ABSTRACT
In the adult mammalian brain, Gli1 expressing neural stem cells reside in the subventricular zone and their progeny are recruited to sites of demyelination in the white matter where they generate new oligodendrocytes, the myelin forming cells. Remarkably, genetic loss or pharmacologic inhibition of Gli1 enhances the efficacy of remyelination by these neural stem cells. To understand the molecular mechanisms involved, we performed a transcriptomic analysis of this Gli1-pool of neural stem cells. We compared murine NSCs with either intact or deficient Gli1 expression from adult mice on a control diet or on a cuprizone diet which induces widespread demyelination. These data will be a valuable resource for identifying therapeutic targets for enhancing remyelination in demyelinating diseases like multiple sclerosis.
Competing Interest Statement
A patent on the method of targeting GLI1 as a strategy to promote remyelination has been awarded, with J. L. Salzer, J. Samanta and G. Fishell listed as co-inventors. JLS is a consultant for and has ownership interests in Glixogen Therapeutics.
Footnotes
We have added the FACsorting strategy for all the samples (Fig.2), heatmap data (Fig. 5) and a summary of Ingenuity Pathway Analysis of differentially expressed genes in Gli1HET cuprizone vs Gli1NULL cuprizone groups (Table 3). We have also mentioned the trypan blue viability assay performed with the FACsorted cells in the text. We have also provided the references to prior studies about expression of Gli1 in neural stem cells in the adult SVZ and the tamoxifen protocol.
https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE162683