A Singular Case of Prophage Complementation in Mutational Activation of recET Orthologs in Salmonella enterica Serovar Typhimurium

Abstract

ABSTRACT A class of mutations that suppress the recombination defects of recB mutants in Salmonella enterica serovar Typhimurium strain LT2 activates the normally silent recET module of the Gifsy-1 prophage. Allele sbcE21 is a 794-bp deletion within the immunity region of the prophage. Concomitant with activating recET , sbcE21 stimulates Gifsy-1 excision, resulting in unstable suppression. Early studies found both recB suppression and its instability to depend on the presence of the related Gifsy-2 prophage elsewhere in the chromosome. In cells lacking Gifsy-2, the sbcE21 allele became stable but no longer corrected recB defects. Here, we show that a single Gifsy-2 gene is required for Gifsy-1 recET activation in the sbcE21 background. This gene encodes GtgR, the Gifsy-2 repressor. Significantly, the sbcE21 deletion has one end point within the corresponding gene in the Gifsy-1 genome, gogR , which in strain LT2 is a perfect duplicate of gtgR . The deletion truncates gogR and places the Gifsy-1 left operon, including the recET and xis genes, under the control of the gogR promoter. The ability of GtgR to trans -activate this promoter therefore implies that GtgR and GogR normally activate the transcription of their own genes. Consistent with the symmetry of the system, a similar deletion in Gifsy-2 results in a Gifsy-1-dependent sbc phenotype ( sbcF24 ). Two additional Gifsy-1 deletions ( sbcE23 and sbcE25 ) were characterized, as well. The latter causes all but the last codon of the gogR gene to fuse, in frame, to the second half of recE . The resulting hybrid protein appears to function as both a transcriptional regulator and a recombination enzyme.