Physiological studies on the t gene defect in T4-infected Escherichia coli.
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Escherichia coli cells carrying lambda cI857 prophage lyse 40 min after lambda thermoinduction; the lysis depends on the lambda genes Q, R, and S. If chloramphenicol (CAP) is added within 20 min after lambda cI857 induction, an early, unproductive lysis occurs. This lysis is independent of the genes int, rex, O, P, Q, and all late genes. Instead, early lysis depends upon the kil gene. The early lysis is under the positive control of lambda gene N and the negative control of gene cro. One or more events specifically connected with lambda induction appear to be necessary for the occurrence of early lysis, since early lysis cannot be observed after lambda infection. Induced lambda kil+ lysogens are more sensitive to osmotic shock than induced lambda kil- lysogens. CAP-induced early lysis can be prevented in a hypertonic medium. These results suggest that induction of lambda causes an osmotic fragility due to a damage of the cell envelope which requires repair; in the absence of protein synthesis the cell envelope is not repaired and cell lysis ensues.
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 degrees) 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 product in a late stage of phi 80 development are discussed.