The Arabidopsis PILZ group genes encode tubulin-folding cofactor orthologs required for cell division but not cell growth

  1. Katharina Steinborn1,7,
  2. Christoph Maulbetsch1,7,
  3. Bianca Priester1,
  4. Susanne Trautmann1,6,
  5. Tobias Pacher1,
  6. Bernd Geiges1,5,
  7. Frank Küttner1,
  8. Loic Lepiniec2,
  9. York-Dieter Stierhof3,
  10. Heinz Schwarz4,
  11. Gerd Jürgens1, and
  12. Ulrike Mayer1,8
  1. 1ZMBP, Entwicklungsgenetik, Universität Tübingen, D-72076 Tübingen, Germany; 2Laboratoire de Biologie des Semences, INRA, Versailles, France; 3ZMBP, Mikroskopie, Universität Tübingen, D-72076 Tübingen, Germany; 4Max-Plank-Institut für Entwicklungsbiologie, D-72076 Tübingen, Germany

Abstract

Plant microtubules are organized into specific cell cycle-dependent arrays that have been implicated in diverse cellular processes, including cell division and organized cell expansion. Mutations in fourArabidopsis genes collectively called the PILZ group result in lethal embryos that consist of one or a few grossly enlarged cells. The mutant embryos lack microtubules but not actin filaments. Whereas the cytokinesis-specific syntaxin KNOLLE is not localized properly, trafficking of the putative auxin efflux carrier PIN1 to the plasma membrane is normal. The four PILZ group genes were isolated by map-based cloning and are shown to encode orthologs of mammalian tubulin-folding cofactors (TFCs) C, D, and E, and associated small G-protein Arl2 that mediate the formation of α/β-tubulin heterodimers in vitro. The TFC C ortholog, PORCINO, was detected in cytosolic protein complexes and did not colocalize with microtubules. Another gene with a related, although weaker, embryo-lethal phenotype,KIESEL, was shown to encode a TFC A ortholog. Our genetic ablation of microtubules shows their requirement in cell division and vesicle trafficking during cytokinesis, whereas cell growth is mediated by microtubule-independent vesicle trafficking to the plasma membrane during interphase.

Keywords

Footnotes

  • Present addresses: 5Biologie III, Universität Freiburg, D-79104 Freiburg, Germany; 6Department of Molecular Genetics and Microbiology, University of Massachusetts Medical School, Worcester, MA 01605, USA.

  • 7 These authors contributed equally to this work.

  • 8 Corresponding author.

  • E-MAIL ulrike.mayer{at}zmbp.uni-tuebingen.de; FAX 49-7071-295797.

  • Article and publication are at http://www.genesdev.org/cgi/doi/10.1101/gad.221702.

    • Received November 30, 2001.
    • Accepted February 15, 2002.
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