Defective dendrite elongation but normal fertility in mice lacking the rho-like GTPase activator Dbl

Emilio Hirsch, Michela Pozzato, Alessandro Vercelli, Laura Barberis, Ornella Azzolino, Chiara Russo, Cristina Vanni, Lorenzo Silengo, Alessandra Eva, Fiorella Altruda

Research output: Contribution to journalArticlepeer-review

Abstract

Dbl is the prototype of a large family of GDP-GTP exchange factors for small GTPases of the Rho family. In vitro, Dbl is known to activate Rho and Cdc42 and to induce a transformed phenotype. Dbl is specifically expressed in brain and gonads, but its in vivo functions are largely unknown. To assess its role in neurogenesis and gametogenesis, targeted deletion of the murine Dbl gene was accomplished in embryonic stem cells. Dbl-null mice are viable and did not show either decreased reproductive performances or obvious neurological defects. Histological analysis of mutant testis showed normal morphology and unaltered proliferation and survival of spermatogonia. Dbl-null brains indicated a correct disposition of the major neural structures. Analysis of cortical stratification indicated that Dbl is not crucial for neuronal migration. However, in distinct populations of Dbl-null cortical pyramidal neurons, the length of dendrites was significantly reduced, suggesting a role for Dbl in dendrite elongation.

Original languageEnglish
Pages (from-to)3140-3148
Number of pages9
JournalMolecular and Cellular Biology
Volume22
Issue number9
DOIs
Publication statusPublished - 2002

ASJC Scopus subject areas

  • Molecular Biology
  • Genetics
  • Cell Biology

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