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. Author manuscript; available in PMC: 2022 Oct 6.
Published in final edited form as: Neuron. 2021 Aug 13;109(19):3104–3118.e6. doi: 10.1016/j.neuron.2021.07.018

Fig. 5: Rnf43 controls OPC differentiation through negative regulation of Wnt.

Fig. 5:

(A) Differentiation of Pdgfrα (green) OPCs into mature MBP (red) expressing OL, from OPCs isolated from RZ fl/fl control and Olig1cre:RZ fl/fl mice, in the presence (+Wnt3a) or absence of Wnt3a added to the media. (B) Quantification of OPC differentiation into MBP+ cells from the above RZ fl/fl control and Olig1cre:RZ fl/fl mice when treated with increasing concentrations (marked on x axis) of Wnt3a (n=3 independent experiments). Numbers are expressed as percentage of total cells that were MPB+. (C) qPCR for Wnt targets Axin2 and Notum mRNA in RZ fl/fl OPCs and Olig1cre:RZ fl/fl OPCs with 100ng/ml Wnt3a treatment, depicted as fold change normalized to the mRNA levels in RZ fl/fl OPCs without Wnt3a treatment (n=3 independent experiments). (D) qPCR for Rnf43 mRNA expression levels in the Oli-neu oligodendroglial cell line transfected with control vector or Rnf43 expression vector (n=3 independent experiments). (E) Wnt target Axin2 mRNA levels in Oli-neu cells transfected with control vector or Rnf43 expression vector in the presence of increasing Wnt3a stimulation (concentrations marked on x axis; n=3 independent experiments). (F) MBP mRNA levels in Oli-neu cells treated with Wnt3a and transfected with either control vector or Rnf43 expression vector (n = 3 independent experiments). (G) Axin2 mRNA is significantly upregulated (arrowheads) in 7dpl remyelinating lesions (lesion boundaries marked with dotted lines) from both PDGFRα-creER:APCfl/fl (G) and Olig1cre:RZfl/fl (H) mice compared to their respective APCfl/fl and RZfl/fl non cre controls. Values in all graphs are mean±s.d. NS not significant, *p<0.05, ** p<0.01, *** p<0.001. Scale bar in (A) is 100μm. See also Fig. S7.