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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, Vol. 1140, 06.04.2007, p. 161-9.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Schüller, U & Rowitch, DH 2007, 'Beta-catenin function is required for cerebellar morphogenesis', BRAIN RES, vol. 1140, pp. 161-9. https://doi.org/10.1016/j.brainres.2006.05.105

APA

Schüller, U., & Rowitch, D. H. (2007). Beta-catenin function is required for cerebellar morphogenesis. BRAIN RES, 1140, 161-9. https://doi.org/10.1016/j.brainres.2006.05.105

Vancouver

Schüller U, Rowitch DH. Beta-catenin function is required for cerebellar morphogenesis. BRAIN RES. 2007 Apr 6;1140:161-9. https://doi.org/10.1016/j.brainres.2006.05.105

Bibtex

@article{8340932cc5b24400b2ce7ed01064861c,
title = "Beta-catenin function is required for cerebellar morphogenesis",
abstract = "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.",
keywords = "Animals, Cerebellum, Embryo, Mammalian, Gene Expression Regulation, Developmental, Intermediate Filament Proteins, Mice, Mice, Transgenic, Morphogenesis, Nerve Tissue Proteins, Nestin, Signal Transduction, Wnt Proteins, beta Catenin, Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't",
author = "Ulrich Sch{\"u}ller and Rowitch, {David H}",
year = "2007",
month = apr,
day = "6",
doi = "10.1016/j.brainres.2006.05.105",
language = "English",
volume = "1140",
pages = "161--9",
journal = "BRAIN RES",
issn = "0006-8993",
publisher = "Elsevier",

}

RIS

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 -