# Molecular mechanisms initiating cell migrations in Caonorhabditis elegans

> **NIH NIH R01** · RBHS-ROBERT WOOD JOHNSON MEDICAL SCHOOL · 2020 · $337,428

## Abstract

Molecular mechanisms initiating cell migrations
Project Summary/Abstract
The process by which extracellular signals act through receptors at the plasma membrane to
influence cell function is a fundamental requirement for life. Cytoskeletal elements, including
branched actin, transmit signals throughout the cell. When branched actin is not properly
polarized this can result in serious health problems like defective neuronal development or
cancer metastases. We study how the actin cytoskeleton interprets extracellular signals to
carry out polarized functions, including polarized cell migrations and polarized intracellular
trafficking. We established a genetically amenable system in which signaling to specific
tissues can be analyzed. Our system also identifies the relevant signals that promote specific
developmental processes, uncovers novel components contributing to the propagation of the
signal, and uses live imaging to provide insights into the cell biology controlled by the signals.
Previously we identified and characterized three signals that pattern membrane recruitment
of the GTPase Rac1/CED-10, which in turn recruit the branched actin regulator WAVE/Scar
to regulate the dynamics of F-actin during a cell migration. Now we are ready to address:
1) How does branched actin promote the Cadherin trafficking that sets up proper apical/basal
polarity? 2) Which Rac GEF(s) specifically convert signals received by the epidermis into
epidermal motility cues? 3) How does branched-actin-dependent adhesion support tissue-
tissue movements? Clinical relevance: The human homolog of one of the genes we study
in C. elegans, WAVE3, is considered a biomarker for high grade, triple negative breast
cancer (Kulkarni et al., 2012) and is associated with invasive prostate and colon cancers
(Fernando et al., 2010; Zhang et al., 2012). Understanding the signals that regulate actin
dynamics through the WAVE/Scar complex during cell migrations will suggest new
biomarkers for altered actin regulation in human disease.

## Key facts

- **NIH application ID:** 10072777
- **Project number:** 2R01GM081670-10A1
- **Recipient organization:** RBHS-ROBERT WOOD JOHNSON MEDICAL SCHOOL
- **Principal Investigator:** Martha C. Soto
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $337,428
- **Award type:** 2
- **Project period:** 2009-07-15 → 2024-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10072777

## Citation

> US National Institutes of Health, RePORTER application 10072777, Molecular mechanisms initiating cell migrations in Caonorhabditis elegans (2R01GM081670-10A1). Retrieved via AI Analytics 2026-05-21 from https://api.ai-analytics.org/grant/nih/10072777. Licensed CC0.

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