The molecular events involved in the induction of petite yeast mutants by fluorinated pyrimidines
The molecular events involved in the induction of petite yeast mutants by fluorinated pyrimidines
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氟化嘧啶诱导小酵母突变体涉及的分子事件
DOI：
10.1007/bf00701248
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发表时间：
1976
期刊：
影响因子：
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通讯作者：
D. Williamson
中科院分区：
文献类型：
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作者：
S. Oliver;D. Williamson
摘要氟代嘧啶类化合物5-氟尿嘧啶(5FU)和5-氟胞嘧啶(5FC)高效诱导酿酒酵母细胞质微小突变。研究发现，为了诱导突变，必须首先将5FC脱氨基为5FU。然而，诱变并不依赖于5FU进一步转化为其脱氧核苷(5FUDR)并随后阻断细胞内胸苷合成，因为5FUDR本身没有突变，并且5FU诱导的突变不能通过向DTMP可渗透的菌株供应胸苷一磷酸(DTMP)而被拮抗。无论如何，对对数期细胞中伴随着微小诱导的分子变化的观察排除了突变仅仅是由于复制受阻的mitDNA分子被稀释而导致的可能性，因为突变体的出现与改变的mitDNA分子的合成相吻合。在不同的菌株中，产生的缺陷分子要么保持不变，产生抑制的ρ−小体，要么完全降解，获得中性ρ0突变体的纯克隆。推测这一降解过程是5FU掺入RNA的结果。
SummaryThe fluorinated pyrimidines 5-fluorouracil (5FU) and 5-fluorocytosine (5FC) induce the cytoplasmic petite mutation in the yeastSaccharomyces cerevisiae with high efficiency. It was found that in order to induce the mutation, 5FC must first be deaminated to 5FU. However, mutagenesis does not depend on the further conversion of 5FU to its deoxyriboside (5FUDR) and subsequent blockade of intracellular thymidine synthesis, since 5FUDR itself was found not to be mutagenic, and 5FU-induced mutagenesis was not antagonised by supplying thymidine monophosphate (dTMP) to a dTMP permeable strain. In any case, observations of the molecular changes accompanying petite induction in log phase cells ruled out the possibility that mutagenesis resulted simply from the dilution out of replication-blocked mitDNA molecules, since the appearance of mutants coincided with the synthesis of altered mitDNA molecules. In different strains, the resulting defective molecules were either maintained, giving rise to suppressiveρ− petites, or completely degraded, to give pure clones of neutralρ0 mutants. It is suggested that this degradative process was a consequence of the incorporation of 5FU into RNA.