Opposing Actions of Fgf8a on Notch Signaling Distinguish Two Muller Glial Cell Populations that Contribute to Retina Growth and Regeneration

Publication date: 25 April 2017
Source:Cell Reports, Volume 19, Issue 4
Author(s): Jin Wan, Daniel Goldman
The teleost retina grows throughout life and exhibits a robust regenerative response following injury. Critical to both these events are Muller glia (or, Muller glial cells; MGs), which produce progenitors for retinal growth and repair. We report that Fgf8a may be an MG niche factor that acts through Notch signaling to regulate spontaneous and injury-dependent MG proliferation. Remarkably, forced Fgf8a expression inhibits Notch signaling and stimulates MG proliferation in young tissue but increases Notch signaling and suppresses MG proliferation in older tissue. Furthermore, cessation of Fgf8a signaling enhances MG proliferation in both young and old retinal tissue. Our study suggests that multiple MG populations contribute to retinal growth and regeneration, and it reveals a previously unappreciated role for Fgf8a and Notch signaling in regulating MG quiescence, activation, and proliferation.

Graphical abstract

Teaser

Muller glia contribute to growth and regeneration in the zebrafish retina. Wan and Goldman report that Fgf8a influences these processes by regulating Notch signaling. They identify an age-related change in Fgf8a-to-Notch signaling that suggests that multiple Muller glial cell populations contribute to spontaneous and injury-dependent proliferation of Muller glia.


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