Narumi Issay, Satoh Katsuya, Cui Suzhen, Funayama Tomoo, Kitayama Shigeru, Watanabe Hiroshi
Research Group for Biotechnology Development, Department of Ion-beam-applied Biology, Japan Atomic Energy Research Institute, Takasaki 370-1292, Japan.
Mol Microbiol. 2004 Oct;54(1):278-85. doi: 10.1111/j.1365-2958.2004.04272.x.
The extraordinary radiation resistance of Deinococcus radiodurans results from the efficient capacity of the bacterium to repair DNA double-strand breaks. By analysing the DNA damage repair-deficient mutant, KH311, a unique radiation-inducible gene (designated pprA) responsible for loss of radiation resistance was identified. Investigations in vitro showed that the gene product of pprA (PprA) preferentially bound to double-stranded DNA carrying strand breaks, inhibited Escherichia coli exonuclease III activity, and stimulated the DNA end-joining reaction catalysed by ATP-dependent and NAD-dependent DNA ligases. These results suggest that D. radiodurans has a radiation-induced non-homologous end-joining repair mechanism in which PprA plays a critical role.
耐辐射球菌的超强辐射抗性源于该细菌修复DNA双链断裂的高效能力。通过分析DNA损伤修复缺陷型突变体KH311,鉴定出了一个导致辐射抗性丧失的独特的辐射诱导基因(命名为pprA)。体外研究表明,pprA的基因产物(PprA)优先结合带有链断裂的双链DNA,抑制大肠杆菌核酸外切酶III的活性,并刺激由ATP依赖性和NAD依赖性DNA连接酶催化的DNA末端连接反应。这些结果表明,耐辐射球菌具有一种辐射诱导的非同源末端连接修复机制,其中PprA起着关键作用。