A [phi]80 function inhibitory for growth of lambdoid phage in him mutants of Escherichia coli. Deficient in integration host factor II. Physiological analysis of the abortive infection

Abstract

Derivatives of phage [lambda] with the rightmost 3% of the genome (the QSR region) from the related phage [phi]80 fail to grow at low temperatures (e.g., 32[deg]) in Escherichia coli. hosts deficient in either protein component of IHF (integration host factor), the products of the himA and hip/himD genes. The abortive infection of [lambda](QSR)80 in mutants defective for IHF was studied in detail. This infection is characterized by a lack of cell lysis and an inhibition of phage DNA replication after an initial period of normal synthesis. An inhibition of host DNA replication also occurs after a similar period of apparently normal synthesis, and the abortive [lambda](QSR)80 infection is lethal to the host. An assay of [beta]-galactosidase activity in [lambda](QSR)80-infected cells provided indirect evidence that RNA and protein synthesis continue late into the abortive infection. The defective growth is imposed by the product of the rha gene located in the (QSR)80 genetic material. Two-dimensional electrophoretic analysis of phage proteins produced in ultraviolet (uv)-irradiated phage-infected host cells has demonstrated the existence of a protein that is encoded or whose synthesis is regulated by the rha locus. Based on these findings, possible roles for a HimA-Hip/HimD-controlled rha gene product in a late stage of [phi]80 development are discussed.