연사 : 송미령교수 (광주과학기술원)
연제 : STAT3 maintains the stemness of radial glia at mid-neurogenesis
일시 : 2015년 5월 22일 (금) 오후 4시
장소 : 하나과학관 A동 101호
초청교수 : 백자현교수
Abstract
Radial glial cells are stem cell-like populations of glial nature that supply neurons either
directly or indirectly via basal progenitors that give rise to neurons. Here we show that STAT3
signaling is active during neurogenesis in radial glia (RG), but not in basal progenitors.
Enhanced STAT3 signaling in cortical progenitors caused more radial glia to persist rather than
become neurons. Targeted deletion or RNAi-mediated knockdown of Stat3 resulted in fewer
radial glial cells and more basal progenitors and led to premature neurogenesis. The neuronal
populations affected in Stat3 mutant mice were the late-born neurons that constitute the upper
cortical layers rather than early-born neurons, thus supporting the view that the role of STAT3
at mid-neurogenesis is layer-specific. Analysis of dividing radial glia revealed that STAT3
selectively increased the proportion of dividing RGs, while downregulation of STAT3 reduced
the proportion. Consistently, STAT3 activity in dividing radial glia was frequently associated
with vertical cleavage. Pair cell analysis showed that elevated STAT3 activity correlated with
symmetric division of radial glia producing more radial glia, whereas elimination of STAT3
generated more neurogenic cells. Together, our results suggest that STAT3 maintains the
stemness of radial glia and inhibits their transition to basal progenitors at mid-neurogenesis, so
probably preserving a pool of radial glia for later neurogenesis or gliogenesis.