Monitoring perturbation of ER-mitochondria interactions linked to genetic modulation of protein of the VDAC1/Grp75/IP3R1 complex by in situ PLA. Representative.

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Monitoring perturbation of ER-mitochondria interactions linked to genetic modulation of protein of the VDAC1/Grp75/IP3R1 complex by in situ PLA. Representative PLA images (at left, ×63 and scale bar = 20 μm) and quantitative analysis of both Grp75/IP3R1 and VDAC1/IP3R1 interactions (at right) in HuH7 cells transfected either with specific siRNA or transient expressing vectors during 48 h. Monitoring perturbation of ER-mitochondria interactions linked to genetic modulation of protein of the VDAC1/Grp75/IP3R1 complex by in situ PLA. Representative PLA images (at left, ×63 and scale bar = 20 μm) and quantitative analysis of both Grp75/IP3R1 and VDAC1/IP3R1 interactions (at right) in HuH7 cells transfected either with specific siRNA or transient expressing vectors during 48 h. Genetic invalidation of VDAC1 (A) and Grp75 (B) significantly reduce Grp75/IP3R1 as well as VDAC1/IP3R1 interactions. Transient overexpression of Grp75 significantly increases both Grp75/IP3R1 and VDAC1/IP3R1 interactions (C). Silencing of Mfn2 decreases both VDAC1/IP3R1 and Grp75/IP3R1 interactions (D), whereas overexpression of Mfn2 significantly increases them (E). Linker-mediated tethering between mitochondria and ER following rapamycin treatment (100 nmol/L, 2 min) induces VDAC1/IP3R1 interactions in HuH7 cells (F). *P < 0.05 vs. respective control. n = 3 independent experiments. Co, control. Emily Tubbs et al. Diabetes 2014;63:3279-3294 ©2014 by American Diabetes Association