Extended Data Fig. 3: Validation of the mouse models for MARK4 selective expression in either haematopoietic cells or cardiomyocytes.
From: MARK4 controls ischaemic heart failure through microtubule detyrosination
a, b, Confirmation of MARK4 deficiency in CD45+ cells of chimeric wild-type mice reconstituted with bone marrow (BM) cells from Mark4−/− mice (strategy is shown in Extended Data Fig. 1c). a, Representative image with arrows pointing to CD45+ cells in the infarct area. Scale bars, 20 μm (a). b, Quantification of the percentage of MARK4+ cells (green) within CD45+ cells (red). n = 3 mice per group. c, Confirmation of Mark4 deletion in cardiomyocytes (strategy is shown in Extended Data Fig. 1d). Real-time PCR of Mark4 level in primary cardiomyocytes isolated from Myh6-mcm+/−;Mark4fl/fl (also known as αMHC-mcm+/−;Mark4fl/fl) (n = 4) and control mice (n = 3) at day 7 after the last tamoxifen injection. d, Assessment of LVEF of a different group (compared with Fig. 2e) of Mark4 cKO and control mice (n = 6 per group) at day 1 after myocardial infarction. e, Infarct size at 24 h after myocardial infarction (n = 6 per group). Scale bar, 2 mm. b–e, Data are mean ± s.e.m.; two-tailed unpaired t-test; P values are indicated.
