m6A mosaics: transcriptional regulation of developing cardiomyocytes

This thesis investigates new therapeutic strategies for heart disease by exploring early cardiac development. Cardiomyocytes, the heart’s contractile cells, lose their ability to repair themselves after birth, leading to permanent damage after injury. This research focuses on the molecular modification m6A, which acts as a switch to regulate gene activity during heart development. The study demonstrates that m6A is essential for forming heart cells, and disruptions in its regulation can lead to abnormal development. Additionally, the thesis identifies a novel RNA molecule unique to humans, which plays a key role in heart formation without producing protein. This RNA is modified by m6A and is activated alongside a key cardiogenic transcription factor during cardiac differentiation. These findings suggest that the RNA and m6A play a significant role in regulating heart cell formation and that targeting these pathways may offer new treatment strategies for repairing damaged heart tissue in heart disease patients.