# Dynamics of FGF and its integration with other pathways during human germ layer differentiation

> **NIH NIH F32** · UNIVERSITY OF MICHIGAN AT ANN ARBOR · 2022 · $78,550

## Abstract

Abstract
Gastrulation is the stage of early embryonic development during which the body plan is
established. Using the mouse as a model, it has been established that mammalian gastrulation
is primarily regulated by BMP, FGF, WNT, and NODAL signaling pathways and disruption of these
pathways can lead to developmental defects or early embryonic lethality which ay infest as
infertility. However, it remains unclear how cells interpret multiple signaling pathways to make
specific cell fate decisions. Moreover, findings in mice cannot directly be compare to human
development. For example, disruption of FGF signaling at blastocyst stage leads to defects in
visceral endoderm development in mice but not in human. Human pluripotent stem cells (hPSCs)
have been an ideal model system to study gastrulation because they mimic many aspects of
gastrulation and allow for high throughput, quantitative analysis and time resolved experiments in
vitro. Using micropatterned hPSC gastrulation model and directed primitive streak like cell
differentiation model, my data suggests that higher FGF/ERK signaling activity is spatially
restricted to PSLCs and functional experiments that block FGF signaling results in a failure of
PSLC differentiation as well as downregulation of WNT3 ligand expression. Based on this, my
overarching hypothesis is that FGF/ERK signaling is spatially and temporally regulated by
expression of FGF ligands and heparin sulfate proteogylcan (HSPG) modulators and act in
parallel to BMP upstream of WNT and NODAL to create combined signaling patterns that induce
different cell fate outcome. I will test this hypothesis by 1) determining how FGF activity is
spactially and temporally regulated by FGF ligands and HSPG modulators, 2) dissecting the
dynamics of multiple signaling activity underlying cell fate acquisition during in vitro gastrulation.

## Key facts

- **NIH application ID:** 10465300
- **Project number:** 1F32HD108980-01
- **Recipient organization:** UNIVERSITY OF MICHIGAN AT ANN ARBOR
- **Principal Investigator:** Kyoung Ha Jo
- **Activity code:** F32 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2022
- **Award amount:** $78,550
- **Award type:** 1
- **Project period:** 2022-07-01 → 2024-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10465300

## Citation

> US National Institutes of Health, RePORTER application 10465300, Dynamics of FGF and its integration with other pathways during human germ layer differentiation (1F32HD108980-01). Retrieved via AI Analytics 2026-05-22 from https://api.ai-analytics.org/grant/nih/10465300. Licensed CC0.

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