Molecular Mechanism of Cell Death at Stationary Phase in Escherichia coli
| Project/Area Number |
09680698
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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 |
Cell biology
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| Research Institution | Yamaguchi University |
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Principal Investigator |
YAMADA Mamoru Yamaguchi University, Agriculture Associate Professor, 農学部, 助教授 (30174741)
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| Project Period (FY) |
1997 – 1998
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| Project Status |
Completed (Fiscal Year 1998)
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| Budget Amount *help |
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 1998: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1997: ¥2,400,000 (Direct Cost: ¥2,400,000)
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| Keywords | Escherichia coli / cell death / stationary phase / ssnA / rpoS / rpoE / SSnA / rpos |
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| Research Abstract |
From the original genomic gene analysis, I found that the ssnA gene is involved in the large decline of living cell number at the transition period from log to stationary phase. The dead cell number is increased to be more than 99% in the rpoS background, and this increase is suppressed by the ssnA mutation. Moreover, ssnA is expressed at stationary phase under the negative control of RpoS.From these facts, I assume that the decline of living cell number at the specific period may be programmed, which contributes to the maintenance of the living cell number in stationary phase. To elucidate the mechanism of the cell death at the beginning of stationary phase, I obtained the following results in this study. 1) The ssnA clone showed extremely repressed cell growth probably because of the inhibition of cell division. 2) SsnA is a cytoplasmic protein and was purified as a dimmer. 3) The domain for the growth inhibition activity may be located at the C-terminus of SsnA.4) SsnA homologues se
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em to occur not only in some Gram-negative bacteria but also in some Gram-positive bacteria. 5) Two suppressors for the ssnA-dependent growth inhibition were isolated using transposon. One (suppressor 1) has the insertion in the rseA gene encoding a negative regulator for RpoE activity. Consistently, the rpoF clone suppressed the ssnA-dependent growth inhibition. The other (suppressor II) was found to be different from rseA.6) The suppressor I and the rpoE clone showed decreased turbidities at stationary phase but their viable cell numbers were nearly the same as that of the wild-type. 7) The expression of rpoE was increased at the late log phase even under non-heat shock conditions. 8) Both suppressors I and Ii showed decreased expression of two proteins of about 39 kDa in the membrane fractions. All together, SsnA may induce the cell death at the beginning of stationary phase by causing growth inhibition. RpoE.may contribute to the acquisition of nutrients to maintain viable cell number in stationary phase although the mechanism of its suppression of the ssnA-dependent growth inhibition has not been elucidated. Less
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Report
(3 results)
Research Products
(12 results)
