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首页> 外文期刊>Journal of bacteriology >Phage-Borne Factors and Host LexA Regulate the Lytic Switch in Phage GIL01
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Phage-Borne Factors and Host LexA Regulate the Lytic Switch in Phage GIL01

机译：噬菌体因子和宿主LexA调节噬菌体GIL01中的裂解开关

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The Bacillus thuringiensis temperate phage GIL01 does not integrate into the host chromosome but exists stably as an independent linear replicon within the cell. Similar to that of the lambdoid prophages, the lytic cycle of GIL01 is induced as part of the cellular SOS response to DNA damage. However, no CI-like maintenance repressor has been detected in the phage genome, suggesting that GIL01 uses a novel mechanism to maintain lysogeny. To gain insights into the GIL01 regulatory circuit, we isolated and characterized a set of 17 clear plaque (cp) mutants that are unable to lysogenize. Two phage-encoded proteins, gp1 and gp7, are required for stable lysogen formation. Analysis of cp mutants also identified a 14-bp palindromic dinBox1 sequence within the P1-P2 promoter region that resembles the known LexA-binding site of Gram-positive bacteria. Mutations at conserved positions in dinBox1 result in a cp phenotype. Genomic analysis identified a total of three dinBox sites within GIL01 promoter regions. To investigate the possibility that the host LexA regulates GIL01, phage induction was measured in a host carrying a noncleavable lexA (Ind?) mutation. GIL01 formed stable lysogens in this host, but lytic growth could not be induced by treatment with mitomycin C. Also, mitomycin C induced β-galactosidase expression from GIL01-lacZ promoter fusions, and induction was similarly blocked in the lexA (Ind?) mutant host. These data support a model in which host LexA binds to dinBox sequences in GIL01, repressing phage gene expression during lysogeny and providing the switch necessary to enter lytic development.
机译：苏云金芽孢杆菌（Bacillus thuringiensis）温带噬菌体GIL01不整合到宿主染色体中，而是作为独立的线性复制子稳定存在于细胞内。与lambdoid噬菌体相似，GIL01的裂解周期被诱导为细胞对DNA损伤的SOS反应的一部分。但是，在噬菌体基因组中未检测到类似CI的维持阻遏物，这表明GIL01使用了一种新的机制来维持溶原性。为了深入了解GIL01调节电路，我们分离并鉴定了一组17个无法溶原的透明噬菌斑（ cp ）突变体。稳定的溶原形成需要两个噬菌体编码的蛋白gp1和gp7。对 cp 突变体的分析还发现，在 P1 - P2 启动子区域内有一个14 bp回文的 dinBox 1序列。类似于革兰氏阳性细菌的已知LexA结合位点。 dinBox 1中保守位置的突变会导致 cp 表型。基因组分析确定了GIL01启动子区域内总共三个 dinBox 位点。为了研究宿主LexA调节GIL01的可能性，在携带不可切割 lexA （Ind ？）突变的宿主中测量了噬菌体诱导。 GIL01在该宿主中形成稳定的溶原原，但丝裂霉素C不能诱导溶菌生长。此外，丝裂霉素C诱导了GIL01- lacZ 启动子融合体的β-半乳糖苷酶表达，并且类似地阻断了诱导 lexA （Ind ？）突变宿主。这些数据支持一种模型，其中宿主LexA与GIL01中的 dinBox 序列结合，在溶血原过程中抑制噬菌体基因的表达，并提供进入裂解发育所必需的转换。

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