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. 2012 Mar 1;26(5):433–438. doi: 10.1101/gad.179416.111

Figure 5.

Figure 5.

ATRX loss results in increased association of mH2A1 at telomeres and the α-globin cluster, concomitant with loss of α-globin expression. (A) shRNA-mediated knockdown of ATRX (sh90 and sh92) in K562 cells. β-Actin was used for loading. (B) ChIP reveals increased association of mH2A1 with telomeres in the absence of ATRX. (Right) Densitometry quantitation. One of two biological replicates is shown. (C) Loss of ATRX results in decreased α-globin protein and HBA mRNA. (D) Capture of the University of California at Santa Cruz Genome Browser showing an ∼50-kb region around the α-globin locus. ChIP-seq-enriched peaks are shown for mH2A1 (sh92 and shluc), ATRX (Law et al. 2010), and input (shluc). Significant peaks (MACS) are shown below each panel as black bars. (Bottom) RefSeq annotated genes. The threshold line was set at 35 to facilitate visualization.