Project description:To study the function of Mettl3 during retinal development, we used Six3-Cre and Mettl3floxed mice to conditionally knock out Mettl3 from retinal progenitor cells. The mutant mice show defects in late-stage retinogenesis and structural and physiological homeostasis of the retina.
Project description:Mettl3 was conditionally knocked out from retinal progenitor cells. Metll3 deficient retinas exhibited disrupted cell cycle during late retinogenesis and abnormality in retinal architecture and physiology.
Project description:The purpose of this project is to explore the changes in signaling pathways after Mettl3 knockout, and to identify potential downstream target proteins of Mettl3 along with the signaling pathways they are involved in. Ultimately elucidating the molecular mechanisms underlying Mettl3 pathogenesis. Retina of control and Mettl3 knockout mice were collected, and samples were then used for proteomic analysis. After tissue collection, a series of cutting-edge technologies, including protein extraction, enzyme digestion, liquid chromatography-tandem mass spectrometry, and bioinformatics analysis, were employed to investigate the quantitative proteome of the samples.