Elements in the λ immunity region regulate phage development: beyond the 'Genetic Switch'.
Elements in the λ immunity region regulate phage development: beyond the 'Genetic Switch'.
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α免疫区的元素调节噬菌体发育：超越“基因开关”。
DOI：
10.1111/mmi.14394
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发表时间：
2019
影响因子：
3.6
通讯作者：
Court,DonaldL
中科院分区：
文献类型：
--
作者：
Thomason,LynnC;Morrill,Kathleen;Murray,Gillian;Court,Carolyn;Shafer,Brenda;Schneider,ThomasD;Court,DonaldL
λ噬菌体免疫区的遗传元件有助于整合的大肠杆菌噬菌体的稳定维持和同步诱导，在溶原性和溶原性生长之间存在一个由CI和Cro阻遏物协调的双向开关，该阻遏物作用于溶原性（PL和PR）和溶原性（PRM）启动子，称为遗传开关。噬菌体免疫区中其他不太好表征的元件包括PLIT启动子和免疫终止子TIMM。在λ溶原菌中，PLIT启动子被细菌莱克萨蛋白抑制。莱克萨阻遏物和λ CI阻遏物一样，在DNA损伤的SOS反应过程中失活，这种调节确保了PLIT启动子和裂解性PL和PR启动子同步激活。适当的RexA和RexB蛋白水平对于从溶原性到溶解性生长的转变至关重要。PLIT突变降低了RexB相对于RexA的水平，损害了细胞能量学并导致裂解性噬菌体产量降低10倍。RexA和RexB蛋白在细菌双杂交系统中相互作用。我们还发现转录终止子TIMM是一种Rho-独立的内在终止子。TIMM的失活对λ溶原化或原噬菌体诱导的影响最小。
Genetic elements in the bacteriophage λ immunity region contribute to stable maintenance and synchronous induction of the integratedEscherichia coliprophage.There is a bistable switch between lysogenic and lytic growth that is orchestrated by the CI and Cro repressors acting on the lytic (PLandPR) and lysogenic (PRM) promoters, referred to as the Genetic Switch. Other less well‐characterized elements in the phage immunity region include thePLITpromoter and the immunity terminator,TIMM. ThePLITpromoter is repressed by the bacterial LexA protein in λ lysogens. LexA repressor, like the λ CI repressor, is inactivated during the SOS response to DNA damage, and this regulation ensures that thePLITpromoter and the lyticPLandPRpromoters are synchronously activated. Proper RexA and RexB protein levels are critical for the switch from lysogeny to lytic growth. Mutation ofPLITreduces RexB levels relative to RexA, compromising cellular energetics and causing a 10‐fold reduction in lytic phage yield. The RexA and RexB proteins interact with themselves and each other in a bacterial two‐hybrid system. We also find that the transcription terminator,TIMM, is a Rho‐independent, intrinsic terminator. Inactivation ofTIMMhas minimal effect on λ lysogenization or prophage induction.