ニコチン酸の制限は,UTI中にカンジダアデシンの静止を調節する
Renee Domergue1, Irene Castaño, Alejandro De Las Peñas
1Department of Molecular Biology and Genetics, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Science (New York, N.Y.)
|March 19, 2005
まとめ
Candida glabrataは,宿主細胞粘着のためのEPA遺伝子を使用し,ニコチン酸 (NA) の不足によって尿路感染症の間に活性化されます. この代謝適応は,C. glabrata.の宿主環境をシグナルする.
科学分野:
- 微生物学 微生物学とは
- 分子生物学は分子生物学である.
- ホストと病原体の相互作用
背景:
- キャンディダ・グラブラタの宿主細胞への粘着は,感染にとって極めて重要です.
- アデシンをコードするEPA遺伝子は,典型的には,サブテロメア位置で転写的に静止されます.
- EPA遺伝子の調節を理解することは,C. glabrataの感染を制御する鍵です.
研究 の 目的:
- ネズミの尿路感染症 (UTI) 中のEPA遺伝子の発現を調査する.
- C. glabrataにおけるEPA遺伝子発現を誘発する環境信号を特定する.
- ニコチン酸 (NA) がEPA遺伝子発現とC. glabrataの適応に影響するメカニズムを解明する.
主な方法:
- 尿路感染症のマウスモデル.
- 感染中のEPA遺伝子発現の分析.
- ニコチン酸 (NA) とニコチナミドアデニン・ディヌクレオチド (NAD+) の代謝に関する調査.
- NAD+依存ヒストン脱酸化酵素Sir2p.の役割を評価する.
主要な成果:
- 通常,静かなEPA遺伝子は,ネズミの尿路感染症で発現します.
- ニコチン酸 (NA) 制限は,EPA遺伝子発現を誘発する信号です.
- C. glabrataはNAに対するオクスオトロフィックであり,NA誘発のEPA発現はNA+の可用性低下と相関する.
- このプロセスは,NAD+に依存するヒストン脱酸化酵素Sir2p.を伴う.
結論:
- C. glabrataは,ニコチン酸 (NA) に対するオクスオトロフィーを利用して宿主環境に適応します.
- NAの制限は,EPAの遺伝子発現を誘発し,尿路感染症中に宿主細胞の結合を促進します.
- この研究は,C. glabrataにおける代謝状態とウイルス性遺伝子調節の間の関連性を明らかにしている.
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