Expression of the unassembled capsid protein during infection of Shigella sonnei by bacteriophage T7 results in DNA damage that is repairable by bacteriophage T3, but not T7, DNA ligase.
The abortive infection of bacteriophage T7 in Shigella sonnei D2 371-48 is characterized by a premature inhibition of phage DNA replication and nucleolytic breakdown of all phage DNA. Mutations in T7 gene 10 which are recessive to the presence of the wild-type allele can alleviate the restriction of phage growth. Phage T3 productively infects S. sonnei D2 371-48, as does a T7-T3 hybrid phage that contains, in particular, a gene 10 of T7 origin. It is the presence of T3 DNA ligase that allows phage growth on S. sonnei D2 371-48, and this enzyme can also rescue wild-type T7 from the abortive infection. T7+ is therefore functionally ligase deficient during the infection of S. sonnei D2 371-48; this deficiency is a result of the expression of the phage capsid protein, but it is independent of the assembly of the protein into a procapsid or other morphogenetic structure.
D002213:Capsid / Q000096:biosynthesis*; D011088:DNA Ligases / Q000378:metabolism*; D004279:DNA, Viral / Q000096:biosynthesis / Q000378:metabolism*; D011118:Polynucleotide Ligases / Q000378:metabolism*; D012764:Shigella sonnei; D013604:T-Phages / Q000201:enzymology / Q000254:growth & development / Q000378:metabolism*
D004279:DNA, Viral; D011088:DNA Ligases; D011118:Polynucleotide Ligases