Article

  • The EMBO Journal (2005) 24, 54 - 62
  • doi:10.1038/sj.emboj.7600497

Published online: 9 December 2004

RalA interacts with ZONAB in a cell density-dependent manner and regulates its transcriptional activity

Paul Frankel1, Ami Aronheim2, Emma Kavanagh3, Maria S Balda3, Karl Matter3, Tom D Bunney4 and Christopher J Marshall1

  1. Oncogene Team, Cancer Research UK Centre for Cell and Molecular Biology, Chester Beatty Laboratories, Institute of Cancer Research, London, UK
  2. Department of Molecular Genetics, the B Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, Haifa, Israel
  3. Division of Cell Biology, Institute of Ophthalmology, University College London, London, UK
  4. Lipid Signalling Team, Cancer Research UK Centre for Cell and Molecular Biology, Chester Beatty Laboratories, Institute of Cancer Research, London, UK

Correspondence to:

Christopher J Marshall, Cancer Research UK Centre for Cell and Molecular Biology, Chester Beatty Laboratories, Institute of Cancer Research, 237 Fulham Road, London SW3 6JB, UK. Tel.: +44 207 352 9772; Fax: +44 207 352 5630; E-mail: chris.marshall@icr.ac.uk

Received 23 June 2004; Accepted 5 November 2004


Ral proteins are members of the Ras superfamily of small GTPases and are involved in signalling pathways for actin cytoskeleton remodelling, cell cycle control, cellular transformation and vesicle transport. To identify novel RalA effector proteins, we used the reverse Ras recruitment system and found that RalA interacts with a Y-box transcription factor, ZO-1-associated nucleic acid-binding protein (ZONAB), in a GTP-dependent manner. The amount of the RalA–ZONAB complex increases as epithelial cells become more dense and increase cell contacts. The RalA–ZONAB interaction results in a relief of transcriptional repression of a ZONAB-regulated promoter. Additionally, expression of oncogenic Ras alleviates transcriptional repression by ZONAB in a RalA-dependent manner. The data presented here implicate the RalA/ZONAB interaction in the regulation of ZONAB function.

  • Keywords:

    • cell–cell contact,
    • RalA,
    • signal transduction,
    • transcription,
    • ZONAB
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