Farnesylated RhoB inhibits radiation-induced mitotic cell death and controls radiation-induced centrosome overduplication

Cell Death Differ. 2005 May;12(5):492-501. doi: 10.1038/sj.cdd.4401586.


Our previous results demonstrated that expressing the GTPase ras homolog gene family, member B (RhoB) in radiosensitive NIH3T3 cells increases their survival following 2 Gy irradiation (SF2). We have first demonstrated here that RhoB expression inhibits radiation-induced mitotic cell death. RhoB is present in both a farnesylated and a geranylgeranylated form in vivo. By expressing RhoB mutants encoding for farnesylated (RhoB-F cells), geranylgeranylated or the CAAX deleted form of RhoB, we have then shown that only RhoB-F expression was able to increase the SF2 value by reducing the sensitivity of these cells to radiation-induced mitotic cell death. Moreover, RhoB-F cells showed an increased G2 arrest and an inhibition of centrosome overduplication following irradiation mediated by the Rho-kinase, strongly suggesting that RhoB-F may control centrosome overduplication during the G2 arrest after irradiation. Overall, our results for the first time clearly implicate farnesylated RhoB as a crucial protein in mediating cellular resistance to radiation-induced nonapoptotic cell death.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Death / radiation effects*
  • Cell Survival / radiation effects
  • Centrosome / pathology*
  • Centrosome / radiation effects*
  • Flow Cytometry
  • Fluorescein-5-isothiocyanate
  • Fluorescent Antibody Technique, Indirect
  • Fluorescent Dyes
  • G2 Phase / radiation effects
  • Gamma Rays
  • Mice
  • Microscopy, Fluorescence
  • Mitosis / radiation effects*
  • NIH 3T3 Cells
  • rhoB GTP-Binding Protein / genetics
  • rhoB GTP-Binding Protein / metabolism*


  • Fluorescent Dyes
  • rhoB GTP-Binding Protein
  • Fluorescein-5-isothiocyanate