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[P1.23]: Repression of the proneural factor Ascl1 by retinoid signalling restricts neuronal fate choices in the ventral spinal cord
Author(s) -
Jacob J.,
Moore S.,
Milton C.,
GonzalezQuevedo R.,
Terriente J.,
Briscoe J.
Publication year - 2010
Publication title -
international journal of developmental neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.761
H-Index - 88
eISSN - 1873-474X
pISSN - 0736-5748
DOI - 10.1016/j.ijdevneu.2010.07.064
Subject(s) - neuroscience , spinal cord , biology , retinoid , psychological repression , microbiology and biotechnology , signalling , retinoic acid , genetics , gene , gene expression
determined by time-lapse imaging using a SNAP-tagged HMGB1 construct and by immunocytochemistry. The induction of Fezf2 in response to LPS stimulation was analysed by quantitative PCR. NT2 cells were found to express TLR4, the co-receptor CD14, and the adaptor proteins MyD88 and TRIF, and TLR4 was localised to the plasma membrane. Activation of TLR4 with LPS resulted in NF B translocation and TNF expression within 30 min as well as IRF3 phosphorylation and induction of IFN . LPS also stimulated NT2 cell proliferation (significant at 1 and 10 ug/mL p < 0.01), and enhanced differentiation of NT2 in the presence of retinoic acid. Significantly, Fezf2 was also induced by TLR4 activation. These results suggest that Fezf2 may be a key regulator of neural progenitor cell development in response to immune insult. Future studies are aimed at confirming the key TLR4 adaptor molecules required for Fezf2 activity and to analyse the response to TLR4 stimulation when Fezf2 is inhibited. References: