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. 2020 Apr 1;12(9):688–699. doi: 10.1093/jmcb/mjaa011

Figure 4.

Figure 4

Asxl1 is required for H2AK119 deubiquitylation at the Pten promoter. (A) RT-qPCR analysis of relative mRNA levels of Asxl1 and Bap1 after IL3 withdrawal at the indicated time points. (B) WB analysis of H2AK119ub1, H3K27me3, and H3K4me3 in WT and Asxl1-KO 32D cells under culture conditions with or without IL3. H3 and β-actin were used as loading controls. (C and D) ChIP-qPCR analysis of Asxl1 and Bap1 (C) as well as H2AK119ub1 and H3K27me3 (D) in WT and Asxl1−/− 32D cells under culture conditions with or without IL3. IgG was used as a negative control. Significance level was determined using Student’s two-sided t-tests. The error bars denote SD, n = 3; *P ≤ 0.05, **P ≤ 0.01. (E) The model for the role of Asxl1 in regulation of the Pten promoter. Anti-proliferative signals like IL3 deprivation lead to enrichment of Asxl1 and Bap1 at the Pten promoter, accompanied with H2AK119 deubiquitylation and decreased H3K27me3 levels for Pten activation, thereby inhibiting cell proliferation. Asxl1 loss leads to insufficiency of H2AK119 deubiquitylation and thereby maintains Pten silencing, which allows sustained activation of AKT signaling for cellular transformation.