Bacteriophage T4 Alc protein: a transcription termination factor sensing local modification of DNA

Cell. 1993 Oct 8;75(1):147-54.


Bacteriophage T4 Alc protein participates in shutting off host transcription after infection of E. coli. It is demonstrated that Alc acts as a site-specific termination factor. The Alc sites occur frequently in E. coli DNA, resulting in early cessation of elongation in several tested transcription units. Alc-dependent termination requires unimpeded propagation of the elongating complex as it approaches the Alc site. Temporary halting of RNA polymerase within 10-15 bp before the Alc site prevents termination. Bacteriophage T4 transcription is protected from the action of Alc by overall substitution of cytosine with 5-hydroxymethyl cytosine in T4 DNA. In vitro methylation of CpG sequences in the vicinity of an Alc site abolishes the effect of Alc. Thus, Alc-dependent termination involves local sensing of the state of cytosine modification and a short-term "memory" of recent pausing.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Bacteriophage T4 / genetics
  • Bacteriophage T4 / metabolism*
  • Base Sequence
  • DNA, Viral / metabolism*
  • DNA-Directed RNA Polymerases / metabolism*
  • Dinucleoside Phosphates / metabolism
  • Escherichia coli / genetics
  • Escherichia coli / metabolism*
  • Methylation
  • Molecular Sequence Data
  • Oligodeoxyribonucleotides
  • Substrate Specificity
  • Templates, Genetic
  • Terminator Regions, Genetic*
  • Transcription Factors / metabolism*
  • Transcription, Genetic*
  • Viral Proteins / metabolism*


  • Alc protein, Enterobacteria phage T4
  • DNA, Viral
  • Dinucleoside Phosphates
  • Oligodeoxyribonucleotides
  • Transcription Factors
  • Viral Proteins
  • cytidylyl-3'-5'-guanosine
  • DNA-Directed RNA Polymerases