Characterization of the double mutant of Deinococcus radiodurans lexA1 and lexA2  

作　　者：ZHOU Qing CHEN WeiWei ZHANG XinJue XU Hong XU BuJin HUA YueJin 

机构地区：[1]Institute of Nuclear-Agricultural Sciences, Zhejiang University, Hangzhou 310029, China [2]James D. Watson Institute of Genome Sciences, Zhejiang university, Hangzhou 3100081 China

出　　处：《Chinese Science Bulletin》2007年第8期1046-1052,共7页

基　　金：Supported by the National Natural Science Foundation of China(Grant No.30330020),;National Basic Research Program of China(Grant No.2004CB19604);and the State Funds for Distinguished Young Scientists of China(Grant No.30425038)

摘　　要：LexA and RecA play a crucial role in SOS response in Escherichia coli.In classical SOS response,LexA functions as a repressor to regulate the expression of many genes including RecA after DNA damage occurs.Previous studies showed that LexA1 or LexA2 is not involved in RecA induction in Deinococ- cus radiodurans.In this study,we constructed a double mutant of lexA1 and lexA2.Results showed that mutation of lexA1 and lexA2 resulted in an apparent decrease in growth rate and an increased re- sistance to ultraviolet and hydrogen peroxide compared with wild type R1 and two single mutants. However,this double mutant did not exhibit any remarkably increased constitutive expression of RecA under normal conditions,just like wild type R1 and two single mutants,suggesting that neither LexA1 nor LexA2 is involved in the induced expression of RecA.Further transcriptional assay showed that LexA1 and LexA2 together participated in many regulatory pathways involved in cell division,protein synthesis,antioxidant process,transcription regulation and other mechanisms.These results indicate that there should be a new mechanism by which these damage-induced proteins are regulated in D. radiodurans.LexA and RecA play a crucial role in SOS response in Escherichia coli. In classical SOS response, LexA functions as a repressor to regulate the expression of many genes including RecA after DNA damage occurs. Previous studies showed that LexA1 or LexA2 is not involved in RecA induction in Deinococ- cus radiodurans. In this study, we constructed a double mutant of lexA 1 and lexA2. Results showed that mutation of lexA1 and lexA2 resulted in an apparent decrease in growth rate and an increased re- sistance to ultraviolet and hydrogen peroxide compared with wild type R1 and two single mutants. However, this double mutant did not exhibit any remarkably increased constitutive expression of RecA under normal conditions, just like wild type R1 and two single mutants, suggesting that neither LexA1 nor LexA2 is involved in the induced expression of RecA. Further transcriptional assay showed that LexA1 and LexA2 together participated in many regulatory pathways involved in cell division, protein synthesis, antioxidant process, transcription regulation and other mechanisms. These results indicate that there should be a new mechanism by which these damage-induced proteins are regulated in D. radiodurans.

关 键 词：耐辐射球菌 双突变体 LexA1 LexA2 缺失性突变 

分 类 号：Q933[生物学—微生物学] Q937