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  • The EMBO Journal (2001) 20, 2171 - 2179
  • doi:10.1093/emboj/20.9.2171

cdc42 regulates the exit of apical and basolateral proteins from the trans-Golgi network

Anne Müsch2, David Cohen1, Geri Kreitzer1 and Enrique Rodriguez-Boulan3

  1. Dyson Institute of Vision Research, Joan and Sanford Weill Medical College of Cornell University, New York, NY 10021, USA
  2. Department of Biochemistry Joan and Sanford Weill Medical College of Cornell University, New York, NY 10021, USA
  3. Department of Cell Biology, Joan and Sanford Weill Medical College of Cornell University, New York, NY 10021, USA

Correspondence to:

Anne Müsch, E-mail: amuesch@mail.med.cornell.edu

Enrique Rodriguez-Boulan, E-mail: boulan@mail.med.cornell.edu

Received 11 December 2000; Accepted 14 March 2001; Revised 9 March 2001

It is well established that Rho-GTPases regulate vesicle fusion and fission events at the plasma membrane through their modulatory role on the cortical actin cytoskeleton. In contrast, their effects on intracellular transport processes and actin pools are less clear. It was recently shown that cdc42 associates with the Golgi apparatus in an ARF-dependent manner, similarly to coat proteins involved in vesicle formation and to several actin-binding proteins. We report here that mutants of cdc42 inhibited the exit of basolateral proteins from the trans-Golgi network (TGN), while stimulating the exit of an apical marker, in two different transport assays. This regulation may result from modulation of the actin cytoskeleton, as GTPase-deficient cdc42 depleted a perinuclear actin pool that rapidly exchanges with exogenous fluorescent actin.

  • Keywords:

    • cdc42,
    • Golgi,
    • protein transport