Extended Data Fig. 9: Probing the role of PP2A inhibition by CIP2A in the maintenance of genome integrity in BRCA-deficient cells.
a, Immunoblots showing levels of B56α (left), B56γ (middle) and of B6L and the destabilization domain (DD) from the empty virus (EV) (right) after 72 h of siRNA treatment and 48 h of AS1 induction. Representative of two independent immunostainings. b, Quantitation of micronuclei (MNi) in DLD1 BRCA2-/- cells stably transduced with a B6L-encoding lentivirus and transfected with control (siCTRL) or B56α and B56γ-targeting siRNAs. B6L expression was induced by AS1 addition for 48 h. Data presented as the mean ± S.D. n = 3 independent MNi counts; analyzed with a two-tailed t-test, assuming data is normally distributed, **p = 0.0031, **p = 0.0072. c, Representative micrographs of the experiment in (b). Arrowheads indicate micronuclei. d, LacR/LacO assay assessing the interaction between endogenous CIP2A, HA-tagged B56α or B56γ and FLAG-LacR-TOPBP1. Data presented as the intensity of the signal at the LacR-TOPBP1 focus over background (dashed line). Bars represent the mean ± S.D. aggregated from two independent localization assays measuring 15 cells per experiment. e, Representative micrographs of the experiment in (d). Statistical analyses and full blots are found in Source Data ED Fig. 9.
