺失（di）会导致VP序列下游的移码和终止密码子的丢失。所得移码肽前体不会进入下丘脑神经元的分泌途径，从而阻止VP和其他肽的神经分泌。然而，从出生开始，di / di大鼠中的神经元亚群会缓慢积累具有半合子野生型表型的回复细胞。由于输注加压素可减缓衰老过程中的逆转速率，因此有必要考虑这些现象，并与最近有关单细胞细菌和酵母中“适应性”突变的观察结果相关联，这些突变能够逆转在营养条件下阻止细胞分裂的突变赤字。在考虑可能在原核生物和真核生物的非分裂细胞中产生可逆表型的机制时，我们注意到转录偶联修复和SOS“易错”修复的相关性。

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