Project description:In mammals, retinal damage is followed by Müller glia cell activation and proliferation. While retinal gliosis persists in adult mammals after an insult or disease, some vertebrates, including zebrafish, have the capacity to regenerate. We believe we are the first group to show that gliosis is a fibrotic-like process in mammals’ eyes caused by differential activation of canonical and non-canonical TGFβ signaling pathways.
Project description:By removing MLL1 from mouse retinal progenitors, we discovered that MLL1 plays multiplex roles in retinal development by regulating: 1) progenitor cell proliferation and cell cycle progression; 2) retinal cell composition; 3) maintenance of horizontal neurons; 4) formation of functional synapses between neuronal layers; and 5) visual function development. Altogether, our results suggest that MLL1 is an indispensable regulator for the development of retinal structure and function.