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FimK regulation on the expression of type 1 fimbriae in Klebsiella pneumoniae CG43S3
Update time:2013-08-08 01:47:27   【 Font: Large  Medium Small


Klebsiella pneumoniae CG43, a heavy encapsulated liver abscess isolate, mainly expresses type 3 fimbriae. Type 1 fimbriae expression was only apparent in CG43S3ΔmrkA (the type 3 fimbriae-deficient strain). The expression of type 1 fimbriae in CG43S3ΔmrkA was reduced by deleting the fimK gene, but was unaffected by removing the 3'end of fimK encoding the C-termial EIL domain (EILfimK). Quantitative reverse-transcription PCR and promoter activity analysis showed that the putative DNA binding region at the N-terminus, but not the C-terminal EIL domain, of FimK positively affects transcription of type 1 fimbrial major subunit, fimA. An electrophoretic mobility shift assay demonstrated that the recombinant FimK could specifically bind to fimS, that is located upstream of fimA and contains a vegetative promoter for the fim operon, also reflecting possible transcriptional regulation. EILfimK was shown to encode a functional phosphodiesterase (PDE) via enhancing motility in Escherichia coli JM109 and in vitro using PDE activity assays. Moreover, EILfimK exhibited higher PDE activity than FimK implying that the N-terminal DNA binding domain may negatively affect the PDE activity of FimK. FimA expression was detected in CG43S3 expressing EILfimK or AILfimK suggesting that FimA expression is not directly influenced by the c-di-GMP level. In summary, FimK influences type 1 fimbriation by binding to fimS at the N-terminal domain, and thereafter, the altered protein structure may activate C-terminal PDE activity to reduce the intracellular c-di-GMP level.

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Source:Microbiology      by ZC Wang, CJ Huang, YJ Huang, CC Wu
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