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