バクテリオファージが子孫を守る新戦略を解明(U of T researchers reveal how bacterial viruses protect their offspring to maximize spread)

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2025-08-28 トロント大学(U of T)

トロント大学の研究で、バクテリオファージ(細菌ウイルス)が子孫の感染効率を高める仕組みが解明された。ファージはZipタンパク質を産生し、宿主細菌の菌毛形成を抑制する。菌毛は感染の足場であるため、これを減らすことで新たに放出された子孫ファージが既感染細胞に無駄に再感染せず、未感染の細菌に効率よく拡散できる。実験ではZipを持つ場合、一晩で100万個/mLの子孫が確認されたのに対し、欠失株ではわずか500個/mLにとどまった。さらにZip発現は細菌の密度センサーにより調節され、状況に応じて保護効果を強めることも判明。この「anti-Kronos効果」は複数のファージに保存されており、自己再感染を防ぐ進化的戦略とされる。

バクテリオファージが子孫を守る新戦略を解明(U of T researchers reveal how bacterial viruses protect their offspring to maximize spread)
Screenshot from a video showing the movement of fibres called pili – which are located on the bacterial surface and function as a docking station for phages – on typical Pseudomonas bacteria (oval shapes) (video by Matthias Koch)

<関連情報>

プロファージは細胞表面受容体を遮断し、ウイルス子孫を保護する Prophages block cell surface receptors to preserve their viral progeny

Véronique L. Taylor,Pramalkumar H. Patel,Megha Shah,Ahmed Yusuf,Cayla M. Burk,Kristina M. Sztanko,Zemer Gitai,Alan R. Davidson,Matthias D. Koch & Karen L. Maxwell
Nature   Published:16 July 2025
DOI:https://doi.org/10.1038/s41586-025-09260-z

Abstract

In microbial communities, viruses compete for host cells and have evolved diverse mechanisms to inhibit competitors. One strategy is superinfection exclusion, whereby an established viral infection prevents a secondary infection of the same cell1. This phenomenon has been shown to have an important role in the spread of eukaryotic viruses. Here we determine that superinfection exclusion proteins in bacterial viruses (bacteriophages, hereafter phages) perform a similar role, promoting viral spread through the bacterial community. We characterize a phage protein that alters the dynamics of a common phage receptor, the type IV pilus. This protein, known as Zip, does not abrogate pilus activity, but fine-tunes it, providing a strong phage defence without a fitness cost. Notably, Zip also prevents internalization and destruction of newly released phage progeny, a phenomenon that we call the anti-Kronos effect after the Greek god who consumed his offspring. Zip activity promotes the accumulation of free phages in bacterial lysogen communities, thereby enhancing viral spread. We further demonstrate that the anti-Kronos effect is conserved across diverse prophage-encoded superinfection exclusion systems. Our results identify the mechanistic basis of a superinfection exclusion system that safeguards phage progeny and provide insights into the conservation of viral defence mechanisms among bacterial and eukaryotic systems.

細胞遺伝子工学
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