作者: M. Shibata , H. Nakao , H. Kiyonari , T. Abe , S. Aizawa
DOI: 10.1523/JNEUROSCI.5085-10.2011
关键词:
摘要: microRNA-9-2 and microRNA-9-3 double-mutant mice demonstrate that microRNA-9 (miR-9) controls neural progenitor proliferation differentiation in the developing telencephalon by regulating expression of multiple transcription factors. As suggested our previous study, Foxg1 was elevated, production Cajal-Retzius cells early-born neurons suppressed miR-9-2/3 pallium. At embryonic day 16.5 (E16.5), however, no longer elevated. The an AU-rich RNA-binding protein Elavl2 increased at E16.5, Elav2 associated with 3' untranslated region (UTR), it countered suppression miR-9. Later, reduced pallium decrease Nr2e1 Pax6 increase Meis2 expression. analyses suggest indirectly inhibits suppressing In contrast, together Elavl1 Msi1, targets mRNA UTR to enhance Concomitantly, cortical layers were reduced, each projection malformed, tangential migration interneurons into impaired double mutants. miR-9 also Gsh2 UTR, Gsh2, as well Foxg1, elevated subpallium. subpallium enhanced, development basal ganglia including striatum globus pallidus suppressed. Pallial/subpallial boundary shifted dorsally, ventral lost. Corridor thalamocortical corticofugal axons misrouted