Viral Satellites Exploit Phage Proteins to Escape Degradation of the Bacterial Host Chromosome.

Amelia C McKitterick, Stephanie G Hays, Fatema-Tuz Johura, Munirul Alam, Kimberley D Seed
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Abstract

Phage defense systems are often found on mobile genetic elements (MGEs), where they constitutively defend against invaders or are induced to respond to new assaults. Phage satellites, one type of MGE, are induced during phage infection to promote their own transmission, reducing phage production and protecting their hosts in the process. One such satellite in Vibrio cholerae, phage-inducible chromosomal island-like element (PLE), sabotages the lytic phage ICP1, which triggers PLE excision from the bacterial chromosome, replication, and transduction to neighboring cells. Analysis of patient stool samples from different geographic regions revealed that ICP1 has evolved to possess one of two syntenic loci encoding an SF1B-type helicase, either of which PLE exploits to drive replication. Further, loss of PLE mobilization limits anti-phage activity because of phage-mediated degradation of the bacterial genome. Our work provides insight into the unique challenges facing parasites of lytic phages and underscores the adaptions of satellites to their ever-evolving target phage.

病毒卫星利用噬菌体蛋白质逃避细菌宿主染色体的降解。
噬菌体防御系统通常存在于可移动遗传元件(MGE)上,在那里它们组成性地防御入侵者或被诱导对新的攻击做出反应。噬菌体卫星是MGE的一种,在噬菌体感染过程中被诱导以促进其自身的传播,减少噬菌体的产生并在此过程中保护其宿主。霍乱弧菌中的一种卫星,噬菌体诱导型染色体岛状元件(PLE),破坏裂解噬菌体ICP1,从而触发PLE从细菌染色体上切除、复制和转导到邻近细胞。对来自不同地理区域的患者粪便样本的分析表明,ICP1已进化为拥有编码SF1B型解旋酶的两个同基因座之一,PLE利用其中任何一个来驱动复制。此外,由于噬菌体介导的细菌基因组降解,PLE动员的丧失限制了抗噬菌体活性。我们的工作深入了解了裂解噬菌体寄生虫面临的独特挑战,并强调了卫星对其不断进化的目标噬菌体的适应。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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