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P2 Growth Restriction on an rpoC Mutant Is Suppressed by Alleles of the Rz1 Homolog lysC

Dmitry Markov,¹ Gail E. Christie,² Brian Sauer,^3, Richard Calendar,³ Taehyun Park,⁴ Ry Young,⁴ and Konstantin Severinov^1*

Waksman Institute and Department of Molecular Biology and Biochemistry, State University of New Jersey, Rutgers, Piscataway, New Jersey 08854,¹ Department of Microbiology and Immunology, Virginia Commonwealth University, Richmond, Virginia 23298,² Department of Molecular and Cell Biology, University of California, Berkeley, California 94720,³ Department of Biochemistry and Biophysics, Texas A&M University, College Station, Texas 77843-2128⁴

Received 16 February 2004/ Accepted 14 April 2004

Escherichia coli strain 397c carries a temperature-sensitive mutation, rpoC397, that removes the last 50 amino acids of the RNA polymerase ß' subunit and is nonpermissive for plating of bacteriophage P2. P2 gor mutants productively infect 397c and define a new gene, lysC, encoded by a reading frame that extensively overlaps the P2 lysis accessory gene, lysB. The unusual location of lysC with respect to lysB is reminiscent of the Rz/Rz1 lysis gene pair of phage . Indeed, coexpression of lysB and lysC complemented the growth defect of Rz/Rz1 null mutants, indicating that the LysB/C pair is similar to Rz/Rz1 in both gene arrangement and function. Cells carrying the rpoC397 mutation exhibited an early onset of P2-induced lysis, which was suppressed by the gor mutation in lysC. We propose that changes in host gene expression resulting from the rpoC397 mutation result in changes in the composition of the bacterial cell wall, making the cell more susceptible to P2-mediated lysis and preventing accumulation of progeny phage sufficient for plaque formation.

Present address: Stowers Institute for Medical Research, Kansas City, MO 64110.

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