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. Author manuscript; available in PMC: 2024 Aug 27.
Published in final edited form as: Nature. 2017 Apr 5;544(7649):245–249. doi: 10.1038/nature21722

Fig. 3: Characterisation of neurogenic and repressive Myt1l domains.

Fig. 3:

a, Truncation and mutation screen identifies Myt1l domains essential for induced neurogenesis from MEFs upon reprogramming for 14 days with Ascl1. Highlighted are nuclear localisation signals (NLS), aspartic acid/glutamic acid-rich (Asp/Glu-rich), serine-rich (Ser-rich), MYT1, coiled-coil domains, CCHC-type zinc fingers (ZF) and mutants (mtZF). b, Conversion activity compared to Myt1l wt based on number of TUJ1-positive cells with neuronal morphology (black) or TauEGFP expression (grey). n = 3, error bars = SD, t-test * p < 0.005. c, Representative immunofluorescence of iN cells in A; TUJ1 (red), DAPI staining (blue), scale bar 50 μm. d, Representative action potential (AP) traces of iN cells in A upon maturation for 21 days on mouse glia. e, SELEX DNA binding experiments of Myt1l ZF fragments enrich same Myt1l AAGTT-core motif (green arrows). f, Immunoprecipitation show binding of SIN3b to full length and minimal Myt1l in DNase-treated MEF cell lysates two days after transgene overexpression. g, GST pull down from MEF cell lysates identify minimal SIN3b interaction region within functional Myt1l domain. h, Overlapping ChIP-seq chromatin occupancy profiles of overexpressed Myt1l (left, blue), endogenous SIN3b (middle, violet) and HDAC1 (right, green) at Myt1l promoter target sites in MEFs two days after reprogramming induction. n = 2.