C. GP40 plays a direct role in shutoff of both host DNA and RNA synthesis, and gp38 and gp39 regulate the timing of both shutoffs.

Mutational analysis showed that gp40 was required for normal shutoff of host DNA, RNA, and protein synthesis. Shutoff of host DNA synthesis was accelerated by the 39- mutation, and that effect was suppressed by the 40- mutation. Shutoff of host RNA synthesis was accelerated by the 38-39- double mutant (but usually not by the 38- or 39- single mutants), and that effect too was suppressed by the 40- mutation. Thus, gp40 is required for normal shutoff of host DNA and RNA synthesis, gp38 and gp39 regulate the timing of both shutoffs, and gp40 is also required for the accelerated shutoffs that occur in the absence of gp38 and/or gp39 (11). Since the shutoffs of both host DNA and RNA synthesis occur with roughly similar timing early in infection, and since the 39- mutation and the 44-50-51- triple mutation each affect the two shutoffs differently, it is unlikely that either shutoff is an indirect result of the other. Thus, gp40 probably participates directly in the shutoff of both host DNA and RNA synthesis.

A. General Introduction to bacteriophage SPO1.

B. GP44, gp50, and gp51 regulate the shutoff of host biosyntheses indirectly, by regulating expression of the genes of the host-takeover module.

C. GP40 plays a direct role in shutoff of both host DNA and RNA synthesis, and gp38 and gp39 regulate both shutoffs, by direct participation in the shutoff processes.

D. GP56 (possibly assisted by gp57 and gp58) inhibits host cell division.

E. GP55-53 may inhibit host protein synthesis.

F. Antibiotic Activities of SPO1 Proteins.

References