K27M and K36M mutations on non canonical Histone 3.3 promote redistribution of antagonistic chromatin marks, disrupted development, and tumorigenesis. K27M and K36M mutations on non canonical Histone 3.3 promote redistribution of antagonistic chromatin marks, disrupted development, and tumorigenesis

We conducted RNA-seq analysis to identify genes that are differentially expressed in H3K27M and H3K36M oncohistones compared to wt and control eye tissue (eye discs), followed by smRNA-seq profiling based on our results and to confirm upregulation of piRNAs Overall design: 3 data types (RNA-seq, smRNA-seq and ChIP-seq data). RNA-seq and smRNA-seq experiments has 12 samples, which is composed of 3 replicates of 4 genotypes (H3K27M, H3K36M, histone WT and control eye tissue (Yw)). Additional RNA-seq RNAi experiments has been performed on 10 sets (3 replicates each, 30 samples total). H3K27me3 and H3K36me2 ChIP-seq was also performed (14 samples)