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The unique differentiation potential of rosette cells yields improved access to therapeutically relevant neuron types.Insights from our study on the molecular mechanisms controlling rosette state should enhance basic understanding of NSC biology.Maintenance of R-NSCs is promoted by activation of SHH and Notch pathways.In the absence of these signals, R-NSCs rapidly lose rosette organization and progress to a more restricted NSC stage.( The formation of neural rosettes (Supplemental Fig.1) was initiated by the acquisition of cell polarity in h ESC progeny illustrated by the redistribution of ZO-1, a tight junction protein (Itoh et al.
These studies demonstrated that single factors act instructively to specify neuronal versus glial fate choice (Johe et al. Two major challenges have limited the use of NSCs to study neural differentiation and to develop cell-based strategies for brain repair: First, under most growth conditions, NSCs show increased gliogenic bias and concomitant loss of neurogenic potential in culture. 2005), although potential for regional specification was not addressed.R-NSCs can be derived from human and mouse ESCs or from neural plate stage embryos.While R-NSCs express markers classically associated with NSC fate, we identified a set of genes that specifically mark the R-NSC state.In contrast, embryonic stem cell (ESC) progeny readily yield region-specific neuronal fates in response to appropriate developmental signals.Here we demonstrate prospective and clonal isolation of neural rosette cells (termed R-NSCs), a novel NSC type with broad differentiation potential toward CNS and PNS fates and capable of in vivo engraftment.
Neural stem cells (NSCs) are defined by their ability to clonally give rise to the three major CNS lineages: neurons, astrocytes, and oligodendrocytes.