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. 2022 May 2;132(9):e155468. doi: 10.1172/JCI155468

Figure 2. STRIPAK-MST1/2 undergoes dynamic assembly in response to DNA damage.

Figure 2

(A and B) Gels showing DNA damage–triggered stabilization of the SIKE1-SLMAP arm at the protein level. Here, 293A cells were pretreated with the indicated dose of etoposide (A) or with other DNA-damaging agents (B) for 1 hour, and then harvested 2 hours after removal of the chemicals. (C–E) Gels and plots showing a DNA damage–induced mutually exclusive pattern between SIKE1-SLMAP protein levels and MST1/2 kinase activity. Cells were exposed to 10 μM etoposide for 1 hour and then collected at the indicated time points after removal of the drug to determine the (C) protein levels of both SIKE1 and SLMAP in 293A cells and (D) MST1/2 kinase activity in HGC-27 cells. (E) Quantitative data from HGC-27 cells. (F) Dynamic assembly of STRIPAK-MST1/2 induced by DNA damage. 293A cells transiently transfected with the indicated constructs for 24 hours were treated with DMSO or etoposide (1 h) and then harvested at an early (2 h) or late (18 h) stage before being subjected to BioID analysis. (G) Co-IP assay to validate the BioID results. 293A cells were treated and harvested as in C before processing for STRN3 IP. (H) Cartoon representation of a loosening of the assembly of the Hippo-containing STRIPAK complex in response to DNA damage. See also Supplemental Figure 3.