Roles of genes 38, 39, and 40 in shutoff of host biosyntheses during infection of Bacillus subtilis by bacteriophage SPO1.
A nonsense mutation in SPO1 gene 40 prevented normal shutoff of both host DNA and host RNA synthesis, showing that gp40 is required for the normal occurrence of both shutoffs. A gene 39 nonsense mutation caused accelerated shutoff of both host DNA and host RNA synthesis (aided by a gene 38 nonsense mutation), showing that gp39 (aided by gp38) limits the rate at which both shutoffs occur. The 40(-) mutation suppressed the accelerative effects of the 39(-) and 38(-) mutations, showing that gp40 also plays an essential role in the accelerated shutoffs. To the best of our knowledge, proteins with the particular activities implied for gp39 and gp40 have not been identified in any other bacteriophage. SPO1 has at least three different mechanisms that have the effect of delaying the shutoff of host DNA and RNA synthesis.
Stewart
Charles R
CR
Department of Biochemistry and Cell Biology, Rice University, Houston, TX 77251, USA. crs@rice.edu
Yip
Tameson K S
TK
Myles
Bati
B
Laughlin
Laura
L
D017103:Bacillus Phages / Q000235:genetics / Q000378:metabolism / Q000502:physiology*; D001412:Bacillus subtilis / Q000378:metabolism / Q000821:virology*; D018389:Codon, Nonsense; D004269:DNA, Bacterial / Q000096:biosynthesis; D015964:Gene Expression Regulation, Bacterial; D016297:Mutagenesis, Site-Directed; D012367:RNA, Viral / Q000096:biosynthesis; D014764:Viral Proteins / Q000235:genetics*; D014779:Virus Replication
D018389:Codon, Nonsense; D004269:DNA, Bacterial; D012367:RNA, Viral; D014764:Viral Proteins