# Diversity Supplement (Pilar Andrade) for Molecular Basis of Outer Retina Development and Repair

> **NIH NIH R01** · BAYLOR COLLEGE OF MEDICINE · 2021 · $72,198

## Abstract

PROJECT SUMMARY
Vision begins when light detecting photoreceptors in the outer retina sense and respond to visual input and
relay this information to interneurons. Both the development of these connections and their long-term integrity
must be precisely regulated in space and time to ensure visual information is correctly relayed. Understanding
the mechanisms that coordinate these events is central to understanding the basis of many visual diseases.
We have identified that the serine-threonine kinase LKB1 is differentially required for the emergence and long-
term fidelity of the outer retina. Our preliminary evidence suggests that deletion of LKB1 during development
inhibits outer retina synaptic formation, while deletion in adulthood causes premature synaptic decline. We are
therefore extremely interested to understand how LKB1 orchestrates these distinct processes at both the
cellular and molecular level. Our preliminary evidence suggests that the cells and signaling pathways that
initiate and regulate these events are independent. Adults require LKB1 signaling in rods to ensure the
organization of their synapses, while development of the outer retina requires LKB1 driven extension of cone
axons. Moreover, LKB1 signals through district pathways to mediate these events: in adults LKB1 controls
synaptic fidelity through the AMP activated kinase AMKP, while LKB1 functions independently of AMPK in
development. Our first Aim will determine the precise cellular requirement for LKB1 in the outer retina during
development and adulthood using cell-specific knockout mice, live imaging, and single cell reconstruction. We
will also interrogate the impact of outer retina defects on the molecular organization the synapses that reside
there using 3D nanoscopic imaging techniques. Our second aim will determine the mechanism by which LKB1
functions using genetic analyses of LKB1-kinase pathways and cell-specific transcriptional approaches. Finally,
we will test whether manipulating AMPK or other targets can prevent or reverse visual decline. These studies
will lead to the identification of novel molecular pathways for manipulating retina circuits that may ultimately be
useful for repairing them.

## Key facts

- **NIH application ID:** 10428900
- **Project number:** 3R01EY030458-03S1
- **Recipient organization:** BAYLOR COLLEGE OF MEDICINE
- **Principal Investigator:** Melanie A Samuel
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2021
- **Award amount:** $72,198
- **Award type:** 3
- **Project period:** 2019-09-01 → 2024-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10428900

## Citation

> US National Institutes of Health, RePORTER application 10428900, Diversity Supplement (Pilar Andrade) for Molecular Basis of Outer Retina Development and Repair (3R01EY030458-03S1). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/10428900. Licensed CC0.

---

*[NIH grants dataset](/datasets/nih-grants) · CC0 1.0*