# Elucidating transcriptional mechanisms of motor neuron subtype specification

> **NIH NIH F31** · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · 2020 · $36,511

## Abstract

PROJECT SUMMARY
 Every movement requires fine control of the strength and speed of muscle contractions. The nervous
system achieves graded control of muscle by recruiting motor neuron (MN) subtypes with diverse functional
properties, such as target muscle fiber type, electrophysiology, or role in behavior. The functional diversity of
MNs is vital to locomotion, but we still lack a basic understanding of how it is created. During development, the
identity of MN subtypes is determined by transcriptional codes. We know much about how anatomical MN
subtypes defined by target muscle are specified, but the molecular logic by which functional MN subtypes
develop is practically unknown.
 Though anatomical MN subtypes are well segregated in tetrapods, functional subtypes are heavily
intermingled complicating their study. A model system where functional subtypes of MNs are segregated and
easily identifiable, like in the zebrafish, provides a unique opportunity to dissect their molecular determinants.
The zebrafish has three main functional subtypes of MNs responsible for slow, intermediate, and fast
swimming. These functional subtypes can be identified based on their soma position, muscle fiber type,
birthdate, recruitment order during swimming, and intrinsic properties.
 Through preliminary analysis, I have found two transcription factors, Evi1 and Prdm16, that are
expressed in clustered subpopulations of post-mitotic axial MNs in the zebrafish spinal cord. Evi1 and Prdm16
are known to be important for cell fate and subtype specification in other cell types, but have not yet been
studied in the spinal cord. Based on their expression pattern and preliminary behavioral data of mutant
animals, I hypothesize Evi1 and Prdm16 specify a functional subtype of MNs responsible for intermediate
speed swimming. In Aim 1, I will determine the MN subtype Evi1 and Prdm16 mark using histological
approaches and molecular analyses. In Aim 2, I will determine if Evi1 and Prdm16 specify subtype identity
using loss-of-function and gain-of-function methods. This project will elucidate the roles of Evi1 and Prdm16 in
MN specification and could reveal molecular mechanisms responsible for the determination of functional
properties.

## Key facts

- **NIH application ID:** 10004194
- **Project number:** 5F31NS110235-03
- **Recipient organization:** NEW YORK UNIVERSITY SCHOOL OF MEDICINE
- **Principal Investigator:** Kristen D'Elia
- **Activity code:** F31 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $36,511
- **Award type:** 5
- **Project period:** 2018-09-15 → 2021-09-14

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10004194

## Citation

> US National Institutes of Health, RePORTER application 10004194, Elucidating transcriptional mechanisms of motor neuron subtype specification (5F31NS110235-03). Retrieved via AI Analytics 2026-05-27 from https://api.ai-analytics.org/grant/nih/10004194. Licensed CC0.

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