Transcript expression profiles of stria vascularis in Mitf-m knockout mice

Objective: Mitf-m gene plays an important role in the development of cochlear stria vascularies. The mutation of Mitf-m gene can cause severe hearing loss, such as Wanderburg syndrome. However, the gene expression change caused by Mitf-m has not been systemically studied. In this paper, we studied the transcriptome of Mitf-m knockout mouse on cochlear stria vascularies. Methods: Total RNA extracted from the stria vascularies of the Mitf-m knockout mice (Mitf^{mi-ΔM/mi-ΔM}, MM group) and the wild type mice (Mitf-m^+/+, WW group) were used for RNA-Seq analysis. The clean reads were mapped to the reference sequence and cufflinks were used to evaluate the RNA sequencing results and gene expression. The program edgeR and DESeq were applied to identify the differentially expressed genes (DEGs). The down-regulated DEGs were further analyzed. Results: A total of 42,463,888 and 39,718,542 clean reads have been mapped to the reference sequence in the MM group and the WW group, respectively. For screening DEGs, 88.7% and 87.4% of the reads were uniquely mapped to the reference sequence suggesting a confidence of the RNA-Seq result. Out of the 45 DEGs, 7 genes were found to be up-regulated and 38 genes were down-regulated. GO enrichment analysis indicated that the down-regulated genes were mainly enriched in pigmentation, the melanin biosynthetic and metabolic process. In addition, these DEGs were involved with the inward rectifier potassium channel activity (Kcnj10 and Kcnj13). KEGG enrichment analysis showed that the down-regulated DEGs mainly enriched in melanogenesis pathways. Conclusion: Our data provide a large amount of useful information about mRNAs that are related in Mitf-m related pathways. The result will help researchers to further understand the functions of Mitf-m as a master regulator in more pathways, such as cell proliferation, DNA repair, cell cycle, apoptosis, proliferation, malanosome, and Na⁺/K⁺ iron pathway. Together, our data provide a novel insight for Mitf-m network function.