ArticleBrain research2006
Absence of the basilar pons in mice lacking a functional Large glycosyltransferase gene suggests a defect in pontine neuron migration.
Article in Brain research, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed, 7 citations in OpenAlex.
- Model organisms inform the search for the genes and developmental pathology underlying malformations of the human hindbrain.Seminars in pediatric neurology · 2009Review
- Muscular dystrophies due to defective glycosylation of dystroglycan.Acta myologica : myopathies and cardiomyopathies : official journal of the Mediterranean Society of Myology · 2007Review
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Several forms of congenital muscular dystrophy result from mutations in glycosyltransferases that modify alpha-dystroglycan. As pontine hypoplasia has been reported in some clinical cases of congenital muscular dystrophy, we have begun to examine whether these glycosyltransferases are required for the normal development of the basilar pons, one of several precerebellar nuclei of the hindbrain. In veils (Large(vls)) mice, which carry a loss-of-function mutation in the Large glycosyltransferase gene, the basilar pons is absent. Instead, ectopic clusters of pontine neurons are found lateral to their normal site, suggesting that these neurons are unable to migrate to their appropriate site. Two other precerebellar nuclei, the lateral reticular nucleus and the inferior olive, are present in Large(vls) mice. In addition, the basilar pons forms normally in dystrophin-deficient mice. These results demonstrate that the Large glycosyltransferase but not dystrophin is required for normal basilar pontine development.
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