Cas13誘発の細胞休眠状態は,CRISPRに抵抗する細菌菌の増殖を防ぐ
Alexander J Meeske1, Sandra Nakandakari-Higa2, Luciano A Marraffini3,4
1Laboratory of Bacteriology, The Rockefeller University, New York, NY, USA. ameeske@rockefeller.edu.
Nature
|May 31, 2019
まとめ
タイプVIのCRISPRシステムであるCas13酵素は,宿主細胞のトランスクリプトを割ってDNAファグから防御します. このトランスクリバージはファグの複製を止め,細菌を保護し,耐性ファグの出現を防ぎます.
科学分野:
- 微生物学
- 分子生物学
- 遺伝学
背景:
- クラスタ化された,定期的に間隔のある,短いパリンドロミックリピート (CRISPR) システムは,CRISPR RNAs (crRNAs) を利用して,外来核酸標的化のためのCRISPR関連 (Cas) 核酸を誘導する.
- タイプVIのCRISPRシステム,特にCas13ヌクレアゼはRNAガイドを使ってRNA分子を割ります.
- Cas13はRNA分裂で知られているが,二重鎖DNA (dsDNA) ファージに対する防御における役割は不明である.
研究 の 目的:
- Cas13がdsDNAファグに対して防御するメカニズムを調査する.
- Cas13のシスおよび/またはトランスRNA分裂活動がファグ防御に関与するかどうかを決定する.
- Cas13がDNAを標的とするCRISPRシステムに抵抗するファグに対する免疫をどのように与えるかを理解する.
主な方法:
- dsDNAファグに対するバクテリアの防御におけるCas13の活性に関する実験調査.
- 病原菌感染中のCas13のシス-およびトランス-RNA分裂機能の分析
- Cas13の活性化によってもたらされるファグ中和と宿主免疫の評価.
主要な成果:
- 宿主細胞のトランスクリプトのCas13媒介によるトランスクリバージは,ファグの成長を止め,感染サイクルを中止するのに十分です.
- このトランス・クリバージはファグ集団を枯渇させ,感染していない細菌に集団免疫を与えます.
- Cas13は,宿主トランスクリプトをターゲットにすることで,DNAを標的とするCRISPRシステムを回避する変異を持つファグを効果的に中和します.
結論:
- タイプVIのCRISPRシステムは,宿主トランスクリプトに対するCas13のトランスクリバージング活動を通じて,dsDNAファグに対する強力な防御を提供します.
- このメカニズムは,ファグに直接作用するのではなく,宿主細胞に作用し,広範な保護を提供します.
- Cas13媒介による防御は,CRISPR耐性ファグの出現を防止し,ファグの発生を緩和します.
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