Abstract
Assembly of the essential, tubulin-like FtsZ protein into a ring-shaped structure at the nascent division site determines the timing and position of cytokinesis in most bacteria and serves as a scaffold for recruitment of the cell division machinery. Here we report that expression of bacteriophage λ kil, either from a resident phage or from a plasmid, induces filamentation of Escherichia coli cells by rapid inhibition of FtsZ ring formation. Mutant alleles of ftsZ resistant to the Kil protein map to the FtsZ polymer subunit interface, stabilize FtsZ ring assembly, and confer increased resistance to endogenous FtsZ inhibitors, consistent with Kil inhibiting FtsZ assembly. Cells with the normally essential cell division gene zipA deleted (in a modified background) display normal FtsZ rings after kil expression, suggesting that ZipA is required for Kil-mediated inhibition of FtsZ rings in vivo. In support of this model, point mutations in the C-terminal FtsZ-interaction domain of ZipA abrogate Kil activity without discernibly altering FtsZ-ZipA interactions. An affinity-tagged-Kil derivative interacts with both FtsZ and ZipA, and inhibits sedimentation of FtsZ filament bundles in vitro. Together, these data inspire a model in which Kil interacts with FtsZ and ZipA in the cell to prevent FtsZ assembly into a coherent, division-competent ring structure. Phage growth assays show that kil+ phage lyse ∼30% later than kil mutant phage, suggesting that Kil delays lysis, perhaps via its interaction with FtsZ and ZipA.
Highlights
The replication and lytic functions of bacteriophage l rapidly diminish Escherichia coli viability and lead to ultimate host death by lysis [1]
Viruses that infect bacteria can kill their host, and some prevent the bacterial cell from reproducing during that process
Our report focuses on E. coli and l, a well-studied phage that infects it. l contains a gene, kil, whose expression prevents E. coli from dividing, causing cells to grow into long filaments that die
Summary
The replication and lytic functions of bacteriophage l rapidly diminish Escherichia coli viability and lead to ultimate host death by lysis [1]. A series of nested deletions beginning at attL and int, and removing successive prophage genes toward PL, initially defined the region of this secondary, lysis-independent killing function [3]. These deletions identified a putative gene located in this region named kil (host killing by an induced l prophage) responsible for host cell filamentation, loss of viability, and ultimate death. Separate experiments inducing expression of the annotated kil open reading frame from a plasmid verified that this region was responsible for causing cell filamentation and a loss of viability [7]
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