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易出错的DNA修复与跨损伤DNA合成。II:诱导性SOS假说。

Error-prone DNA repair and translesion DNA synthesis. II: The inducible SOS hypothesis.

作者信息

Bridges Bryn A

机构信息

Genome Damage and Stability Centre, University of Sussex, Falmer, Brighton BN1 9RQ, UK.

出版信息

DNA Repair (Amst). 2005 Jun 8;4(6):725-6, 739. doi: 10.1016/j.dnarep.2004.12.009.

Abstract

Evelyn Witkin hypothesized in 1967 that bacterial cell division is controlled by a repressor which, like the lambda repressor, is inactivated by a complex process that starts with the presence of replication-blocking lesions in the DNA. She further suggested that this might not be the only cellular function to show induction by DNA damage. Three years later, Miroslav Radman, in a privately circulated note, proposed that one such function might be an inaccurate (mutation-prone) DNA polymerase under the control of the recA and lexA genes. Thus was born the SOS hypothesis.

摘要

伊夫林·维特金在1967年提出假说,认为细菌细胞分裂受一种阻遏物控制,这种阻遏物与λ噬菌体阻遏物类似,会通过一个复杂过程失活,该过程始于DNA中出现复制阻断损伤。她还进一步提出,这可能不是唯一受DNA损伤诱导的细胞功能。三年后,米罗斯拉夫·拉德曼在一份私下传阅的笔记中提出,一种这样的功能可能是受recA和lexA基因控制的一种不准确(易出错)的DNA聚合酶。于是,SOS假说诞生了。

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