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Your search keyword '"Norton, Christine R."' showing total 3 results
Start Over Author "Norton, Christine R." Topic signal transduction
3 results on '"Norton, Christine R."'

1. Fine-tuning of Notch signaling sets the boundary of the organ of Corti and establishes sensory cell fates.

Author

Basch ML, Brown RM 2nd, Jen HI, Semerci F, Depreux F, Edlund RK, Zhang H, Norton CR, Gridley T, Cole SE, Doetzlhofer A, Maletic-Savatic M, Segil N, and Groves AK

Subjects
Animals, Glucosyltransferases, Glycosyltransferases genetics, Mice, Mutation, Proteins genetics, Glycosyltransferases metabolism, Organ of Corti embryology, Proteins metabolism, Receptors, Notch metabolism, Signal Transduction
Abstract

The signals that induce the organ of Corti and define its boundaries in the cochlea are poorly understood. We show that two Notch modifiers, Lfng and Mfng, are transiently expressed precisely at the neural boundary of the organ of Corti. Cre-Lox fate mapping shows this region gives rise to inner hair cells and their associated inner phalangeal cells. Mutation of Lfng and Mfng disrupts this boundary, producing unexpected duplications of inner hair cells and inner phalangeal cells. This phenotype is mimicked by other mouse mutants or pharmacological treatments that lower but not abolish Notch signaling. However, strong disruption of Notch signaling causes a very different result, generating many ectopic hair cells at the expense of inner phalangeal cells. Our results show that Notch signaling is finely calibrated in the cochlea to produce precisely tuned levels of signaling that first set the boundary of the organ of Corti and later regulate hair cell development., Competing Interests: The authors declare that no competing interests exist.

Published
2016
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2. Notch signal reception is required in vascular smooth muscle cells for ductus arteriosus closure.

Author

Krebs LT, Norton CR, and Gridley T

Subjects
Animals, Calcium-Binding Proteins genetics, Calcium-Binding Proteins metabolism, Intercellular Signaling Peptides and Proteins genetics, Intercellular Signaling Peptides and Proteins metabolism, Jagged-1 Protein, Membrane Proteins genetics, Membrane Proteins metabolism, Mice, Muscle, Smooth, Vascular cytology, Serrate-Jagged Proteins, Ductus Arteriosus embryology, Muscle, Smooth, Vascular embryology, Muscle, Smooth, Vascular metabolism, Receptors, Notch metabolism, Signal Transduction
Abstract

The ductus arteriosus is an arterial vessel that shunts blood flow away from the lungs during fetal life, but normally occludes after birth to establish the adult circulation pattern. Failure of the ductus arteriosus to close after birth is termed patent ductus arteriosus, and is one of the most common congenital heart defects. Our previous work demonstrated that vascular smooth muscle cell expression of the Jag1 gene, which encodes a ligand for Notch family receptors, is essential for postnatal closure of the ductus arteriosus in mice. However, it was not known what cell population was responsible for receiving the Jag1-mediated signal. Here we show, using smooth muscle cell-specific deletion of the Rbpj gene, which encodes a transcription factor that mediates all canonical Notch signaling, that Notch signal reception in the vascular smooth muscle cell compartment is required for ductus arteriosus closure. These data indicate that homotypic vascular smooth muscle cell interactions are required for proper contractile smooth muscle cell differentiation and postnatal closure of the ductus arteriosus in mice., (© 2016 Wiley Periodicals, Inc.)

Published
2016
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3. Notch signal reception is required in vascular smooth muscle cells for ductus arteriosus closure

Author

Krebs, Luke T., Norton, Christine R., and Gridley, Thomas

Subjects
congenital, hereditary, and neonatal diseases and abnormalities, Receptors, Notch, Calcium-Binding Proteins, Membrane Proteins, Ductus Arteriosus, Article, Muscle, Smooth, Vascular, Mice, embryonic structures, cardiovascular system, Animals, Intercellular Signaling Peptides and Proteins, Serrate-Jagged Proteins, cardiovascular diseases, Jagged-1 Protein, Signal Transduction
Abstract

The ductus arteriosus is an arterial vessel that shunts blood flow away from the lungs during fetal life, but normally occludes after birth to establish the adult circulation pattern. Failure of the ductus arteriosus to close after birth is termed patent ductus arteriosus, and is one of the most common congenital heart defects. Our previous work demonstrated that vascular smooth muscle cell expression of the Jag1 gene, which encodes a ligand for Notch family receptors, is essential for postnatal closure of the ductus arteriosus in mice. However, it was not known what cell population was responsible for receiving the Jag1-mediated signal. Here we show, using smooth muscle cell-specific deletion of the Rbpj gene, which encodes a transcription factor that mediates all canonical Notch signaling, that Notch signal reception in the vascular smooth muscle cell compartment is required for ductus arteriosus closure. These data indicate that homotypic vascular smooth muscle cell interactions are required for proper contractile smooth muscle cell differentiation and postnatal closure of the ductus arteriosus in mice.

Published
2016

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