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

被引:23
作者
Hirsch, E
Pozzato, M
Vercelli, A
Barberis, L
Azzolino, O
Russo, C
Vanni, C
Silengo, L
Eva, A
Altruda, F
机构
[1] Univ Turin, Dipartimento Genet Biol & Biochim, I-10126 Turin, Italy
[2] Univ Turin, Dipartimento Anat Farmacol & Med Forense, I-10126 Turin, Italy
[3] Ist Giannina Gaslini, Mol Biol Lab, I-16147 Genoa, Italy
关键词
D O I
10.1128/MCB.22.9.3140-3148.2002
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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.
引用
收藏
页码:3140 / 3148
页数:9
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