Late effect of bacteriophage T4D on the permeability barrier of Escherichia coli.
Cold centrifugation of lysis-inhibited Escherichia coli B infected with wild-type T4D results in extensive lysis beginning around 20 min after infection at 37 degrees C. Infection with an e mutant, which fails to make lysozyme, prevents lysis, but does not prevent a marked loss of K+ and Mg3+. The t gene product, thought to disrupt the cytoplasmic membrane in natural lysis, is not required for this handling-induced cation loss or lysis. Three lines of evidence argue that late protein synthesis is required to develop this potential for cation loss; the potential does not develop in infections by: (i) mutants defective in DNA synthesis, (ii) mutants defective in gene 55, and (iii) wild-type T4 when chloramphenicol is added at 6 min after infection. All late mutants examined, which are blocked in the major pathways of morphogenesis, do not prevent development of the potential. The evidence argues for a new, late effect of T4 infection on the cytoplasmic membrane.
D002463:Cell Membrane Permeability; D003080:Cold Temperature; D003090:Coliphages / Q000235:genetics / Q000254:growth & development*; D004926:Escherichia coli / Q000378:metabolism*; D008242:Lysogeny; D008274:Magnesium / Q000378:metabolism; D009113:Muramidase / Q000235:genetics; D009154:Mutation; D011188:Potassium / Q000378:metabolism; D014764:Viral Proteins / Q000235:genetics; D014779:Virus Replication
D014764:Viral Proteins; D009113:Muramidase; D008274:Magnesium; D011188:Potassium