Regulation of bacteriophage λ int gene expression

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Abstract

The int gene of bacteriophage lambda can be transcribed from pI in the presence of cII product or from pL in the presence of N product. On infection Int is expressed only from pI, while in an induced prophage Int can be expressed from pL. The critical difference is the b+ region, which is adjacent to int in an infecting phage, but is separate in a prophage. When a prophage is constructed in which b+ is adjacent to int, the synthesis of Int under pL control is strongly inhibited.

We have constructed lacZ-pI and lacZ-pL fusions, where the fusion is 252 basepairs to the left of the attP site, within the b region. These fusions permit us to analyze the effects of various mutations on the ability of cII to activate pI and on the expression of the int gene. We find that the expression of lacZ from pL takes place in the b53 deletion (−252 base-pairs to −160 base-pairs) but not in wild-type phage. The b53 deletion thus removes the tI terminator. It also removes the region containing the sib mutations (Guarneros & Galindo, 1979); as expected, it permits the expression of int from pL during infection. The tI terminator is suppressed by N-function acting on transcription from pL, and is active in a rho15 mutant.

The cII-independent pI mutation pintc226 acts as a weak promoter which is not further stimulated by cII. Since intc226 is a G · C to A · T change at −11, this suggests that the interaction between pI and cII product may involve sequences in the Pribnow box region of this promoter.

We have found that pI is not activated in hosts carrying the himA or hip mutations, and we have demonstrated that this is due to the failure of cII product synthesis in these host mutants.

Our results substantiate the general model of retroregulation of Int expression based on a transcript-specific terminator in the b region (Guarneros et al., 1982).

References (45)

  • J. Abraham et al.

    J. Mol. Biol

    (1981)
  • M. Belfort

    Gene

    (1980)
  • F. Bolivar et al.

    Gene

    (1977)
  • K. Bøvre et al.

    Virology

    (1969)
  • S. Chung et al.

    Virology

    (1977)
  • L.W. Enquist et al.

    Methods Enzymol

    (1979)
  • C. Epp et al.

    Gene

    (1981)
  • M.E. Gottesman et al.

    J. Mol. Biol

    (1968)
  • M.E. Gottesman et al.

    J. Mol. Biol

    (1980)
  • S. Gottesman et al.

    J. Mol. Biol

    (1980)
  • G. Guarneros et al.

    Virology

    (1979)
  • A. Honigman

    Gene

    (1981)
  • A.S. Hopkins et al.

    J. Mol. Biol

    (1976)
  • N. Katzir et al.

    Virology

    (1976)
  • H.A. Lozeron et al.

    Virology

    (1976)
  • D. Luzzati

    J. Mol. Biol

    (1970)
  • H.I. Miller

    Cell

    (1981)
  • D.L. Wulff et al.

    J. Mol. Biol

    (1980)
  • J. Abraham et al.
  • F. Blattner et al.

    Science

    (1977)
  • A. Campbell
  • M. Castellazzi et al.

    Mol. Gen. Genet

    (1972)
  • Cited by (0)

    This work was supported in part by the United States Israel Binational Science Foundation.

    Present address: Department of Microbiological Chemustry, Hebrew University, Hadassah Medical School, Jerusalem, Israel.

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