Enterococcus faecalis cytolysinの2つの成分レギュレータは,クオラムセンシング自動誘導に反応する
Wolfgang Haas1, Brett D Shepard, Michael S Gilmore
1Department of Microbiology and Immunology, University of Oklahoma Health Sciences Center, Oklahoma City 73104, USA.
Nature
|January 10, 2002
まとめ
2つの新しい遺伝子である,cylR1とcylR2は,Enterococcus faecalis.で細胞リン生成を抑制する. この細菌毒素の発現は,特定の細胞密度でクオラムセンシングメカニズムによって自動的に誘発されます.
科学分野:
- 微生物学 微生物学とは
- バクテリア病原菌の発生
- 分子生物学は分子生物学である.
背景:
- Enterococcus種は,病院で感染する主な原因である.
- Enterococcus faecalisは,細菌の毒性を高めるエキゾトキシンであるサイトリシンを生成します.
- サイトリシンは,グラム陽性細菌に対する殺菌作用も示しています.
研究 の 目的:
- Enterococcus faecalis.でサイトリシン発現を制御する規制メカニズムを解明する.
- サイトリシン生成の調節に関与する遺伝的要因を特定する.
主な方法:
- 細胞リン調節における2つの新しい遺伝子,シルR1とシルR2の機能を調査した.
- サイトリシン生成に関連する遺伝子発現とタンパク質の局所化を分析した.
- サイトリシン自己誘導のモデルを開発した.
主要な成果:
- サイトリシン遺伝子転写の新型抑制剤として cylR1 と cylR2 を特定した.
- サイトリシン脱圧が特定の細胞密度で発生することを実証した.
- 細胞外サイトリシンサブユニット濃度が脱圧を誘発することを示した.
結論:
- cylR1 と cylR2 は共鳴して,細胞リンシンセシスを抑制する.
- サイトリシン発現は,二要素の規制システムを含むクオラムセンシングメカニズムによって制御されます.
- この研究は,細菌毒素の自己誘導のための新しいモデルを提供します.
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