Increased Excision of the Salmonella Prophage ST64B Caused by a Deficiency in Dam Methylase

摘要: Salmonella enterica mutants defective in Dam methylase are strongly attenuated virulence and release a large amount of proteins to the extracellular medium. The extent which these two phenotypes linked is unknown. Using proteomic approach, we identified Sb6, Sb13, Sb36 as present larger amounts culture supernatants an S. serovar Typhimurium dam mutant than those wild-type strain. These three encoded prophage ST64B. Higher ST64B phage DNA tailless viral capsids were also detected supernatant extracts mutant, suggesting that methylation negatively regulates excision Reverse transcription-PCR analysis revealed expression genes encoding putative antirepressor replication protein increases mutant. SOS response augments Infection assays performed with phage-cured strains demonstrated does not carry required for mouse model. Evidence was obtained discarding relationship between high envelope instability or attenuation phenotype. Taken together, data indicate excises at rate due loss repression exerted by on induction characteristic mutants. exacerbated however contribute incapacity cause disease.