Beta-catenin function is required for cerebellar morphogenesis
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Beta-catenin function is required for cerebellar morphogenesis. / Schüller, Ulrich; Rowitch, David H.
in: BRAIN RES, Jahrgang 1140, 06.04.2007, S. 161-9.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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TY - JOUR
T1 - Beta-catenin function is required for cerebellar morphogenesis
AU - Schüller, Ulrich
AU - Rowitch, David H
PY - 2007/4/6
Y1 - 2007/4/6
N2 - Because of the failure to form embryonic mid-hindbrain structures in conventional Wnt1 knockout animals, ongoing roles for Wnt signaling at later stages have been difficult to resolve. Here, we used Nestin-cre to ablate beta-catenin at midgestation in developing CNS precursors to investigate beta-catenin-dependent Wnt signaling in the development of late-derived structures such as the cerebellum. At 14.5 dpc, we found evidence for premature neural precursor cell fate commitment. At P0, we observed vermian hypoplasia and failure to fuse the cerebellar hemispheres and caudal midbrain, a phenotype reminiscent of the swaying (Wnt1(sw/sw)) mouse mutant. Our findings indicate general functions for beta-catenin beyond the neural plate stage during brain development and a particular role for beta-catenin-dependent Wnt signaling during morphogenesis of the caudal midbrain and the cerebellum. We discuss our results with respect to genetic pathways that regulate formation of derivatives of the embryonic midbrain-hindbrain region.
AB - Because of the failure to form embryonic mid-hindbrain structures in conventional Wnt1 knockout animals, ongoing roles for Wnt signaling at later stages have been difficult to resolve. Here, we used Nestin-cre to ablate beta-catenin at midgestation in developing CNS precursors to investigate beta-catenin-dependent Wnt signaling in the development of late-derived structures such as the cerebellum. At 14.5 dpc, we found evidence for premature neural precursor cell fate commitment. At P0, we observed vermian hypoplasia and failure to fuse the cerebellar hemispheres and caudal midbrain, a phenotype reminiscent of the swaying (Wnt1(sw/sw)) mouse mutant. Our findings indicate general functions for beta-catenin beyond the neural plate stage during brain development and a particular role for beta-catenin-dependent Wnt signaling during morphogenesis of the caudal midbrain and the cerebellum. We discuss our results with respect to genetic pathways that regulate formation of derivatives of the embryonic midbrain-hindbrain region.
KW - Animals
KW - Cerebellum
KW - Embryo, Mammalian
KW - Gene Expression Regulation, Developmental
KW - Intermediate Filament Proteins
KW - Mice
KW - Mice, Transgenic
KW - Morphogenesis
KW - Nerve Tissue Proteins
KW - Nestin
KW - Signal Transduction
KW - Wnt Proteins
KW - beta Catenin
KW - Journal Article
KW - Research Support, N.I.H., Extramural
KW - Research Support, Non-U.S. Gov't
U2 - 10.1016/j.brainres.2006.05.105
DO - 10.1016/j.brainres.2006.05.105
M3 - SCORING: Journal article
C2 - 16824494
VL - 1140
SP - 161
EP - 169
JO - BRAIN RES
JF - BRAIN RES
SN - 0006-8993
ER -