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核糖体蛋白L3样蛋白（ribosomal protein L3-like，RPL3L）是一类横纹肌特异性核糖体蛋白，人类RPL3L的突变与儿童心肌病及年龄相关性心房颤动密切相关。作为普遍表达的核糖体蛋白RPL3的旁系同源蛋白（paralogue），该蛋白在心脏与骨骼肌中的功能仍未得到充分解析。为填补这一研究空白，本研究构建并研究了Rpl3L基因敲除的纯合突变小鼠（null mutant mice）。本次基因芯片分析（microarray analyses）旨在对比Rpl3L缺失突变小鼠心脏（不表达RPL3L）与野生型对照心脏（wild-type control hearts）的转录组谱（transcriptional profiles），以阐明Rpl3L缺失对小鼠心脏转录组谱的调控效应。