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. Author manuscript; available in PMC: 2019 Jan 11.
Published in final edited form as: Nature. 2018 Jul 25;560(7717):198–203. doi: 10.1038/s41586-018-0372-z

Extended Data Fig. 7 ~. CMPK2 deficiency does not affect inflammasome subunit expression nor NLRP3 activator-induced mitochondrial damage.

Extended Data Fig. 7 ~

a, Immunoblot analysis of pro-IL-1β, NLRP3, ASC, pro-Casp1 and NEK7 in the lysates of wild-type (shCtrl) and CMPK2-deficient (shCmpk2) BMDMs before and after LPS priming. Results are typical of three separate experiments. b, NLRP3 activator-induced changes in Ψm in LPS-primed shCtrl and shCmpk2 BMDMs were measured by TMRM fluorescence. Data are mean ± s.d. (n = 3 biological replicates). c, Relative amounts of mtROS measured by MitoSOX fluorescence in LPS-primed shCtrl and shCmpk2 BMDMs after stimulation with the indicated NLRP3 activators. Data are mean ± s.d. (n = 3 biological replicates). d, Representative fluorescent microscopy images of EdU-labelled wild-type BMDMs transduced with either shCtrl-or shCmpk2-encoding lentiviruses that were stimulated with or without LPS (200 ng ml−1) for 6 h. Scale bars, 5 μm. e, Percentages of cells with mtDNA replication as determined in d. Data are mean ± s.d. (n = 3 different microscopic fields per group; original magnification, ×40). f, Relative amounts of total mtDNA in wild-type and Irf1−/− BMDMs before and after treatments with the indicated TLR agonists. Data are mean ± s.d. (n = 3 biological replicates). g, Relative amounts of total mtDNA in shCtrl-or shCmpk2-encoding lentivirus-transduced wild-type BMDMs before and after treatments with the indicated TLR agonists. Data are mean ± s.d. (n = 3 biological replicates). *P < 0.05; **P < 0.01; ***P < 0.001; two-sided unpaired t-test.