# Molecular mechanisms driving cessation of neural crest migration and aggregation into cranial ganglia

> **NIH NIH F31** · CALIFORNIA INSTITUTE OF TECHNOLOGY · 2021 · $46,836

## Abstract

Proposal Summary
 Neural crest cells are an important stem-like cell population characterized by their multipotency and
migratory ability. Originating within the forming central nervous system, neural crest cells undergo a
spatiotemporally regulated epithelial-to-mesenchymal transition (EMT) to leave the neural tube and become
migratory. They then migrate extensively throughout the developing embryo, giving rise to a wide range of
derivatives as diverse as elements of the craniofacial skeleton and peripheral nervous system. In the post-
migratory phase, neural crest cells condense into different structures, a process that involves loss of migratory
characteristics, perhaps reflecting the reverse of the EMT process. While neural crest EMT has been studied
extensively, the mechanisms underlying the condensation of neural crest cells to form final derivatives is far less
well characterized. To address this knowledge gap, we propose to identify transcriptional changes that
occur during gangliogenesis with the goal of identifying those mediating alterations in intercellular
adhesion required for neural crest condensation into peripheral ganglia. Our hypothesis is that the gene
regulatory mechanisms that play a role during peripheral ganglion formation may reflect a reversal of the EMT
process. The goal is to uncover the molecular mechanisms that drive condensation of neural crest cells into
ganglia. These may in turn lead to clues regarding the underlying cause of certain types of neurocristopathies
like familial dysautonomia and neural crest-derived cancers like neuroblastoma and pheochromocytoma.
Aim 1: RNA-sequencing of pure populations of post-migratory cranial neural crest cells: RNA-sequencing
of isolated condensing cranial neural crest cells will allow us to identify novel transcription factors and adhesion
molecules that may drive neural crest condensation into cranial ganglia.
Aim 2: Functional analysis of genes selectively upregulated upon condensation to form ganglia:
Identified upregulated genes in condensing cranial neural crest cells will be validated by in situ hybridization and
Hybridization Chain Reaction. We will then perform systematic loss-of-function and ectopic expression
experiments on selected genes to examine their role in regulating condensation into and differentiation of
peripheral ganglia.
Aim 3: Characterization of cis-regulatory elements modulating gene expression during ganglion
condensation: To identify putative enhancers driving gene expression during cranial neural crest condensation,
we will perform ATAC-sequencing to identify conserved noncoding regions in the genome that are accessible to
transcription factors during cranial neural crest condensation.

## Key facts

- **NIH application ID:** 10309332
- **Project number:** 1F31DE031154-01
- **Recipient organization:** CALIFORNIA INSTITUTE OF TECHNOLOGY
- **Principal Investigator:** Hugo Alexander Urrutia
- **Activity code:** F31 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2021
- **Award amount:** $46,836
- **Award type:** 1
- **Project period:** 2021-07-01 → 2026-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10309332

## Citation

> US National Institutes of Health, RePORTER application 10309332, Molecular mechanisms driving cessation of neural crest migration and aggregation into cranial ganglia (1F31DE031154-01). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/10309332. Licensed CC0.

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