ctr1, a gene involved in a signal transduction pathway of the gliding motility in the cyanobacterium Synechocystis sp. PCC 6803

FEBS Letters

Kang, Kye-Won²  Cho, Mi-Sun³  Lee, Kyun-Min²  Park, Young Mok³  Chung, Young-Ho³  Moon, Yoon-Jung³  Choi, Jong-Soon³  Park, Youn-Il¹  Yoo, Yong-Cheol³ 

[1] Department of Biology, Chungnam National University, 220 Kung-dong, Yusung-ku, Taejon 305-764, South Korea;Department of Biological Sciences, Korea Advanced Institute of Science and Technology, 373-1 Kusong-dong, Yusung-ku, Taejon 305-701, South Korea;Biomolecule Research Team, Korea Basic Science Institute, 52 Yeoeun-dong, Yusung-ku, Taejon 305-333, South Korea

关键词: Methyl-accepting chemotaxis protein;    Gliding motility;    Pilus production;    Transposon mutagenesis;    Synechocystis 6803;    Syn6803;    Synechocystis sp. PCC 6803;    MCP;    methyl-accepting chemotaxis protein;    RT-PCR;    reverse transcriptase-mediated polymerase chain reaction;   

DOI  :  10.1016/S0014-5793(01)02227-X

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

We generated random Tn5 mutations in Synechocystis sp. PCC 6803 in search for genes involved in the signal transduction cascade for the cyanobacterial gliding motility. One of the non-gliding Tn5 mutants, S1-105, had an insertional inactivation in the slr1044 gene encoding a putative methyl-accepting chemotaxis protein. Interposon mutation on the slr1044 (named ctr1) in the bacterium also eliminated gliding motility. In the interposon mutant, the expression of pilA1 was 5-fold decreased compared with that of wild-type and thick pili, that are believed to be the motor for gliding, could not be observed by an electron microscope. Therefore, we suggest that the Ctr1 protein functions as a transducer that regulates the expression of pilA1, and thus is required for the biogenesis of thick pili.

【 授权许可】

Unknown