Transcription of the SCL/TAL1 interrupting Locus (Stil) is required for cell proliferation in adult Zebrafish Retinas

Lei Sun; Ping Li; Aprell L Carr; Ryne Gorsuch; Clare Yarka; Jingling Li; Michael Bartlett; Delaney Pfister; David R Hyde; Lei Li

doi:10.1074/jbc.M113.506295

Transcription of the SCL/TAL1 interrupting Locus (Stil) is required for cell proliferation in adult Zebrafish Retinas

J Biol Chem. 2014 Mar 7;289(10):6934-6940. doi: 10.1074/jbc.M113.506295. Epub 2014 Jan 27.

Authors

Affiliations

¹ Department of Biological Sciences, University of Notre Dame, Notre Dame, Indiana 46556; Department of Physiology, Nankai University, Tianjin, China 370001.
² Department of Biological Sciences, University of Notre Dame, Notre Dame, Indiana 46556.
³ Department of Biological Sciences, University of Notre Dame, Notre Dame, Indiana 46556; Center for Zebrafish Research, University of Notre Dame, Notre Dame, Indiana 46556.
⁴ Department of Biological Sciences, University of Notre Dame, Notre Dame, Indiana 46556; Center for Zebrafish Research, University of Notre Dame, Notre Dame, Indiana 46556. Electronic address: Li.78@nd.edu.

Abstract

The human oncogene SCL/TAL1 interrupting locus (Stil) is highly conserved in vertebrate species. Previously, we identified a homolog of the Stil gene in zebrafish mutant (night blindness b, nbb), which showed neural defects in the retina (e.g. dopaminergic cell degeneration and/or lack of regeneration). In this research, we examined the roles of Stil in cell proliferation after degeneration in adult zebrafish retinas. We demonstrated that knockdown of Stil gene expression or inhibition of Sonic hedgehog (Shh) signaling transduction decreases the rate of cell proliferation. In contrast, activation of Shh signal transduction promotes cell proliferation. In nbb(+/-) retinas, inhibition of SUFU (a repressor in the Shh pathway) rescues the defects in cell proliferation due to down-regulation of Stil gene expression. The latter data suggest that Stil play a role in cell proliferation through the Shh signal transduction pathway.

Keywords: Cell Proliferation; Neurons; Oncogene; Retina; Zebrafish.

Publication types

Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't

MeSH terms

Animals
Basic Helix-Loop-Helix Transcription Factors / genetics
Basic Helix-Loop-Helix Transcription Factors / physiology*
Cell Proliferation*
Ependymoglial Cells / drug effects
Ependymoglial Cells / metabolism
Ependymoglial Cells / pathology
Gene Expression
Gene Knockdown Techniques
Hedgehog Proteins / genetics
Hedgehog Proteins / metabolism*
Oxidopamine / pharmacology
Proto-Oncogene Proteins / genetics
Proto-Oncogene Proteins / physiology*
Repressor Proteins / genetics
Retina / drug effects
Retina / metabolism
Retina / pathology*
Retinal Degeneration / chemically induced
Retinal Degeneration / pathology
Retinal Rod Photoreceptor Cells / drug effects
Retinal Rod Photoreceptor Cells / metabolism
Retinal Rod Photoreceptor Cells / pathology
Signal Transduction
T-Cell Acute Lymphocytic Leukemia Protein 1
Zebrafish / genetics
Zebrafish / metabolism*
Zebrafish Proteins / genetics
Zebrafish Proteins / metabolism*
Zebrafish Proteins / physiology*

Substances

Basic Helix-Loop-Helix Transcription Factors
Hedgehog Proteins
Proto-Oncogene Proteins
Repressor Proteins
Shha protein, zebrafish
Sufu protein, zebrafish
T-Cell Acute Lymphocytic Leukemia Protein 1
Zebrafish Proteins
tal1 protein, zebrafish
Oxidopamine

Abstract

Publication types

MeSH terms

Substances

Grants and funding