Premium
Retinal regeneration in adult zebrafish requires regulation of TGFβ signaling
Author(s) -
Lenkowski Jenny R.,
Qin Zhao,
Sifuentes Christopher J.,
Thummel Ryan,
Soto Celina M.,
Moens Cecilia B.,
Raymond Pamela A.
Publication year - 2013
Publication title -
glia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.954
H-Index - 164
eISSN - 1098-1136
pISSN - 0894-1491
DOI - 10.1002/glia.22549
Subject(s) - zebrafish , muller glia , biology , retinal regeneration , retina , regeneration (biology) , microbiology and biotechnology , retinal , progenitor cell , neuroglia , neuroscience , stem cell , anatomy , central nervous system , genetics , biochemistry , gene
Müller glia are the resident radial glia in the vertebrate retina. The response of mammalian Müller glia to retinal damage often results in a glial scar and no functional replacement of lost neurons. Adult zebrafish Müller glia, in contrast, are considered tissue‐specific stem cells that can self‐renew and generate neurogenic progenitors to regenerate all retinal neurons after damage. Here, we demonstrate that regulation of TGFβ signaling by the corepressors Tgif1 and Six3b is critical for the proliferative response to photoreceptor destruction in the adult zebrafish retina. When function of these corepressors is disrupted, Müller glia and their progeny proliferate less, leading to a significant reduction in photoreceptor regeneration. Tgif1 expression and regulation of TGFβ signaling are implicated in the function of several types of stem cells, but this is the first demonstration that this regulatory network is necessary for regeneration of neurons. GLIA 2013;61:1687–1697