# Role of Maturin in retinal development and homeostasis

> **NIH NIH R21** · UPSTATE MEDICAL UNIVERSITY · 2020 · $202,500

## Abstract

Project Summary
 Establishing and maintaining a postmitotic state is essential for normal development and organ function.
Cells that fail to exit, or reenter, the cell cycle commonly die or continue proliferating unchecked. Despite the
importance of these processes the mechanisms that drive cells into, and maintain them in, a non-proliferative
state are incompletely understood. The long-term goal of this research is to identify the mechanisms that
control these processes in the mammalian retina. The objectives of this application are to characterize a new
molecule we have identified that is implicated in maintaining postmitotic retinal cells in a non-proliferative state.
Our preliminary data support a central hypothesis that Maturin, regulates postnatal retinogenesis, and Maturin
loss is sufficient for differentiated retinal cells to reenter the cell cycle and generate additional retina. The
rationale for the proposed experiments is that that they will distinguish between two distinct models. Maturin
may be required 1) to prevent the production of excess retinal cells, or 2) for normal retina formation,
independent of proliferation. In Aim 1, morphometric analysis, flow cytometry and EdU labelling will determine
where defects are first detected, if and when retinal cell number is altered, and if cycling RPCs are observed
with retinal expansion. In Aim 2, we precisely define the temporal and spacial expression pattern to determine
which cell types express Maturin, and if that expression is restricted to postmitotic cells. In Aim 3, mice with
tamoxifen-inducible null alleles of Maturin will be used to determine precisely when Maturin loss triggers retinal
expansion. This work is significant, as Maturin may be required, independent of proliferation, for normal retina
development or maintenance. Alternatively, Maturin may control retina size by inhibiting reentry of retinal cells
into the cell cycle. This would be an exciting possibility as it would suggest inhibiting Maturin could potentially
reactivate retinogenesis in the mammalian eye. Therefore, this project perfectly fits within the NEI's audacious
goal to “Regenerate neurons and neural connections in the eye and visual system.”

## Key facts

- **NIH application ID:** 9999604
- **Project number:** 5R21EY030654-02
- **Recipient organization:** UPSTATE MEDICAL UNIVERSITY
- **Principal Investigator:** Michael E Zuber
- **Activity code:** R21 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $202,500
- **Award type:** 5
- **Project period:** 2019-09-01 → 2022-08-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9999604

## Citation

> US National Institutes of Health, RePORTER application 9999604, Role of Maturin in retinal development and homeostasis (5R21EY030654-02). Retrieved via AI Analytics 2026-05-22 from https://api.ai-analytics.org/grant/nih/9999604. Licensed CC0.

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