| Project/Area Number |
59480002
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
遺伝学
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| Research Institution | KUMAMOTO UNIVERSITY (1986)
Kyoto University (1984-1985) |
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Principal Investigator |
HIRAGA SOTA KUMAMOTO UNIVERSITY MEDICAL SCHOOL, PROFESSOR, 医学部, 教授 (40027321)
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| Co-Investigator(Kenkyū-buntansha) |
NAGAI KAZUO TOKYO UNIVERSITY, ASSOCIATE PROFESSOR, 農学部, 助教授 (00011974)
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| Project Period (FY) |
1984 – 1986
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| Project Status |
Completed (Fiscal Year 1986)
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| Budget Amount *help |
¥6,400,000 (Direct Cost: ¥6,400,000)
Fiscal Year 1986: ¥1,900,000 (Direct Cost: ¥1,900,000)
Fiscal Year 1985: ¥1,900,000 (Direct Cost: ¥1,900,000)
Fiscal Year 1984: ¥2,600,000 (Direct Cost: ¥2,600,000)
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| Keywords | PLASMID / PARTITION OF DNA / SEX FACTOR / 大腸菌染色体 |
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| Research Abstract |
The F plasmid of Escherichia coli is known to be stably maintained in dividing cells, despite its low copy number per cell. We have found the partition mechanism controlled by plasmid genes. This mechanism acts for equipartition of plasmid DNA molecules to daughter cells. The mechanism depends on two trans-acting genes (sopA and sopB)and the cis-acting DNA site(sopC)of the plasmid. We determined the DNA sequence of the entire partition region. Twelve 43 base-pair direct repeats exist in the sopC region without any spacer regions. Purified SopB protein binds to the sopC DNA segment. The SopB protein can be recovered from the membrane fraction in the presence of the magnesium ion. Products of host chromosomal genes are involved in the partition mechanism of the mini-F plasmid. Host mutants defective in stable maintenance of the plasmid. They are classified into five linkage groups. Four linkage groups of mutants among them allow normal replication of the plasmid DNA, however mutants of the 5th linkage group cause abnormal replication, resuting linear multimer molecules of the plasmid DNA. The former four linkage groups of mutants are presumably defective in equipartition of plasmid DNA molecules into dauther cells.
We have found another mechanism, named the ccd mechanism, controlled by the plasmid genes ccdA and ccdB. This mechanism guarantees preferential growth of the plasmid-carrying cells in population by killing plasmid-free segments. When replication or partition of a plasmid carrying the ccdA and ccdB genes is impaired and plasmid-free segregants appear, these segregants are killed by the ccd mechanism after few cell divisions (named Nonviable Segregants Model). It is suggested that the ccdA gene product, which supresses the killing function of the ccdB gene product, is diluted and inactivated according to residual cell divisions of plasmid-free segregants, causing killing segregants.
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