Engelberg-Kulka Hanna, Kumar Sathish
Department of Microbiology and Molecular Genetics, IMRIC, The Hebrew University-Hadassah Medical School, Jerusalem, 91120, Israel.
Mol Microbiol. 2015 May;96(4):689-93. doi: 10.1111/mmi.12969. Epub 2015 Mar 16.
The life cycle of phage λ has been studied extensively. Of particular interest has been the process leading to the decision of the phage to switch from lysogenic to lytic cycle. The principal participant in this process is the λcI repressor, which is cleaved under conditions of DNA damage. Cleaved λcI no longer acts as a repressor, allowing phage λ to switch from its lysogenic to lytic cycle. The well-known mechanism responsible for λcI cleavage is the SOS response. We have recently reported that the Escherichia coli toxin-antitoxin mazEF pathway inhibits the SOS response; in fact, the SOS response is permitted only in E. coli strains deficient in the expression of the mazEF pathway. Moreover, in strains lysogenic for prophage λ, the SOS response is enabled by the presence of λrexB. λRexB had previously been found to inhibit the degradation of the antitoxin MazE, thereby preventing the toxic action of MazF. Thus, phage λ rexB gene not only safeguards the prophage state by preventing death of its E. coli host but is also indirectly involved in the lysogenic-lytic switch.
噬菌体λ的生命周期已得到广泛研究。特别令人感兴趣的是导致噬菌体从溶原周期转变为裂解周期的过程。该过程的主要参与者是λcI阻遏物，它在DNA损伤的条件下会被切割。被切割的λcI不再作为阻遏物起作用，从而使噬菌体λ从其溶原周期转变为裂解周期。负责λcI切割的著名机制是SOS反应。我们最近报道，大肠杆菌毒素-抗毒素mazEF途径会抑制SOS反应；事实上，只有在mazEF途径表达缺陷的大肠杆菌菌株中才会出现SOS反应。此外，在携带原噬菌体λ的溶原性菌株中，λrexB的存在会激活SOS反应。此前已发现λRexB会抑制抗毒素MazE的降解，从而防止MazF的毒性作用。因此，噬菌体λ的rexB基因不仅通过防止其大肠杆菌宿主死亡来维持原噬菌体状态，还间接参与溶原-裂解转换。
