# Determining how membrane fluidity regulates embryonic cell migration

> **NIH NIH R35** · JOHNS HOPKINS UNIVERSITY · 2024 · $409,375

## Abstract

PROJECT SUMMARY/ABSTRACT
 Cells first interact with their environment through the plasma membrane where diverse interactions
between lipids and proteins organize membrane complexes in response to external stimuli. One cellular
behavior in which membrane organization plays a critical role is cell migration, wherein cells traverse
complex three-dimensional landscapes to hone to new destinations. Cell migration events are at the root of
many processes including embryonic tissue morphogenesis, immune cell surveillance, and cancer cell
metastasis. Thus, a mechanistic understanding of how the plasma membrane is organized to orient cell migration
is necessary for our appreciation of the basic principles of cell migration and for the identification and treatment
of aberrant cell migration during human development and disease.
 While significant work has deciphered the adhesion, signaling, and mechanical proteins underlying
migratory behaviors, we know far less about how individual lipids, and the biophysical properties they contribute
to the membrane, regulate migratory behaviors. Research in our laboratory interrogates the role of lipid
metabolism in regulating cell signaling, in vivo migration, and membrane fluidity with the ultimate goal of
identifying new strategies to modulate aberrant cell migration during development and disease. We use the avian
neural crest cell population as an ideal in vivo model to address these previously inaccessible questions due to
their robust and synchronous migratory behavior, the ease by which they can be manipulated and visualized in
vivo and measured for biophysical properties.
 Under this award we will answer the questions 1) how does membrane fluidity orient in vivo cell migration,
and 2) how do cells regulate local membrane fluidity? We hypothesize that migrating cells undergo active lipid
metabolism at the plasma membrane to tune local membrane fluidity, and that the organization of relative fluidity
orients cell migration by positioning receptor proteins necessary for chemotaxis. We will test these hypotheses
using in vivo and ex vivo live cell imaging, optogenetic approaches to locally alter membrane fluidity and protein
localization, measuring transmembrane receptor protein diffusion rates, and performing targeted gene
knockdown and mis-localization experiments. These projects will yield high-impact discoveries that shed new
light on how to prevent cancer metastasis, improve wound healing and inflammation responses, and correct for
atypical tissue morphogenesis. In addition, these experiments will reveal new directions for our lab as we
continue to decipher how plasma membrane organization regulates cell signaling and migration.

## Key facts

- **NIH application ID:** 10940050
- **Project number:** 1R35GM155257-01
- **Recipient organization:** JOHNS HOPKINS UNIVERSITY
- **Principal Investigator:** Michael Louis Piacentino
- **Activity code:** R35 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2024
- **Award amount:** $409,375
- **Award type:** 1
- **Project period:** 2024-08-01 → 2029-07-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10940050

## Citation

> US National Institutes of Health, RePORTER application 10940050, Determining how membrane fluidity regulates embryonic cell migration (1R35GM155257-01). Retrieved via AI Analytics 2026-05-26 from https://api.ai-analytics.org/grant/nih/10940050. Licensed CC0.

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