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. Author manuscript; available in PMC: 2023 Apr 25.
Published in final edited form as: Dev Cell. 2022 Apr 25;57(8):959–973.e7. doi: 10.1016/j.devcel.2022.03.017

Figure 6. Pdlim5 long and short variants regulate cytokinesis in hiPSC-cardiomyocytes.

Figure 6.

A. Quantification of relative expression levels of PDLIM5 long and short isoforms in WT and KO hiPSC-cardiomyocytes by qRT-PCR (n = 4 for WT groups, and 3 for KO groups). B. hiPSC-cardiomyocytes were infected with Ad-Pdlim5-long-mEGFP and Ad-Pdlim5-short-mEGFP and immunostained for GFP and alpha-actinin. White arrows indicate the accumulation of Pdlim5-short variants surrounding nuclei. Yellow arrows indicate Pdlim5 long and short isoforms colocalizing with alpha-actinin at Z-discs. Scale bar: 50 μm C. Quantification of AURKB-positive midbody frequency in WT and KO hiPSC-cardiomyocytes infected with Ad-mEGFP, Ad-Pdlim5-long-mEGFP and Ad-Pdlim5-short-mEGFP (n = 4–6 for WT or KO groups, average 300 cardiomyocytes per group). D. Schematic diagrams showing the function of RBPMS in cardiomyocyte proliferation and WT heart development (top), and loss of Rbpms causes cardiomyocyte binucleation and noncompaction cardiomyopathy (bottom). All data are presented as mean ± SEM.