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 pLit-rexB-tImm (late immunity transcription, LIT RNA) and po-oop-t(o) (OOP RNA) has remained unexplained. The initial assigned sequence for pLit bore no relationship to po. We have identified two promoter sites for independent rexB transcription, denoted here pLit2 and pLit1, which are separated by about 330 bp. The upstream pLit1 site shares with po 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 pLit2. 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 pLit1, suggesting a complex regulatory pattern for rexB expression from this promoter.