2006 Fiscal Year Final Research Report Summary
Molecular Mechanism of Bacterial Chromosome Partitioning dependent on a Centromere like site migS
| Project/Area Number |
16370082
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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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 |
NIKI Hironori National Institute of Genetics, Strain Stock Center, Professor, 系統生物研究センター, 教授 (70208122)
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| Co-Investigator(Kenkyū-buntansha) |
KURUMIZAKA Hitoshi Waseda University, Graduate School of Science and Engineering, Associate professor, 理工学術院, 助教授 (80300870)
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| Project Period (FY) |
2004 – 2006
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| Keywords | E.coli / Chromosome / nuclear division / replication / cetromere |
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| Research Abstract |
We have found a centromere-like element (migS) on the Escherichia coli genome. We searched gene products that genetically interact with migS. Transposon (Tn) insertion mutations of phoU showed a growth defect under migS deletion mutation. It was reported that PhoU functions in phosphate uptake and intercellular phosphate metabolism, although several group claimed those were not its primary functions. The phoU Tn insertion mutant (phoU : : Tn) lacked a few amino acid residues from the carboxyl terminal of phoU gene, and the null mutant did not show the synthetic lethal phenotype with migS mutant. phoU::Tn cells showed mislocated nucleoid from centre of the cells, while in wild type cells have the nucleoid at central region of the cell. Daughter nucleoids were not clearly separated at cell division in the mutant. In fact, frequency of DNA-less cells increased in the phoU mutant. This phenotype was exaggerated in slmA deficient cells where septum inhibition mechanism over unseparated nucl
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eoids was absent. In ΔslmA, phoU : : Tn double mutant cells, frequency of anucleate cells were increased compared to the wild type cells and guillotine typed cells were appeared. We concluded that the truncated PhoU protein perturbed correct positioning of daughter nucleoids and this could lead mitotic catastroph. Furthermore, we would like to focus on study of the molecular mechanism for bipolar migration of DNA in a bacterial cell. Although actin-like proteins have been found in prokaryotes, a motor function to partition chromosomes into daughter cells has not yet been identified on bipolar migration of the chromsome. Presumably, a motor protein works on the process to generate a driving force. Investigation of the molecular mechanism of migS dependent migration is providing vital new clues as how the putative motor protein contributes to chromosome partitioning. Proteomics approaches have already been identified two proteins as migS binding proteins. Further investigation of the genes that encode the migS binding proteins have already been carried out, and the results indicates the genes would be involved in bipolar migration of migS Less
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Research Products
(5 results)
