1996 Fiscal Year Final Research Report Summary
Regulatory mechnism of cell growth in SOS response of Escherichia coli
| Project/Area Number |
06680672
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Molecular biology
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| Research Institution | National Institute of Genetics |
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Principal Investigator |
HIGASHITANI Atsushi National Institute of Genetics, Research Associate, 細胞遺伝研究系, 助手 (40212162)
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| Project Period (FY) |
1994 – 1996
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| Keywords | SOS response / Cell division / Cell cycle / Inhibitor / Protease / DNA repair / Stress response / Single-stranded DNA |
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| Research Abstract |
Regulatory mechnisms of cell growth in the SOS response of E.coli were investigated with emphas is on SulA protein, an SOS-inducible cell-division inhibitor. Direct interaction of SulA with FtsZ,which plays a central role in bacterial cell division was studied. Molecular dissection of SulA and the role of single-stranded DNA as a primary signal for SOS induction in vivo were also analyzed.
1.Using purified SulA protein that was fused to the maltose binding protein, I demonstrated in vitro that SulA interacts with FtsZ to from a stable complex. The reaction required GTP and its hydrolysis. The complex was formed in a molar ratio of approximately one to one of the two proteins.
2.From mutation analyzes, Arg 62, Leu 67, Trp 77, and Lys 87 in the central region of SulA were found essential for the cell-division inhibitory activity. N-terminal residues of SulA ranging from the 3rd to the 27th amino acid and C-terminal 21 residues were dispensable for the activity. The C-terminal 20 residues of SulA were enough for its recognition by and for complexformation with Lon protease. They were necessary, but noy enough, for degradation of SulA by Lon protease.
3.Infection of E.coli with mutant filamentous phage that are defective in the initiation of minus-strand DNA snythesis induced the SOS response as monitored by cellular level of LexA.This observation demonstrated that single-stranded DNA serves as a primary signal for SOS induction in vivo.
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