Rps19bp1 cKO Xmlc2Cre E11.5 mouse heart RNAseq

This study investigates the transcriptomic consequences of cardiomyocyte-specific deletion of Rps19bp1 during mouse embryonic development. Rps19bp1 encodes AROS (Active Regulator of SIRT1), a known negative regulator of p53. To understand its role in cardiac development and cell cycle regulation, we performed RNA sequencing (RNA-seq) on ventricular heart tissues from E11.5 embryos of Rps19bp1 conditional knockout (cKO) mice and littermate controls. The data reveal widespread gene expression changes and activation of p53 signaling in Rps19bp1-deficient hearts, providing mechanistic insights into how Rps19bp1 modulates cardiomyocyte proliferation and embryonic heart morphogenesis. Overall design: Rps19bp1 floxed mice (Rps19bp1 fl/fl) were crossed with Xmlc2-Cre mice to generate cardiomyocyte-specific knockout animals (Rps19bp1 fl/fl; Xmlc2-Cre +/-). Embryos were harvested at embryonic day 11.5 (E11.5). Ventricular heart tissues were dissected under a stereomicroscope, and total RNA was extracted using TRIzol reagent. RNA integrity was confirmed using Agilent Bioanalyzer prior to library preparation. Four biological replicates were collected for each genotype (cKO and control). Libraries were prepared using the Illumina TruSeq stranded mRNA kit and sequenced on the Illumina HiSeq 6000 platform to a depth of ~30 million paired-end reads per sample.