The roles of the bacteriophage T4 r genes in lysis inhibition and fine-structure genetics: a new perspective.


Journal Article

Seldom has the study of a set of genes contributed more to our understanding of molecular genetics than has the characterization of the rapid-lysis genes of bacteriophage T4. For example, T4 rII mutants were used to define gene structure and mutagen effects at the molecular level and to help unravel the genetic code. The large-plaque morphology of these mutants reflects a block in expressing lysis inhibition (LIN), the ability to delay lysis for several hours in response to sensing external related phages attacking the cell, which is a unique and highly adaptive attribute of the T4 family of phages. However, surprisingly little is known about the mechanism of LIN, or how the various r genes affect its expression. Here, we review the extensive old literature about the r genes and the lysis process and try to sort out the major players affecting lysis inhibition. We confirm that superinfection can induce lysis inhibition even while infected cells are lysing, suggesting that the signal response is virtually instantaneous and thus probably the result of post-translational regulation. We identify the rI gene as ORF tk.-2, based on sequence analysis of canonical rI mutants. The rI gene encodes a peptide of 97 amino acids (Mr = 11.1 kD; pI = 4.8) that probably is secreted into the periplasmic space. This gene is widely conserved among T-even phage. We then present a model for LIN, postulating that rI is largely responsible for regulating the gpt holin protein in response to superinfection. The evidence suggests that the rIIA and B genes are not directly involved in lysis inhibition; rather, when they are absent, an alternate pathway for lysis develops which depends on the presence of genes from any of several possible prophages and is not sensitive to lysis inhibition.

Full Text

Duke Authors

Cited Authors

  • Paddison, P; Abedon, ST; Dressman, HK; Gailbreath, K; Tracy, J; Mosser, E; Neitzel, J; Guttman, B; Kutter, E

Published Date

  • April 1998

Published In

Volume / Issue

  • 148 / 4

Start / End Page

  • 1539 - 1550

PubMed ID

  • 9560373

Pubmed Central ID

  • 9560373

International Standard Serial Number (ISSN)

  • 0016-6731


  • eng

Conference Location

  • United States