Defining the effects of Rpl3L-deficiency on transcriptional profiles of mouse hearts

The ribosomal protein L3-like (RPL3L) is a striated muscle-specific ribosomal protein, and mutations in human RPL3L are linked with childhood cardiomyopathy and age-related atrial fibrillation. However, the function served by this protein, a paralogue of the ubiquitously expressed RPL3 protein, remains poorly characterized in both heart and skeletal muscle. To address this, null mutant mice with the Rpl3L gene deleted were generated and studied. The purpose of this microarray analyses was to compare transcriptional profiles of the null mutant hearts (lacking RPL3L) with wild-type control hearts (expressing RpL3L). We used microarrays to elucidate effects of Rpl3L deficiency on transcriptional profile of mouse hearts Hearts were harvested from control and experimental mice on the C57/BL6 background. Total RNA was isolated using the Trizol protocol and submitted to Affymetrix Clariom S array pipeline after quality control analysis using Agilent 2100 Bioanalyzer.