Project description:Genome-wide mapping of H3K4me1, H3K4me3 and H3K27ac in KP and DK ChIP-seq for H3K4me1, H3K4me3 and H3K27ac in KP and DK p63 profiling of DK through ChIP-seq
Project description:We have performed a transcriptome analysis of genes at three different ripening stages of the pink-white fruits and the ripe stage of the red fruits of Chinese bayberry. This analysis provided a total of 119,701 unigenes, of which 41.43% were annotated in the Nr database. Our results showed that the formation of the pink-white color in Chinese bayberry fruits depended on the anthocyanin metabolic pathway, regulated by MYB1. Downregulated expression of key anthocyanin biosynthetic pathway genes, such as UFGT, F3’H, and ANS at the late stage of fruits development compared with DK3 fruits resulted in the failure to form red fruits. Our findings shed light on the regulatory mechanisms and metabolic processes that control color development in the fruits of Chinese bayberry.
Project description:Diabetes mellitus (DM) is a complex metabolic disorder. Long-term hyperglycemia may induce diabetic keratopathy (DK), which is mainly characterized by delayed corneal epithelial regeneration. MicroRNAs (miRNAs) have been reported to play regulatory roles during tissue regeneration. However, the molecular mechanism by which miRNAs influence epithelial regeneration in DK is largely unknown. In this study, we performed miRNA and mRNA sequencing of regenerative corneal epithelium tissue from streptozotocin-induced type 1 diabetic (T1DM) and wild-type mice to screen for differentially expressed miRNAs and mRNAs. Based on regulatory network analysis, miR-223-5p was selected for subsequent experiments and Hpgds was then identified as a direct target gene. MiR-223-5p downregulation significantly promoted diabetic corneal epithelial wound healing and nerve regeneration. However, the beneficial effects of miR-223-5p inhibition were abolished by an Hpgds inhibitor. Furthermore, mechanistic studies demonstrated that miR-223-5p suppression ameliorated inflammation and enhanced cell proliferation signaling in DK. Taken together, our findings revealed that the regulatory role of miR-223-5p in diabetic corneal epithelial and nerve regeneration by mediating inflammatory processes and cell proliferation signaling. And silencing miR-223-5p may contribute to the development of potential therapeutic strategies for DK.
Project description:We generated dCas9-KRAB (dK) Tg mice and gRNA targeting Slc25a44 Tg mice. Slc25a44 knockdown mice were obtained by crossing these two Tg mice. Brown adipose tissue from Slc25a44 KD mice (dK+;gRNA+) and littermate control mice (either dK+ or gRNA+) were collected and subjected to transcriptome profiling by RNA-seq.