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Analysis of gene expression in hindgut cells of EdnrB mutant embryonic day 14 mice

ABSTRACT: Analysis of gene expression in hindgut cells of EdnrB mutant embryonic day 14 mice

PROVIDER: PRJNA576593 | ENA |

REPOSITORIES: ENA

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Analysis of gene expression in hindgut cells of EdnrB mutant embryonic day 14 mice

Project description:Neural Crest Cells (NCC) migrate through the gut during mouse development and are involved in mesenchymal patterning. However, in a Tcof hetrozygous mutant, NCC cells stop their migration at E14.5. Mutation of the EdnrB receptor also inhibits cell migration, but farther back. A FLEX conditional knockout of EdnrB only in NCC cells, also halts migration, however is still permissible for transplantated wt NCC cells. In order to better understand mechanisms of cell migration, the transcriptional environment of the gut was characterized by array analysis of Ednrb mutants.

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Avian ceca are required for hindgut enteric nervous system development by promoting enteric neural crest cell proliferation and inhibiting neuronal differentiation via non-canonical Wnt signaling

Project description:The enteric nervous system (ENS), which is derived from enteric neural crest cells (ENCCs) during gut development, represents the neuronal innervation of the gastrointestinal tract and is critical for regulating normal intestinal function. Compromised ENCC migration can lead to Hirschsprung Disease, which is characterized by an aganglionic distal bowel. We find that removal of the ceca, a paired structure present at the midgut-hindgut junction in avian intestine, leads to severe hindgut aganglionosis, suggesting that the ceca are required for ENS development. To test this, we replaced the ceca of embryonic day 6 (E6) wild-type chicks with ceca from transgenic GFP chicks. Interestingly, the entire hindgut ENS arises from the GFP+ ceca-derived ENCC population. Comparative transcriptome profiling of the cecal buds compared to the interceca region shows that the non-canonical Wnt signaling pathway is preferentially expressed within the ceca. Specifically, Wnt11 is highly expressed in the ceca, as confirmed by RNA in situ hybridization, leading us to hypothesize that cecal expression of Wnt11 is important for ENCC colonization of the hindgut. Organ cultures were prepared using E6 avian intestine, when ENCCs are migrating through the ceca, and showed that Wnt11 inhibits enteric neuronal differentiation. These results reveal an essential role for the ceca during hindgut ENS formation and highlight an important function for non-canonical Wnt signaling in regulating ENCC differentiation and thereby promoting their migration into the colon.

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Effect of IUGR on postnatal day 14 pancreatic islets

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