# Regulation of interneuron formation in the developing retina

> **NIH NIH R01** · UNIVERSITY OF MICHIGAN AT ANN ARBOR · 2021 · $341,173

## Abstract

Abstract/Project Summary
 Retinal disease or injury leading to impaired vision or blindness are human health problems that reduce
quality of life, generating significant human and economic costs. Advances in gene therapy and stem cell
biology have made retinal repair a feasible goal. Nonetheless, rational repair strategies are constrained by
current knowledge of retinal biology and development. The complex cellular composition of the retina, like
other parts of the mammalian central nervous system, is an essential component of the retina’s functional
capabilities, yet remains incompletely understood. The mammalian retina includes more than 100 distinct types
of neurons. The generation of this cellular diversity during retinal development depends in part on sequential
cascades of transcriptional regulators as well as other factors. We found the miR-216b microRNA can
influence retinal development including the formation of amacrine and bipolar interneurons. We identified a
target gene for this microRNA, a transcriptional repressor in the forkhead family, Foxn3, that when inhibited
using RNAi or CRISPR in the developing retina increases amacrine cell formation, and when overexpressed
reduces amacrine cell formation. The target genes of Foxn3 during retinal development are not known. Here
we propose to identify mRNAs regulated by either loss or gain of Foxn3 function in the developing retina. We
will analyze changes in mRNA expression to identify the molecular pathways by which Foxn3 modulates retinal
cell fate decisions. In addition, we will identify genomic sites at which the Foxn3 protein binds in the developing
retina to find candidate target genes. We also propose to analyze retinal development in the absence of miR-
216b or the related miR-216a microRNA, to determine if these miRNAs are required for amacrine cell
differentiation or other functions, and to assess the function of two miR-216a/b genetic variants that may be
linked to retinal disease. These studies will provide new insights into the regulation of development and cell
determination in the mammalian retina. They are expected to provide information that may be relevant to
retinal disease and that may contribute to new strategies to repair retinal tissue.

## Key facts

- **NIH application ID:** 10295556
- **Project number:** 2R01EY024996-04A1
- **Recipient organization:** UNIVERSITY OF MICHIGAN AT ANN ARBOR
- **Principal Investigator:** DAVID L TURNER
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2021
- **Award amount:** $341,173
- **Award type:** 2
- **Project period:** 2016-02-01 → 2024-07-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10295556

## Citation

> US National Institutes of Health, RePORTER application 10295556, Regulation of interneuron formation in the developing retina (2R01EY024996-04A1). Retrieved via AI Analytics 2026-05-26 from https://api.ai-analytics.org/grant/nih/10295556. Licensed CC0.

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