Mutations of bacteriophage P2 which prevent activation of P2 late genes by satellite phage P4

Abstract

Satellite phage P4 multiplies only in the presence of its helper P2 and requires each morphogenesis function of P2 for phage maturation. The helper phage P2 can be present either as prophage or as a co-infecting phage. We have isolated mutant P2 lysogens unable to support P4 growth. These carry mutations lying in the region of P2 early genes. Measurement of P2 lysozyme synthesis indicates that in these mutants, P2 late genes are activated inefficiently during P4 infection. Complementation tests show that the P4 stimulation function, which is absent in the defective lysogens, can be provided in trans by another prophage. This function cannot be assigned to either of the two known early genes of P2 which are required for late gene transcription during P2 vegetative growth; P4 multiplies normally when both P2 early genes A and B are inactivated by amber mutations. A dominant mutation of P2 has been isolated which makes repressed P2 incapable of supporting P4 multiplication. The mutation prevents derepression of the P2 prophage and may alter the P2 repressor. We propose that two different pathways exist for activation of P2 late genes: (1) a pathway dependent on P2 replication and (2) a pathway activated by satellite P4. One component of the P4-dependent pathway is a diffusible P2 early gene function under the control of P2 repressor. This function acts to stimulate the P2 late gene transcription in the P4-dependent pathway.