Premium
Gangliogenesis in the enteric nervous system: Roles of the polysialylation of the neural cell adhesion molecule and its regulation by bone morphogenetic protein‐4
Author(s) -
Faure Christophe,
Chalazonitis Alcmène,
Rhéaume Catherine,
Bouchard Guylaine,
Sampathkumar S.Gopalan,
Yarema Kevin J.,
Gershon Michael D.
Publication year - 2007
Publication title -
developmental dynamics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.634
H-Index - 141
eISSN - 1097-0177
pISSN - 1058-8388
DOI - 10.1002/dvdy.20943
Subject(s) - neural cell adhesion molecule , neural crest , biology , microbiology and biotechnology , bone morphogenetic protein , cell adhesion molecule , cell adhesion , neural tube , neural development , embryo , cell , biochemistry , gene
Abstract The neural crest–derived cells that colonize the fetal bowel become patterned into two ganglionated plexuses. The hypothesis that bone morphogenetic proteins (BMPs) promote ganglionation by regulating neural cell adhesion molecule (NCAM) polysialylation was tested. Transcripts encoding the sialyltransferases, ST8Sia IV (PST) and ST8Sia II (STX), which polysialylate NCAM, were detectable in fetal rat gut by E12 but were downregulated postnatally. PSA‐NCAM‐immunoreactive neuron numbers, but not those of NCAM, were developmentally regulated similarly. Circular smooth muscle was transiently (E16–20) PSA‐NCAM‐immunoreactive when it is traversed by migrating precursors of submucosal neurons. Neurons developing in vitro from crest‐derived cells immunoselected at E12 with antibodies to p75 NTR expressed NCAM and PSA‐NCAM. BMP‐4 promoted neuronal NCAM polysialylation and clustering. N‐butanoylmannosamine, which blocks NCAM polysialylation, but not N‐propanoylmannosamine, which does not, interfered with BMP‐4‐induced neuronal clustering. Observations suggest that BMP signaling enhances NCAM polysialylation, which allows precursors to migrate and form ganglionic aggregates during the remodeling of the developing ENS. Developmental Dynamics 236:44–59, 2007. © 2006 Wiley‐Liss, Inc.