| Project/Area Number |
25870386
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Bacteriology (including mycology)
Applied microbiology
|
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| Research Institution | Dokkyo Medical University (2014-2016)
Osaka University (2013) |
|---|
Principal Investigator |
Otsuka Yuichi 獨協医科大学, 医学部, 助教 (10548861)
|
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| Research Collaborator |
TADA Shunsuke
TAKAHASHI Chisato
|
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| Project Period (FY) |
2013-04-01 – 2017-03-31
|
| Project Status |
Completed (Fiscal Year 2016)
|
| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2015: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2014: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2013: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | トキシン－アンチトキシン系 / 細菌 / ファージ / 非コードRNA / 翻訳 / RNA分解 / 抗ファージ作用 / 抗菌ペプチド / 大腸菌 / 遺伝子発現 / トキシンーアンチトキシン / mRNA分解 / トキシン / アンチトキシン |
|---|
| Outline of Final Research Achievements |
Toxin-antitoxin system (TAS) is widely conserved in prokaryotic plasmids and chromosomes and is linked to many roles in cell physiology. TAS is composed of a stable toxin that inhibits one of essential cellular processes, and a labile antitoxin that inhibits a harmful effect of the cognate toxin. In this study, the new TAS, z3289-sRNA1, encoded by the Enterohemorrhagic E. coli O157:H7 chromosome has been characterized. I elucidated the molecular mechanism of the toxicity caused by the z3289 toxin, the mechanism for the translational repression of the z3289 toxin by the sRNA1 antitoxin, and the physiological role of z3289-sRNA1 as an anti-phage defense. In addition, I demonstrated that the modified z3289 toxin functions as an antimicrobial peptide.
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