TY - JOUR
T1 - Rhes is involved in striatal function
AU - Spano, Daniela
AU - Branchi, Igor
AU - Rosica, Annamaria
AU - Pirro, Maria Teresa
AU - Riccio, Antonio
AU - Mithbaokar, Pratibha
AU - Affuso, Andrea
AU - Arra, Claudio
AU - Campolon, Patrizia
AU - Terracciano, Daniela
AU - Macchia, Vincenzo
AU - Bernal, Juan
AU - Alleva, Enrico
AU - Di Lauro, Roberto
PY - 2004/7
Y1 - 2004/7
N2 - The development and the function of central nervous system depend on thyroid hormones. In humans, the lack of thyroid hormones causes cretinism, a syndrome of severe mental deficiency. It is assumed that thyroid hormones affect the normal development and function of the brain by activating or suppressing target gene expression because several genes expressed in the brain have been shown to be under thyroid hormone control. Among these, the Rhes gene, encoding a small GTP-binding protein, is predominantly expressed in the striatal region of the brain. To clarify the role of Rhes in vivo, we disrupted the Rhes gene by homologous recombination in embryonic stem cells and generated mice homozygous for the Rhes null mutation (Rhes-/-). Rhes-/- mice were viable but weighed less than wild-type mice. Furthermore, they showed behavioral abnormalities, displaying a gender-dependent increase in anxiety levels and a clear motor coordination deficit but no learning or memory impairment. These results suggest that Rhes disruption affects selected behavioral competencies.
AB - The development and the function of central nervous system depend on thyroid hormones. In humans, the lack of thyroid hormones causes cretinism, a syndrome of severe mental deficiency. It is assumed that thyroid hormones affect the normal development and function of the brain by activating or suppressing target gene expression because several genes expressed in the brain have been shown to be under thyroid hormone control. Among these, the Rhes gene, encoding a small GTP-binding protein, is predominantly expressed in the striatal region of the brain. To clarify the role of Rhes in vivo, we disrupted the Rhes gene by homologous recombination in embryonic stem cells and generated mice homozygous for the Rhes null mutation (Rhes-/-). Rhes-/- mice were viable but weighed less than wild-type mice. Furthermore, they showed behavioral abnormalities, displaying a gender-dependent increase in anxiety levels and a clear motor coordination deficit but no learning or memory impairment. These results suggest that Rhes disruption affects selected behavioral competencies.
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U2 - 10.1128/MCB.24.13.5788-5796.2004
DO - 10.1128/MCB.24.13.5788-5796.2004
M3 - Article
C2 - 15199135
AN - SCOPUS:2942753949
VL - 24
SP - 5788
EP - 5796
JO - Molecular and Cellular Biology
JF - Molecular and Cellular Biology
SN - 0270-7306
IS - 13
ER -