Several studies indicate that the TGFβ signaling pathway plays an important role in regulating proliferation of progenitors and cell differentiation during mammalian retinal development and zebrafish retinal regeneration. We are using chemical genetics and genetic approaches in zebrafish to manipulate TGFβ signaling in order to study how the signaling pathway regulates the cell cycle and cell differentiation during retinal development, which has not yet been described, and regeneration of the adult retina. Specifically, TGFβ signaling has been shown to promote Müller glial cell fate, inhibit proliferation, and increase differentiation into photoreceptors during rodent retinal development, and in the regenerating adult zebrafish retina, proliferation and regeneration are impaired when canonical TGFβ signaling is mis-regulated. Our preliminary studies of retinal development in zebrafish using fluorescence immunohistochemistry suggest that the CMZ may be expanded when TGFβ signaling is inhibited. In the adult damaged retina, the initial damage response by Müller glia is extremely similar between mammals and zebrafish, but the zebrafish is able to achieve robust regeneration of destroyed neurons while mammals are limited. In the zebrafish retina, Müller glial cells respond to damage by dedifferentiating and generating a neurogenic progenitor that goes on to regenerate lost neurons. Ongoing experiments are clarifying whether manipulating TGFβ signaling in the adult zebrafish retina promotes a more mammalian-like response to acute retinal injury.