Lytic gene expression in the temperate bacteriophage GIL01 is activated by a phage-encoded LexA homologue.
Lytic gene expression in the temperate bacteriophage GIL01 is activated by a phage-encoded LexA homologue.
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DOI：
10.1093/nar/gky646
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发表时间：
2018-10-12
影响因子：
14.9
通讯作者：
Butala M
中科院分区：
文献类型：
--
作者：
Fornelos N;Browning DF;Pavlin A;Podlesek Z;Hodnik V;Salas M;Butala M
GIL 01噬菌体是感染昆虫病原体苏云金芽孢杆菌的温和噬菌体。在裂解周期中，噬菌体基因转录由三个启动子启动：P1和P2，其控制参与基因组复制的早期噬菌体基因的表达; P3，其控制负责病毒体成熟和宿主裂解的晚期基因的表达。与大多数温和的噬菌体不同，GIL 01溶原性不是由专门的噬菌体阻遏物维持，而是由宿主的SOS反应调节剂莱克萨维持。以前，我们表明，裂解周期诱导的DNA损伤和莱克萨，与噬菌体编码的蛋白质gp 7，抑制P1。在这里，我们研究的裂解/溶原开关更详细，并显示P3也被抑制的LexA-gp 7复合物，结合到串联莱克萨盒内的启动子。我们还表明，从P3的表达是相当延迟DNA损伤后，需要噬菌体编码的DNA结合蛋白，gp 6。令人惊讶的是，gp 6与莱克萨本身同源，因此是直接激活转录的莱克萨同源物的罕见实例。我们建议，这两个莱克萨家族成员之间的相互作用，具有相反的功能，确保GIL 01噬菌体晚期基因的及时表达。
The GIL01 bacteriophage is a temperate phage that infects the insect pathogen Bacillus thuringiensis. During the lytic cycle, phage gene transcription is initiated from three promoters: P1 and P2, which control the expression of the early phage genes involved in genome replication and P3, which controls the expression of the late genes responsible for virion maturation and host lysis. Unlike most temperate phages, GIL01 lysogeny is not maintained by a dedicated phage repressor but rather by the host’s regulator of the SOS response, LexA. Previously we showed that the lytic cycle was induced by DNA damage and that LexA, in conjunction with phage-encoded protein gp7, repressed P1. Here we examine the lytic/lysogenic switch in more detail and show that P3 is also repressed by a LexA–gp7 complex, binding to tandem LexA boxes within the promoter. We also demonstrate that expression from P3 is considerably delayed after DNA damage, requiring the phage-encoded DNA binding protein, gp6. Surprisingly, gp6 is homologous to LexA itself and, thus, is a rare example of a LexA homologue directly activating transcription. We propose that the interplay between these two LexA family members, with opposing functions, ensures the timely expression of GIL01 phage late genes.
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DOI：
10.3390/v6072623
发表时间：
2014-07-09
期刊：
Viruses
影响因子：
--
作者：
Gillis A;Mahillon J
通讯作者：
Mahillon J
影响因子：
64.8
作者：
Abrescia, NGA;Cockburn, JJB;Bamford, JKH
通讯作者：
Bamford, JKH
影响因子：
3.2
作者：
Rabatinova, Alzbeta;Sanderova, Hana;Krasny, Libor
通讯作者：
Krasny, Libor
影响因子：
5.4
作者：
Berjon-Otero, Monica;Lechuga, Ana;Redrejo-Rodriguez, Modesto
通讯作者：
Redrejo-Rodriguez, Modesto
影响因子：
3.4
作者：
Kühner, F;Costa, LT;Gaub, HE
通讯作者：
Gaub, HE