Investigation of the Slitrk6 function in the enteric nervous system development of Sox10 mutant Dominant megacolon mouse
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摘要The enteric nervous system (ENS), which regulates the majority of gut activities, is derived from vagal (the whole gut) and sacral (hindgut only) neural crest cells (NCCs) which migrate into and along the developing gut. Inactivation or mutation of Sox10 leads to defective migration of vagal NCCs, resulting in a loss of neurons and glial cells of ENS in the hind gut, which is called Hirschsprung’s disease (HSCR) in human. Slitrk6 has been known to regulate neurite outgrowth and synaptic development, but its functions in the ENS development are still known. Here, we report that Slitrk6 is expressed in the primary culture NCCs in vitro, and the embryonic gut in vivo; and, its expression is decreased in the NCCs from Sox10 mutant Dominant megacolon mouse (Dom) which is a HSCR animal model. Luciferase assay indicates that Sox10 has the affinity to bind with Slitrk6 promoter sequence and regulates its expression in vitro. Knockdown of Slitrk6 expression in NCCs primary culture results in reduced neuronal cell differentiation efficiency and abnormal neuronal cell morphology. In conclusion, the down-regulation of Slitrk6 affect the normal differentiation of NCCs in the Dom mouse and it may play a role in regulating the development of the ENS in mouse embryos.
著者Taida HUANG, Tiantian PAN, Yonghui HOU, Wood Yee CHAN
會議名稱The 25th International Symposium on Morphological Sciences

上次更新時間 2018-27-04 於 12:29