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Cytoplasmic targeting of IpaC to the bacterial pole directs polar type III secretion in Shigella

Valentin Jaumouillé, Olivera Francetic, Philippe J Sansonetti, Guy Tran Van Nhieu

Author Affiliations

  1. Valentin Jaumouillé1,2,
  2. Olivera Francetic3,
  3. Philippe J Sansonetti1,2 and
  4. Guy Tran Van Nhieu*,1,2
  1. 1 Department of Cell Biology and Infections, Unité de Pathogénie Microbienne Moléculaire, Institut Pasteur, Paris, France
  2. 2 Unité 786, Institut National de la Santé et de la Recherche Médicale (Inserm U786), Paris, France
  3. 3 Unité de Génétique Moléculaire, CNRS URA 2172, Institut Pasteur, Paris, France
  1. *Corresponding author. Department of Cell Biology and Infections, Institut Pasteur, 28 rue du Dr. Roux, Paris Cedex 75724, France. Tel.: +33 1 4568 8315; Fax: +33 1 4568 8953; E-mail: gtranvan{at}pasteur.fr
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Abstract

Type III secretion (T3S) systems are largely used by pathogenic Gram‐negative bacteria to inject multiple effectors into eukaryotic cells. Upon cell contact, these bacterial microinjection devices insert two T3S substrates into host cell membranes, forming a so‐called ‘translocon’ that is required for targeting of type III effectors in the cell cytosol. Here, we show that secretion of the translocon component IpaC of invasive Shigella occurs at the level of one bacterial pole during cell invasion. Using IpaC fusions with green fluorescent protein variants (IpaCi), we show that the IpaC cytoplasmic pool localizes at an old or new bacterial pole, where secretion occurs upon T3S activation. Deletions in ipaC identified domains implicated in polar localization. Only polar IpaCi derivatives inhibited T3S, while IpaCi fusions with diffuse cytoplasmic localization had no detectable effect on T3S. Moreover, the deletions that abolished polar localization led to secretion defects when introduced in ipaC. These results indicate that cytoplasmic polar localization directs secretion of IpaC at the pole of Shigella, and may represent a mandatory step for T3S.

  • Received June 29, 2007.
  • Accepted December 4, 2007.
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