PP2A-Ankle2 promotes BAF dephosphorylation.
A. Phosphoproteomic analysis identified BAF as being hyperphosphorylated at Thr4 and Ser5 upon Ankle2 depletion. D-Mel cells were transfected with dsRNA against Ankle2 or non-target dsRNA (against bacterial KAN gene). Phosphopeptides from tryptic digests were analyzed quantitatively by mass spectrometry. A few additional significantly hyperphosphorylated proteins are labeled as examples (see Table S5 for the full list). B. Competition assay. Top: schematic hypothesis. If Ankle2 occupies the position of a PP2A regulatory subunit, its presence in the PP2A holoenzyme may be outcompeted by Tws (PP2A regulatory subunit). Bottom: the interaction between PP2A-29B-GFP and Ankle2-Myc was monitored by a GFP affinity co-purification assay. Increasing amounts of Myc-Tws plasmid were co-transfected. As a result, increasing amounts of Myc-Tws, and decreasing amounts of Ankle2-Myc, are co-purified with PP2A-29B-GFP. The amounts of co-purified Mts are unchanged. Averages of 3 experiments are shown. All error bars: S.D. * p < 0.05, **p < 0.01, ***<0.001 **** p < 0.0001, ns: non-significant from paired t-tests C. AlphaFold3 predicted model of a complex between Drosophila Ankle2, PP2A-29B and Mts. Residues of Ankle2 with confidence scores below 0.8 are coloured grey. D. Predicted model of a complex between Drosophila Tws, PP2A-29B and Mts. E. Crystal structure of a complex between human PPP2R1A, PPP2CA and B55 (PDB 3DW8) (Xu et al., 2008). Red asterisks denote the positions of the phosphatase catalytic site.