Cardiomyocyte vulnerability to lamin polymer disruption revealed by saturation mutagenesis
Using saturation mutagenesis in human induced pluripotent cells and cardiomyocytes, this study reveals that LMNA mutations causing cardiomyopathy uniquely trigger profound protein loss and cellular toxicity in heart cells due to lamin polymer assembly defects, thereby explaining the tissue-specific vulnerability of cardiomyocytes in laminopathies.