Involvement of two genes of superinfecting phage kappa in curing and induction of prophage psi in Serratia marcescens HY.

Prophage psi carried along with prophage y by Serratia marcescens HY is subject of moderate curing at heteroimmune superinfection of cells from stationary phase with phage kappa. Curing becomes considerably more frequent when the bacteria are non-lysogenic for y. Both psi, y-double-lysogenic and psi-single-lysogenic cells with a mutation in the ink gene are very efficiently cured of psi if infected by kappa tay, although this mutant was characterized as being deficient in transactivation of certain genes in prophage y. On the other hand to get efficiently cured after kappa wild-type infection these cells too must be devoid of a y prophage. Thus a y function turned on by tay+ seems to counteract the elimination of psi. However, interestingly enough psi curing is boosted by a further y function under special circumstances. Efficient curing depends on an intact kappa tap gene, a gene reported to cause transactivation of certain psi genes. Curing at kappa tay infection is specifically accompanied by induction of the psi prophage in a part of the infected cells. However, there is no such induction at kappa wild-type infection, either in the absence or presence of a y prophage. An explanation of these findings is suggested which includes an antirepressive effect exerted on psi and a hypothetical interaction between the products of genes tap and tay.