| pubmed-article:2936651 | pubmed:abstractText | The lysis gene, E, of bacteriophage phi X174 has been subjected to deletion and gene fusion analysis. C-terminal deletions of as few as 17 of the 91 codons inactivate the cloned E gene, which in its intact form can cause lysis of the host cell. Fusion of lacZ to deletion joints at the 59th codon or beyond apparently restores lethal and lytic competence to the respective E deletion alleles, whereas a fusion at the 23rd codon remains non-lethal. The lethal E phi lacZ fusions are also lethal to a mutant, designated slyD, which was isolated as a spontaneous E. coli mutant resistant to the expression of the intact E gene. slyD appears to be linked to rpsE. The data are interpreted in terms of a model in which E-mediated lethality requires oligomerization of the E gene product. Calculations based on the beta-galactosidase activity accumulated by the time of lethal action of E phi lacZ suggest that fewer than 1000 molecules of E gene product are required for lysis and probably fewer than 100 are required for loss of host viability. | lld:pubmed |
