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Learn MoreWe sequenced mRNA from cardiomyocytes derived from hESCS in vitro. By using the Cas9n, we generated the QKI null hESCs. The gene expression level and alternative splicing events were compared between 4 control and 4 QkI KO samples. Here, we applied a widely used cardiomyocyte differentiation protocol that was reported to produce a population of more than 90% cardiac troponin T (TNNT2)-positive cardiomyocytes. And we are able to demonstrate that QKI is indespensible to cardiac sarcomerogenesis and cardiac function through its regulation of alternative splicing in genes involved in Z-disc formation, such as ACTN2, NEBL, ABLIM1, and PDLIM5. SOURCE: Weinian Shou (wshou@iu.edu) - Shou Indiana University
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