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

doi:10.1128/MCB.22.9.3140-3148.2002

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

Mol Cell Biol. 2002 May;22(9):3140-8. doi: 10.1128/MCB.22.9.3140-3148.2002.

Authors

Emilio Hirsch¹, Michela Pozzato, Alessandro Vercelli, Laura Barberis, Ornella Azzolino, Chiara Russo, Cristina Vanni, Lorenzo Silengo, Alessandra Eva, Fiorella Altruda

Affiliation

¹ Dipartimento di Genetica, Biologia e Biochimica, Università di Torino, 10126 Turin, Italy. emilio.hirsch@unito.it

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.

Publication types

Research Support, Non-U.S. Gov't

MeSH terms

Animals
Blotting, Western
Brain / growth & development
Brain / metabolism
Brain / pathology
Cell Movement
Dendrites / metabolism*
Dendrites / pathology*
Female
Fertility*
GTP Phosphohydrolases / metabolism
GTPase-Activating Proteins / deficiency
GTPase-Activating Proteins / genetics
GTPase-Activating Proteins / metabolism*
Gene Deletion
Gonads / embryology
Gonads / metabolism
Guanine Nucleotide Exchange Factors / deficiency
Guanine Nucleotide Exchange Factors / genetics
Guanine Nucleotide Exchange Factors / metabolism*
Male
Mice
Mice, Knockout
Ovary / cytology
Ovary / metabolism
Proto-Oncogene Proteins / deficiency
Proto-Oncogene Proteins / genetics
Proto-Oncogene Proteins / metabolism*
RNA, Messenger / genetics
RNA, Messenger / metabolism
Spermatogenesis
Testis / cytology
Testis / metabolism

Substances

GTPase-Activating Proteins
Guanine Nucleotide Exchange Factors
Mcf2 protein, mouse
Proto-Oncogene Proteins
RNA, Messenger
GTP Phosphohydrolases