RhoG regulates gene expression and the actin cytoskeleton in lymphocytes

Oncogene. 2003 Jan 23;22(3):330-42. doi: 10.1038/sj.onc.1206116.

Abstract

RhoG, a member of the Rho family of GTPases, has been implicated as a regulator of the actin cytoskeleton. In this study, we show a novel function for the small GTPase RhoG on the regulation of the interferon-gamma promoter and nuclear factor of activated T cells (NFAT) gene transcription in lymphocytes. Optimal function of RhoG for the expression of these genes requires a calcium signal, normally provided by the antigen receptor. In addition, RhoG potentiation of NFAT requires the indirect activity of Rac and Cdc42; however, pathways distinct from those activated by Rac and Cdc42 mediate RhoG activation of NFAT-dependent transcription. Using effector domain mutants of RhoG we found that its ability to potentiate NFAT-dependent transcription correlates with its capacity to increase actin polymerization, supporting the suggestion that NFAT-dependent transcription is an actin-dependent process. RhoG also promotes T-cell spreading on fibronectin, a property that is independent of its ability to enhance NFAT-dependent transcription. Hence, these results implicate RhoG in leukocyte trafficking and the control of gene expression induced in response to antigen encounter.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Actins / metabolism*
  • Actins / ultrastructure
  • B-Lymphocytes / physiology
  • B-Lymphocytes / ultrastructure
  • Calcium / metabolism
  • Cell Cycle Proteins*
  • Cells, Cultured
  • Cytoskeleton / metabolism*
  • Cytoskeleton / ultrastructure
  • DNA-Binding Proteins / genetics
  • DNA-Binding Proteins / metabolism
  • Fibronectins / metabolism
  • GTP Phosphohydrolases / genetics
  • GTP Phosphohydrolases / metabolism*
  • Gene Expression Regulation
  • Humans
  • Interferon-gamma / genetics
  • Jurkat Cells
  • Leukocytes / cytology
  • Leukocytes / metabolism
  • Lymphocytes / cytology
  • Lymphocytes / physiology*
  • Lymphocytes / ultrastructure
  • Mutation
  • NFATC Transcription Factors
  • Nuclear Proteins*
  • Proto-Oncogene Proteins / genetics
  • Proto-Oncogene Proteins / metabolism
  • Proto-Oncogene Proteins c-vav
  • Signal Transduction
  • T-Lymphocytes / physiology
  • T-Lymphocytes / ultrastructure
  • Transcription Factors / genetics
  • Transcription Factors / metabolism
  • Transcription, Genetic
  • cdc42 GTP-Binding Protein / genetics
  • cdc42 GTP-Binding Protein / metabolism
  • rac1 GTP-Binding Protein / genetics
  • rac1 GTP-Binding Protein / metabolism
  • rho GTP-Binding Proteins

Substances

  • Actins
  • Cell Cycle Proteins
  • DNA-Binding Proteins
  • Fibronectins
  • NFATC Transcription Factors
  • Nuclear Proteins
  • Proto-Oncogene Proteins
  • Proto-Oncogene Proteins c-vav
  • Transcription Factors
  • VAV1 protein, human
  • RHOG protein, human
  • Interferon-gamma
  • GTP Phosphohydrolases
  • cdc42 GTP-Binding Protein
  • rac1 GTP-Binding Protein
  • rho GTP-Binding Proteins
  • Calcium