Transcriptional changes of adipocyte-deletion of Prmt5 in white adipocytes

Adipose tissue (AT) is a crucial regulator of systemic energy homeostasis, and its dysfunction can lead to insulin resistance and other metabolic complications. Protein arginine methyltransferase 5 (PRMT5) catalyzes symmetrical dimethylation of arginine residues to modulate protein stability and function. Here, we explore the function of PRMT5 in AT through RNA sequencing of wildtype and Prmt5 knockout (Prmt5AKO) mice. Our results demonstrate that Prmt5AKO alters the expression of genes related to metabolism and membrane transport. Specifically, Prmt5AKO induces genes enriched in glucose transport and glycolysis pathways, while suppressing genes encoding fatty acid (FA) transporters. Overall design: RNA-seq profiling of epididymal white adipose tissue (eWAT) from wild-type (WT) and Prmt5 knockout (KO) mice.

脂肪组织（Adipose Tissue, AT）是调控全身能量稳态的关键组织，其功能异常可诱发胰岛素抵抗及其他代谢并发症。蛋白质精氨酸甲基转移酶5（Protein arginine methyltransferase 5, PRMT5）能够催化精氨酸残基发生对称二甲基化修饰，进而调控蛋白质的稳定性与功能。本研究通过对野生型（Wild-Type, WT）与Prmt5基因敲除（Prmt5 knockout, Prmt5AKO）小鼠开展RNA测序，探究了PRMT5在脂肪组织中的生物学功能。实验结果表明，Prmt5AKO可改变代谢与膜转运相关基因的表达谱：具体而言，Prmt5AKO可上调富集于葡萄糖转运与糖酵解通路的基因，同时下调编码脂肪酸（FA）转运蛋白的基因。实验整体设计：对野生型与Prmt5基因敲除（Knockout, KO）小鼠的附睾白色脂肪组织（epididymal white adipose tissue, eWAT）进行RNA-seq表达谱分析。