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  • The EMBO Journal (2006) 25, 377 - 386
  • doi:10.1038/sj.emboj.7600935

Published online: 5 January 2006

Cytokinesis signals truncation of the PodJ polarity factor by a cell cycle-regulated protease

Joseph C Chen1, Alison K Hottes1,2, Harley H McAdams1, Patrick T McGrath1,3, Patrick H Viollier4 and Lucy Shapiro1

  1. Department of Developmental Biology, Stanford University, Stanford, CA, USA
  2. Department of Electrical Engineering, Stanford University, Stanford, CA, USA
  3. Department of Physics, Stanford University, Stanford, CA, USA
  4. Department of Molecular Biology and Microbiology, Case Western Reserve University, Cleveland, OH, USA

Correspondence to:

Lucy Shapiro, Department of Developmental Biology, Stanford University, Beckman Center B300, Stanford, CA 94305, USA. Tel.: +1 650 725 7678; Fax: +1 650 725 7739; E-mail: shapiro@stanford.edu

Received 25 August 2005; Accepted 2 December 2005

We demonstrate that successive cleavage events involving regulated intramembrane proteolysis (Rip) occur as a function of time during the Caulobacter cell cycle. The proteolytic substrate PodJL is a polar factor that recruits proteins required for polar organelle biogenesis to the correct cell pole at a defined time in the cell cycle. We have identified a periplasmic protease (PerP) that initiates the proteolytic sequence by truncating PodJL to a form with altered activity (PodJS). Expression of perP is regulated by a signal transduction system that activates cell type-specific transcription programs and conversion of PodJL to PodJS in response to the completion of cytokinesis. PodJS, sequestered to the progeny swarmer cell, is subsequently released from the polar membrane by the membrane metalloprotease MmpA for degradation during the swarmer-to-stalked cell transition. This sequence of proteolytic events contributes to the asymmetric localization of PodJ isoforms to the appropriate cell pole. Thus, temporal activation of the PerP protease and spatial restriction of the polar PodJL substrate cooperatively control the cell cycle-dependent onset of Rip.

  • Keywords:

    • cell division,
    • differentiation,
    • microarray analysis,
    • pilus,
    • proteolysis