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Open Access Research article

Studies on Escherichia coli HflKC suggest the presence of an unidentified λ factor that influences the lysis-lysogeny switch

Kaustav Bandyopadhyay1, Pabitra K Parua12, Ajit B Datta13 and Pradeep Parrack1*

Author Affiliations

1 Department of Biochemistry, Bose Institute, P 1/12, C.I.T. Scheme VIIM, Kolkata 700 054, India

2 Department of Biochemistry, University of Washington, 1705 NE Pacific St. HSB J-405, Box 357350 Seattle, WA 98195-7350, USA

3 Department of Biophysics & Biophysical Chemistry and Howard Hughes Medical Institute, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA

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BMC Microbiology 2011, 11:34  doi:10.1186/1471-2180-11-34

Published: 17 February 2011



The lysis-lysogeny decision in the temperate coliphage λ is influenced by a number of phage proteins (CII and CIII) as well as host factors, viz. Escherichia coli HflB, HflKC and HflD. Prominent among these are the transcription factor CII and HflB, an ATP-dependent protease that degrades CII. Stabilization of CII promotes lysogeny, while its destabilization induces the lytic mode of development. All other factors that influence the lytic/lysogenic decision are known to act by their effects on the stability of CII. Deletion of hflKC has no effect on the stability of CII. However, when λ infects ΔhflKC cells, turbid plaques are produced, indicating stabilization of CII under these conditions.


We find that CII is stabilized in ΔhflKC cells even without infection by λ, if CIII is present. Nevertheless, we also obtained turbid plaques when a ΔhflKC host was infected by a cIII-defective phage (λcIII67). This observation raises a fundamental question: does lysogeny necessarily correlate with the stabilization of CII? Our experiments indicate that CII is indeed stabilized under these conditions, implying that stabilization of CII is possible in ΔhflKC cells even in the absence of CIII, leading to lysogeny.


We propose that a yet unidentified CII-stabilizing factor in λ may influence the lysis-lysogeny decision in ΔhflKC cells.