# Planar Polarity Mechanisms in Mammalian Inner Ear Development

> **NIH NIH R01** · UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH · 2024 · $494,020

## Abstract

Project Summary:
In the vestibular system of the inner ear, motion is detected via the mechanical deflection of a bundle of
stereocilia located at the top of sensory receptor hair cells. The bundle is morphologically and physiologically
polarized because only movements of the bundle towards a lone kinocilium positioned at one side of the apical
cell surface are able to produce excitatory responses to acceleration or gravity. Thus, the range of motion that
can be detected by an individual hair cell is determined by the polarized orientation of the stereociliary bundle.
The utricle and saccule contain thousands of vestibular hair cells that detect linear accelerations which are
divided between two groups that have opposite stereociliary bundle orientations and therefore respond to motion
in opposite directions. These two groups of hair cells meet at a cellular junction that anatomically divides the
utricle and saccule called the Line of Polarity Reversal (LPR).
Our goal is to identify the cellular and molecular mechanisms that direct the development of planar polarity and
the LPR, and underlie the formation of a sensory representation of gravity and acceleration in the mouse utricle
and saccule. This will be addressed throughout the course of the project using a combination of knockout and
transgenic mouse models, molecular genetic approaches to evaluate the transcriptional regulation of an
essential regulatory kinase called STK32A, and biochemical and proteomics approaches to identify STK32A
substrates. Specifically, we will test the hypothesis that patterns of Stk32a gene expression are determined by
the transcription factor EMX2, and that STK32A guides stereociliary bundle orientation in hair cells that do not
express EMX2. STK32A is a dark kinase with previously unknown function, which my lab has recently shown to
be necessary and sufficient to determine stereociliary bundle orientation. This effort is significant and innovative
because it introduces post-translational modification by kinase signaling as a new regulatory mechanism guiding
hair cell planar polarity, and because it focuses on the EMX2-negative hair cells that were previously excluded
from studies, including my own, that focused specifically on EMX2. Although directed towards the development
of vestibular planar polarity, we anticipate that this research will impact our understanding of auditory planar
polarity as well as other organ systems that rely upon cellular polarization for growth or function.

## Key facts

- **NIH application ID:** 10882625
- **Project number:** 2R01DC013066-12A1
- **Recipient organization:** UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH
- **Principal Investigator:** MICHAEL R DEANS
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2024
- **Award amount:** $494,020
- **Award type:** 2
- **Project period:** 2013-03-25 → 2025-01-15

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10882625

## Citation

> US National Institutes of Health, RePORTER application 10882625, Planar Polarity Mechanisms in Mammalian Inner Ear Development (2R01DC013066-12A1). Retrieved via AI Analytics 2026-05-27 from https://api.ai-analytics.org/grant/nih/10882625. Licensed CC0.

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