| Project/Area Number |
10660099
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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 |
応用微生物学・応用生物化学
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| Research Institution | Tokai University |
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Principal Investigator |
OGURA Mitsuo Tokai University, Faculty of Marine Science and Technology, Associate Professor, 海洋学部, 助教授 (80204163)
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| Co-Investigator(Kenkyū-buntansha) |
TANAKA Teruo Tokai University, Faculty of Marine Science and Technology, Professor, 海洋学部, 教授 (10236606)
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| Project Period (FY) |
1998 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 1999: ¥1,800,000 (Direct Cost: ¥1,800,000)
Fiscal Year 1998: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Keywords | Genetic competence / Lipoprotein / Two-component system / Bacillus subtilis / Extracellular factor / Quorum sensing / RapGフォスファターゼ / DegS-DegU / competence / 転写因子 / Comk |
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| Research Abstract |
A master regulator for B. subtilis competence, ComK, is required for transcription of late competence operons. ComK is inactive in a complex with MecA and ClpC, but is activated upon release from the complex by the action of ComS.
Med has been found as a positive regulator for comK functioning downstream from MecA. It is a putative lipoprotein with a lipid modification signal. An alkaline phosphatase fusion with Med and Western analysis revealed localization of Med on the outer surface of the cell membrane.
Western and Northern analyses showed a decrease of ComK in the med mutant. Unphosphorylated DegU, a response regulator of the DegS-DegU two-component system regulating exoprotease production, is necessary for transcription of comK, whereas phosphoryrlated DegU is necessary for exoprotease production. The effect of the med mutation was suppressed by deletion of degS, suggesting that Med could modulate DegU phosphorylation, I.e., a factor inhibiting DegU phosphorylation might be incorporated by a Med-dependent manner. We have found that multicopy phrG inhibited the expression of aprE-lacZ and caused an increase in comK transcription. Addition of a synthetic PhrG pentapeptide to the culture reduced aprE-lacZ expression. These results suggested that phrG positively regulates transcription of comK possibly through DegU.
Quorum sensing regulation by the PhrC pentapeptide results in activation of a response regulator, ComA, triggering transcription of comS. RapG-PhrG was also identified as the regulatory system for expression of the ComA-controlled genes in addition to RapC-PhrC.
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