| Project/Area Number |
26860223
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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 |
Pathological medical chemistry
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| Research Institution | Kawasaki Medical School |
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Principal Investigator |
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| Project Period (FY) |
2014-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | 肺炎クラミジア / エフェクター / 酵母スクリーニング / 細胞内輸送異常 / 細胞内輸送 / アポトーシス |
|---|
| Outline of Final Research Achievements |
Chlamydia pneumoniae is an obligate intracellular pathogen that causes acute and chronic respiratory infections in humans. We found that C. pneumoniae J138 strain featured a putative protein coded by its 1069 open reading frames (ORFs). A comprehensive bioinformatics approach was applied for annotation taxonomy, and approximately half of the predicted ORFs were found to encode proteins without any known functions. To identify novel C. pneumoniae molecules which determine virulence and pathogenicity, we screened 455 ORFs without any known functions in a yeast expression system. We found E01, localized at mitochondria, caused apoptosis in both yeast and mammalian cells, and E02 involved in aberrant vesicular trafficking in host cells. E02 could interact with the enzyme that modifies chemical reaction in host cells.Our study suggests that a novel C. pneumoniae molecule interacts with the enzyme and could cause aberrant vesicle trafficking.
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