The Rex phenotype of altruistic cell death following infection of a lambda lysogen by T4rII mutants is suppressed by plasmids expressing OOP RNA

The coordinate expression from induced lambda prophages of p(Lit)-rexB-t(Imm) (late immunity transcription, LIT RNA) and p(o)-oop-t(o) (OOP RNA) has remained unexplained. The initial assigned sequence for p(Lit) bore no relationship to p(o). We have identified two promoter sites for independent rexB transcription, denoted here p(Lit2) and p(Lit1), which are separated by about 330 bp. The upstream p(Lit1) site shares with P-o a common 9 bp sequence between the -10 and -35 regions, with strong homology to aspects of the SOS box or LexA operator site. This sequence is also found within OOP RNA, suggesting that OOP RNA, or another regulatory factor recognizing the common sequence, was involved in the regulation of rexB expression and hence Rex exclusion. We measured the influence of OOP synthesis from plasmids on the Rex phenotype, finding that plasmids producing OOP can suppress Rex exclusion by a lambda prophage. The possibility was suggested that low level constitutive rexB transcription occurs from p(Lit2). Potential binding sites were identified for DnaA, for the LexA, CI and Cro repressors and for lambda O protein in the 80 nt DNA interval upstream from and including p(Lit1), suggesting a complex regulatory pattern for rexB expression from this promoter. (C) 1997 Elsevier Science B.V.