Bacteriophage P22 lysogenises efficiently at high multiplicities of infection because Salmonella typhimurium DNA synthetic capacity is limited

Abstract

INFECTIONS of Salmonella typhimurium by wild-type phage P22 generally result in a lytic response at low multiplicities of infection (MOIs) and a lysogenic response at high MOIs¹. At MOIs above 5, more than 90% of all cells are lyso-genised. At an MOI of 3, 45% of the infected cells become lysogens whereas at an MOI of 1, only 23% of the infected cells are lysogenised. The regulation of P22 lysogeny has been studied extensively^1–7. Three structural genes and a cis-active site in the immunity C (immC) region are required to establish lysogeny. Interaction of gene c1 and c3 products at the c27 site stimulates the production of the c2 represser, and at the same time causes a transient retardation in the expression of lytic genes^1,8. A mutant of S. typhimurium, Pox-1, that channels P22 infections at any MOI to lysogeny with an efficiency of 1.0 has a reduced capacity for both host and viral DNA synthesis⁶. Slowed synthesis of DNA in this mutant results in an overproduction of regulatory proteins relative to the levels of viral DNA in infected cells. This, in turn, results in lysogeny at all MOIs. We now propose that the initial decision between lysis and lysogeny in wild-type cells is also a function of the relative amounts of phage DNA and the phage proteins from the immC region.