Abstract

Abstract When gene 2 amber mutants of T4 infect su − cells, whole particles are produced (2.Su − ) which appear normal in electron micrographs. 2.Su − particles plate less than 0.5% as efficiently as wild type phage on su + hosts. These particles adsorb, contract, and kill their host normally. Up to 40% of 2.Su − DNA is rapidly degraded to acid-soluble fragments after infection of Escherichia coli B, E. coli CR63 rgl − and E. coli B 40 SuI. 2.Su − particles provide gene products for in vivo complementation only 10–20% as efficiently as 2.Su + phage. 2.Su − DNA is glucosylated and unnicked inside the phage head. Morphogenesis of 2.Su − progeny is delayed and the burst of 2.Su − phage is decreased compared to wild-type infections. Thus, the absence of gene 2 product during phage synthesis affects both morphogenesis and particle infectivity. 2.Su − particles are defective at an early stage of infection, probably after DNA ejection and before gene expression.

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