MECHANISM FOR GENE CONVERSION IN FUNGI

MECHANISM FOR GENE CONVERSION IN FUNGI
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DOI:
10.1017/s0016672300001233
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发表时间:
1964-01-01
期刊:
影响因子:
1.5
通讯作者:
HOLLIDAY, R
HOLLIDAY, R
中科院分区:
生物学4区
文献类型:
--
作者:
HOLLIDAY, R

文献摘要

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提出的机制克服了许多困难,任何副本选择模型遇到的。有人建议,有效的配对短区域发生在分子水平上的DNA双holices的链的分离,然后从2个同源染色单体的链退火。如果退火区域恰好跨越杂合位点,则会发生碱基错配。这种情况可能类似于被诱变剂损伤的DNA;相同或相似的修复机制可能起作用,这些修复机制通过调整碱基序列以恢复正常的碱基配对,在没有任何遗传复制的情况下引起基因转换。该模型表明如何交叉断裂和染色单体的团聚可能发生在附近的转换。该模型还提出,精细结构图上2个突变位点之间的距离与其说取决于它们之间发生重组事件的频率,不如说取决于突变体本身对遗传配对过程的抑制程度。文献中的数据清楚地表明,突变体对基因内重组有抑制作用,并进行了讨论。
The mechanism proposed overcomes many of the difficulties that any copy choice model encounters. It is suggested that effective pairing over short regions occurs at the molecular level by the separation of the strands of the DNA double holices, followed by the annealing of strands from 2 homologous chromatids. If the annealed region happens to span a heterozygous site, mispairing of bases will occur. Such a situation may be analogous to that in DNA damaged by mutagens; the same or similar repair mechanisms may operate, and these, by adjusting the base sequences in order to restore normal base pairing, would bring about gene conversion in the absence of any genetic replication. The model indicates how crossing over by breakage and reunion of chromatids could occur in the vicinity of the conversion. The model also proposes that the distance between 2 mutant sites on a fine structure map depends not so much on the frequency of a recombinational event occurring between them, but rather on the degree of inhibition of the processes of genetic pairing by the mutants themselves. Data in the literature which clearly indicate that mutants have an inhibiting effect on intragenic recombination are presented and discussed.