The genomic RNA of mengovirus: I. Location of the poly(C) tract

Strains of λ phage containing a mutated cII, cIII, or cy gene in addition to a cro^? mutation were constructed. Each single mutant and the double mutants were analyzed for growth behavior and for expression of specific early and late λ proteins. λc1857cro 16 is unable to grow well at 30° and at 43°. This strain is incapable of turning off early genes (of the b region, of the P_L and P_R operons, and the cU and int genes) and is defective in the expression of late functions. The clear mutations permit phage growth at 30°. They relieve the inhibitory effect conferred by the cro^? mutation on phage growth at 43° to different extents. Our results also indicate that the cII and cIII proteins do not necessarily act at y in the regulation of late functions.     

Superinfection exclusion by λ prophage in lysogens ofSalmonella typhimurium

Lysogens of coliphage λ inSalmonella typhimurium excludeSalmonella phages P22 and L. The λrex function is responsible for exclusion of superinfecting P22, since P22 is not excluded by lysogens of λrex^? mutants. However, λrex^? lysogens still exclude phage L, apparently because they retain another superinfection exclusion mechanism which is identical in specificity to the P22sie B exclusion mechanism. Mutants of λ defective in this new exclusion system (sie^? mutants) have been isolated. The phenotypes of λbio deletion/substitution phages indicate that thesie gene maps between thecIII andN genes, at a position on the λ genome analogous to that of thesie B gene on the P22 genome.     

Rex-dependent exclusion of lambdoid phages. I. Prophage requirements for exclusion

Certain λ lysogens are able to inhibit growth of superinfecting φ80 and λ-P22 hybrid phages with the OPQ region from P22. Superinfection exclusion requires expression of the prophage rex gene and is most evident in λ lysogens in which the prophage carries a mutation (either is or am) in the cI gene. These lysogens also inhibit growth of leaky rII^? mutants of T4 which are able to grow in λ⁺ lysogens. Rex-dependent exclusion of lambdoid phages is not strictly a superinfection exclusion system, as thermal induction of a λrex⁺clts85(OP)-P22 prophage results in “self-exclusion,” that is, in low phage production. These observations are explained by proposing that Rex activity of a λcits lysogen (and other lysogens which produce a modified repressor) is greater than in lysogens carrying a prophage with a wild-type cI gene. The effects of thermal induction and mitomycin C induction on Rex activity are described, and explanations for increased Rex activity in lysogens carrying a prophage with an altered repressor are discussed.     

Cro mutants of phage 434.

Phage 434 cro⁴³⁴ mutants have been isolated and characterized as plaque formers on groN bacteria, which block wild-type 434 and λ development at the level of action of the N gene product (Georgopoulos, 1971). Like the corresponding λ cro^λ mutants, they map within the immunity region and to the right of the cI gene, they overproduce the exonuclease gene product, they are unable to propagate on wild-type bacteria (especially at 42°), and in mixed infections they suppress the growth of heteroimmune but not homoimmune cro⁺ phage.     

Growth of lambda rev in phage P2 lysogenic hosts

Bacteriophage λ rev, a transducing, plaque-forming derivative of λ, carries the Escherichia coli recE(sbcA) region. Though λ rev expresses some of its bacterial genes from a λ promoter under cI control, this expression does not require the λ N antitermination function. Phage λ rev differs from λ in being able to propagate in phage P2 lysogens (Spi^? phenptype). Two λ rev Spi⁺ mutants were shown to be defective in general recombination, which suggests that recE allows λ rev to grow in P2 lysogens. Additional biochemical and genetic evidence suggest the evidence of a λ gam function analog in λ rev, which in the absence of recE function, antagonizes λ rev growth in P2 lysogens.     

The essential role of the cro gene in lytic development by bacteriophage λ

In an effort to understand the physiological role of the Cro repressor protein of bacteriophage λ we have studied the influence of cro^? mutation on lytic and lysogenic development. Effective lytic growth is blocked by cro^? mutation under conditions in which the cI repressor protein is fully active or in which active cI protein is not made; however, a partially active cI protein can substitute for Cro. The blocked lytic development under cro^?cI^? conditions is characterized by a severe inhibition of λ DNA synthesis, and the newly replicated DNA has an aberrant structure. Under cro^?cI⁺ conditions, we have studied the frequency of lysogenization to determine whether the failure of lytic development in this situation results from a complete channeling into the lysogenic pathway. However, the major alteration in the lysogenization pattern for cro^? phage is the appearance of a large fraction of surviving, nonlysogenic cells; we interpret this as a failure of normal lytic growth without a concomitant switch to stable lysogeny. From these results and from previous work on Cro function, we conclude that the repression exerted by Cro is essential for normal lytic development, that Cro probably functions as a “weak” repressor compared to cI, and that at least one of the essential regulatory activities of Cro concerns viral DNA replication.     

Factors determining the susceptibility of NIH swiss mice to erythroleukemia induced by Friend murine leukemia virus

The phage φ80, an Escherichia coli temperate phage, has similarities in sequence and physiology with bacteriophage λ. The isolation of new λ derivatives which carry recombination genes of φ80 (red₈₀ genes) under the control of the λ immunity region is described. Study of these hybrids suggests that the recombination system of φ80 is analogous to the recE system of Escherichia coli. Expression of φ80 recombination in lysogens corrects, like recE, the recombination defect presented by recB^? mutants. The φ80 recombination system also promotes phage recombination in recA hosts, which is also a characteristic of the recE system. The study of recombination defective red₈₀ phages suggests that the φ80 recombination system also determines φ80 growth on P2 lysogens.