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Bone morphogenetic protein regulation of enteric neuronal phenotypic diversity: Relationship to timing of cell cycle exit
Journal of comparative neurology (1911), 2008-08, Vol.509 (5), p.474-492
Chalazonitis, Alcmène
Pham, Tuan D.
Li, Zhishan
Roman, Daniel
Guha, Udayan
Gomes, William
Kan, Lixin
Kessler, John A.
Gershon, Michael D.
2008
Details
Autor(en) / Beteiligte
Chalazonitis, Alcmène
Pham, Tuan D.
Li, Zhishan
Roman, Daniel
Guha, Udayan
Gomes, William
Kan, Lixin
Kessler, John A.
Gershon, Michael D.
Titel
Bone morphogenetic protein regulation of enteric neuronal phenotypic diversity: Relationship to timing of cell cycle exit
Ist Teil von
Journal of comparative neurology (1911), 2008-08, Vol.509 (5), p.474-492
Ort / Verlag
Hoboken: Wiley Subscription Services, Inc., A Wiley Company
Erscheinungsjahr
2008
Link zum Volltext
Quelle
Alma/SFX Local Collection
Beschreibungen/Notizen
The effects of bone morphogenetic protein (BMP) signaling on enteric neuron development were examined in transgenic mice overexpressing either the BMP inhibitor, noggin, or BMP4 under control of the neuron specific enolase (NSE) promoter. Noggin antagonism of BMP signaling increased total numbers of enteric neurons and those of subpopulations derived from precursors that exit the cell cycle early in neurogenesis (serotonin, calretinin, calbindin). In contrast, noggin overexpression decreased numbers of neurons derived from precursors that exit the cell cycle late (γ‐aminobutyric acid, tyrosine hydroxylase [TH], dopamine transporter, calcitonin gene‐related peptide, TrkC). The numbers of TH‐ and TrkC‐expressing neurons were increased by overexpression of BMP4. These observations are consistent with the idea that phenotypic expression in the enteric nervous system (ENS) is determined, in part, by the number of proliferative divisions neuronal precursors undergo before their terminal mitosis. BMP signaling may thus regulate enteric neuronal phenotypic diversity by promoting the exit of precursors from the cell cycle. BMP2 increased the numbers of TH‐ and TrkC‐expressing neurons developing in vitro from immunoselected enteric crest‐derived precursors; BMP signaling may thus also specify or promote the development of dopaminergic TrkC/NT‐3‐dependent neurons. The developmental defects in the ENS of noggin‐overexpressing mice caused a relatively mild disturbance of motility (irregular rapid transit and increased stool frequency, weight, and water content). Although the function of the gut thus displays a remarkable tolerance for ENS defects, subtle functional abnormalities in motility or secretion may arise when ENS defects short of aganglionosis occur during development. J. Comp. Neurol. 509:474–492, 2008. © 2008 Wiley‐Liss, Inc.
Sprache
Englisch
Identifikatoren
ISSN: 0021-9967
eISSN: 1096-9861
DOI: 10.1002/cne.21770
Titel-ID: cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_2592098
Format
–
Schlagworte
Amino Acid Sequence
,
Animals
,
autonomic nervous system
,
Bone Morphogenetic Protein 4 - biosynthesis
,
Bone Morphogenetic Protein 4 - genetics
,
Bone Morphogenetic Protein 4 - physiology
,
Carrier Proteins - biosynthesis
,
Carrier Proteins - genetics
,
Carrier Proteins - physiology
,
Cell Count
,
Cell Cycle - genetics
,
Cell Cycle - physiology
,
Cells, Cultured
,
development
,
enteric nervous system
,
Enteric Nervous System - cytology
,
Enteric Nervous System - embryology
,
Enteric Nervous System - enzymology
,
Female
,
gastrointestinal motility
,
Genetic Variation - physiology
,
Male
,
Mice
,
Mice, Transgenic
,
Molecular Sequence Data
,
Neurons - cytology
,
Neurons - physiology
,
neurotransmitters
,
noggin
,
Phenotype
,
Pregnancy
,
Rats
,
Rats, Sprague-Dawley
,
Time Factors
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