# Gbx2 regulates the development of an atypical amacrine cell.

> **NIH NIH F32** · OREGON HEALTH & SCIENCE UNIVERSITY · 2020 · $69,306

## Abstract

PROJECT SUMMARY
 There are more than 100 distinct neuronal subtypes within the mammalian retina. Recent
studies have made significant progress in our understanding of how specific neuron subtypes
develop, wire into functional circuits, and contribute to disease. However, genetic tools to label and
manipulate single populations of neurons only exist for a small proportion of retinal neurons. Using a
genetic approach, I have identified a single population of retinal neurons based on their selective
expression of the transcription factor Gbx2. These cells are amacrine cells (ACs) and have several
interesting properties. Gbx2+ ACs do not express the inhibitory neurotransmitters, GABA or Glycine.
Rather, Gbx2+ ACs exhibit gap junction coupled connections to bipolar cells, suggesting that the
primary synaptic output for these ACs may be through electrical synapses. I will analyze the
development of Gbx2+ ACs to investigate the role of Gbx2 in their cellular identity, morphology, and
connectivity. In Aim 1, using a Gbx2 conditional knockout mouse, I will determine how Gbx2
regulates the morphology and electrical coupling of Gbx2+ ACs. I will also identify the specific
connexins that mediate electrical synapse formation in Gbx2+ ACs. In Aim 2, I will perform RNAseq
analyses in control and Gbx2 conditional knockout ACs to reveal their molecular profile and identify
the specific effectors of Gbx2. I will also test the hypothesis that Gbx2 functions as a terminal fate
selector to by regulating the expression of genes that endow Gbx2+ ACs with their unique
characteristics. My preliminary data indicate that this occurs in part through the regulation of Robo
receptors, which guide the proper stratification of Gbx2+ AC dendrites within the retina. This study will
provided a comprehensive analysis of the morphological and molecular properties of a previously
unidentified amacrine cell, and will elucidate how Gbx2 regulates the development and function of
these neurons. The results of this study will lead to the generation of genetic tools and targets that will
be useful for future investigations of retina development in health and disease.

## Key facts

- **NIH application ID:** 9931047
- **Project number:** 5F32EY029974-02
- **Recipient organization:** OREGON HEALTH & SCIENCE UNIVERSITY
- **Principal Investigator:** Patrick C Kerstein
- **Activity code:** F32 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $69,306
- **Award type:** 5
- **Project period:** 2019-07-01 → 2022-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9931047

## Citation

> US National Institutes of Health, RePORTER application 9931047, Gbx2 regulates the development of an atypical amacrine cell. (5F32EY029974-02). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/9931047. Licensed CC0.

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