title: Defective dendrite elongation but normal fertility in mice lacking the Rho-like GTPase activator Dbl.
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.
authors.affiliation: Dipartimento di Genetica, Biologia e Biochimica, Università di Torino, 10126 Turin, Italy. emilio.hirsch@unito.it
authors.forename: Emilio
authors.initials: E
authors.lastname: Hirsch
authors.forename: Michela
authors.initials: M
authors.lastname: Pozzato
authors.forename: Alessandro
authors.initials: A
authors.lastname: Vercelli
authors.forename: Laura
authors.initials: L
authors.lastname: Barberis
authors.forename: Ornella
authors.initials: O
authors.lastname: Azzolino
authors.forename: Chiara
authors.initials: C
authors.lastname: Russo
authors.forename: Cristina
authors.initials: C
authors.lastname: Vanni
authors.forename: Lorenzo
authors.initials: L
authors.lastname: Silengo
authors.forename: Alessandra
authors.initials: A
authors.lastname: Eva
authors.forename: Fiorella
authors.initials: F
authors.lastname: Altruda
mesh_terms: D000818:Animals; D015153:Blotting, Western; D001921:Brain / Q000254:growth & development / Q000378:metabolism / Q000473:pathology; D002465:Cell Movement; D003712:Dendrites / Q000378:metabolism* / Q000473:pathology*; D005260:Female; D005298:Fertility; D020558:GTP Phosphohydrolases / Q000378:metabolism; D020690:GTPase-Activating Proteins / Q000172:deficiency / Q000235:genetics / Q000378:metabolism*; D017353:Gene Deletion; D006066:Gonads / Q000196:embryology / Q000378:metabolism; D020662:Guanine Nucleotide Exchange Factors / Q000172:deficiency / Q000235:genetics / Q000378:metabolism*; D008297:Male; D051379:Mice; D018345:Mice, Knockout; D010053:Ovary / Q000166:cytology / Q000378:metabolism; D011518:Proto-Oncogene Proteins / Q000172:deficiency / Q000235:genetics / Q000378:metabolism*; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D013091:Spermatogenesis; D013737:Testis / Q000166:cytology / Q000378:metabolism
chemical_list: D020690:GTPase-Activating Proteins; D020662:Guanine Nucleotide Exchange Factors; C512843:Mcf2 protein, mouse; D011518:Proto-Oncogene Proteins; D012333:RNA, Messenger; D020558:GTP Phosphohydrolases