Kinematics of Intracellular Chlamydiae Provide Evidence for Contact-Dependent Development

We present experimental evidence to provide support for a contact-dependent hypothesis for explaining the trigger involved in differentiation

David P. Wilson; Judith A. Whittum-Hudson; Peter Timms; Patrik M. Bavoil

2009

Scholarcy highlights

  • Members of the Chlamydiaceae are ubiquitous bacterial pathogens in humans and animals
  • At 16ϩ h postinfection, an unknown signal provokes the onset of reticulate body to elementary body differentiation, whereby individual RBs engage in a cellular condensation process, progressing through a poorly defined intermediate body form and ending with the metabolically inactive but highly infectious EB, thereby
  • We have previously proposed a hypothesis for the development of intracellular chlamydiae based on a combination of electron microscopic and other observations and further developed the hypothesis using biomathematical modeling
  • Tenets of the so-called contact-dependent hypothesis of chlamydial development are the following: as RBs, chlamydiae grow strictly in contact with the plasma membranederived chlamydial inclusion membrane, contact with the CIM is mediated by surface projections hypothesized to correspond to T3S injectisomes, and disruption of T3S activity through physical detachment from the CIM is associated with the onset of late differentiation
  • The implied biological significance of the hypothesis is that maintaining contact with the CIM permits continued delivery of chlamydial T3S effectors into the host cell cytosol and subsequent subversion of cellular processes to benefit chlamydial growth; disruption of contact through physical detachment interrupts T3S effector translocation, rendering the host cell less hospitable for chlamydial growth
  • Because contact of chlamydial particles with the CIM, or loss thereof, has direct implications on the ability of chlamydiae to move inside the inclusion, we sought to quantify the movement of individual chlamydial particles at different times along development
  • An attractive hypothesis emerging from these converging results is that T3S-mediated translocation of early midcycle effector(s) to the infected cell cytosol maintains the host in a state optimized for chlamydial exponential growth and that disruption of this state through interruption of T3S translocation may “alert” chlamydiae within the inclusion to initiate late differentiation and subsequent progress of the infection

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