1988 Fiscal Year Final Research Report Summary
Depression of Lethal Activity of Plasmid in Streptomycetes
| Project/Area Number |
62560111
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
発酵・醸造
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| Research Institution | Kyushu University |
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Principal Investigator |
OGATA Seiya Professor, Faculty of Agriculture, Kyushu University, 農学部, 教授 (20038277)
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| Project Period (FY) |
1987 – 1988
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| Keywords | Conjugative plasmid / Lethal activity of plasmid / Spore formation / Aerial mycelium elongation / Thiostrepton production / 胞子形成促進物質 / 気菌糸生育促進物質 / 気菌糸伸長促進 / 細胞分化促進物質 / チオストレプトン生産 |
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| Research Abstract |
We found that some derivatives of Streptomyces azureus ATCC 14921 lost both spore forming ability and Thiostrepton productivity due to the action of a conjugative plasmid pSA1.1, of which original sequence was integrated in the chromosome of wild-type strain. The inhibiting ability of pSA1.1 on the spore formation and Thiostrepton production was depressed by coexistence with a defective plasmid pSA1.2 derived from pSA1.1. Cysteine and cysteine-containing compounds.Such as Bacitracin and Glutathione also depressed the inhibiting action of pSA1.1. These compounds also stimulated the spore formation, aerial mycelium elongation or Thistrepton production of wild-type and plasmid-cured strains: Cysteine showed the spore forming activity, weak activity of aerial mycelium elongation and Thiostrepton productivity; Bacitracin showed the spore forming activity, fairly growth activity on submeriged mycelium and strong elongation activity on areial mycelium; Glutathione showed the spore forming activity. These compounds would enhance the cell metabolism. The inhibiting action of pSA1.1 on the host cells may be depressed by the enhanced metebolism of host cells. The pSA1.1 may code for a protein that can interact in a damage manner with cell membrances.
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