RhoD participates in the regulation of cell-cycle progression and centrosome duplication

Research output: Contribution to journalArticlepeer-review

Authors

  • A. Kyrkou
  • M. Soufi
  • R. Bahtz
  • C. Ferguson
  • M. Bai
  • R. G. Parton
  • I. Hoffmann
  • M. Zerial
  • T. Fotsis

Colleges, School and Institutes

Abstract

We have previously identified a Rho protein, RhoD, which localizes to the plasma membrane and the early endocytic compartment. Here, we show that a GTPase-deficient mutant of RhoD, RhoDG26V, causes hyperplasia and perturbed differentiation of the epidermis, when targeted to the skin of transgenic mice. In vitro, gain-of-function and loss-of-function approaches revealed that RhoD is involved in the regulation of G1/S-phase progression and causes overduplication of centrosomes. Centriole overduplication assays in aphidicolin-arrested p53-deficient U2OS cells, in which the cell and the centrosome cycles are uncoupled, revealed that the effects of RhoD and its mutants on centrosome duplication and cell cycle are independent. Enhancement of G1/S-phase progression was mediated via Diaph1, a novel effector of RhoD, which we have identified using a two-hybrid screen. These results indicate that RhoD participates in the regulation of cell-cycle progression and centrosome duplication.Oncogene advance online publication, 4 June 2012; doi:10.1038/onc.2012.195.

Details

Original languageEnglish
Pages (from-to)1831-1842
JournalOncogene
Volume32
Early online date4 Jun 2012
Publication statusPublished - 2013