Accumulation of components of basal laminae: association with the failure of neural crest cells to colonize the presumptive aganglionic bowel of ls/ls mutant mice.

@article{Payette1988AccumulationOC,
  title={Accumulation of components of basal laminae: association with the failure of neural crest cells to colonize the presumptive aganglionic bowel of ls/ls mutant mice.},
  author={R. Payette and V. Tennyson and H. Pomeranz and T. Pham and T. P. Rothman and M. Gershon},
  journal={Developmental biology},
  year={1988},
  volume={125 2},
  pages={
          341-60
        }
}
Aganglionosis occurs in the terminal colon of the ls/ls mouse because an intrinsic defect of the presumptive aganglionic tissue prevents the entry and colonization of this portion of the bowel by migrating neural crest cells. The current study was undertaken to determine if abnormalities of the extracellular matrix could be identified in this segment that might account for migratory failure. Since basal laminae of the muscularis mucosa are overproduced in the aganglionic segment of adult ls/ls… Expand
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Aggregation chimeras demonstrate that the primary defect responsible for aganglionic megacolon in lethal spotted mice is not neuroblast autonomous.
TLDR
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TLDR
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It is suggested that the extracellular matrix and/or cells of mesenchymal origin of the terminal bowel of the ls/ls mouse may prevent the ing growth of the normal precursors of the glia as well as neurons of the enteric nervous system, but may permit or even encourage the ingrowth of abnormal numbers of extrinsic axons. Expand
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Embryological studies on the mouse indicate that, contrary to the classical concept, all the enteric ganglia are from a single, vagal, neural crest source, and there is no evidence of a lumbosacral origin for any of the intramural ganglia. Expand
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