Figure 4: Epigenomic signature demonstrates switch of lineage-specific active chromatin. | Nature Communications

Figure 4: Epigenomic signature demonstrates switch of lineage-specific active chromatin.

From: CD19 CAR immune pressure induces B-precursor acute lymphoblastic leukaemia lineage switch exposing inherent leukaemic plasticity

Figure 4

ChIP-Seq of H3K27Ac was performed in original disease (E2a:PBX) and four post-CD19-CAR E2a:PBX relapses: a lymphoid CD19-B-ALL (30–4), two mixed B/myeloid samples (5,961 and 252) and a myeloid sample (24–6). (a) ChIP-seq tracks of H3K27ac signal at promoter and enhancer regions for Cd19, Pax5, Ebf1, Sfpi1 (encoding PU.1), Cebpa and Thap2 for the four samples (lymphoid marked in red, myeloid in blue). (b) Transcription factor motif analysis of shared and lineage-specific enhancers was performed, with a more significant P value calculated for more abundant motifs within H3K27Ac-bound chromatin. The Pax5, E2a and Ebf1 motifs were found in regions lost on lineage switch (red box), and absent from newly activated chromatin in samples 59–61, 25–2 and 24–6 (blue box). (c) mRNA expression in fragments per kilobase of transcript per million mapped reads (FPKM) of the transcription factors with enriched motifs (shown in Fig. 4b), grouped according to clustering in Fig. 2d and Supplementary Fig. 5. Error bars represent s.d. *P<0.05.

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