Extended Data Figure 2: Genome-wide chromatin binding of Myt1l.
From: Myt1l safeguards neuronal identity by actively repressing many non-neuronal fates
a, b, ChIP of endogenous Myt1l from E13.5 mouse brain (a) or of wild-type Myt1l (b, left) and Myt1l200–623 (b, right) transgenes from MEF cell lysates 2 days after induction with or without Ascl1 and Brn2. Chromatin immunoprecipitates were analysed by western blotting with Myt1l, Brn2, and Ascl1 antibodies. Input, 0.3% of ChIP input; unbound, 0.3% of ChIP flow-through; ChIP, 3% of ChIP eluates. c, ChIP–seq genome-wide occupancy of endogenous Myt1l in E13.5 mouse brains (n = 2) or Myt1l and Myt1200–623 in MEFs two days after induction with (n = 3) or without (n = 2) Ascl1 and Brn2. A total of 6,911 peaks are sorted on the basis of intensity and corresponding genomic regions are displayed across all datasets; signal is displayed ± 2 kb from summits (see also Fig. 1). d, Chromatin reads for Myt1l, Ascl1 and Brn2 at Ascl1 (top) and Brn2 peaks (bottom)8. e, Chromatin reads of indicated histone marks in uninfected MEFs at the sites at which Myt1l is bound during reprogramming. Signal is displayed ± 2 kb from peak summit. f, Pearson correlation and clustering analysis of ChIP–seq samples highlight high binding overlap between different conditions. g, MA plots from DiffBind and corresponding Venn diagrams showing the distribution of Myt1l ChIP–seq peak intensities between indicated conditions; endogenous Myt1l in mouse brain versus overexpressed Myt1l in BAM MEFs (top), Myt1l overexpression alone versus in combination with Ascl1 and Brn2 (BAM) in MEFs (bottom left), and wild-type Myt1l versus Myt1l200–623 overexpression in MEFs (bottom right). Significantly different peaks are shown in colour and numbers are annotated. Peaks that are significantly changed by the experimental setup are highlighted red.
