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Gastrulation

Gastrulation

Gastrulation establishes the three primary tissues of an embryo: the ectoderm, mesoderm, and endoderm. This developmental process relies on a series of intricate cellular movements, which in humans transforms a flat, “bilaminar disc” composed of two cell sheets into a three-tiered structure. In the resulting embryo, the endoderm serves as the bottom layer, and stacked directly above it is the intermediate mesoderm, and then the uppermost ectoderm. Respectively, these tissue strata...

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Spatial Transcriptomics Analysis: Maternal Obesity Impairs Myogenic Cell Migration and Differentiation during

Yao Gao¹, Md Nazmul Hossain¹, Liang Zhao²

¹Nutrigenomics and Growth Biology Laboratory, Department of Animal Sciences, Washington State University, Pullman, WA 99164, USA.

International Journal of Molecular Sciences

|September 14, 2024

Summary

Maternal obesity (MO) hinders embryonic limb muscle development by impeding myogenic cell migration and differentiation. This study reveals MO

Keywords:

GeoMx spatial RNA sequencing cell migration embryonic myogenesis limb development maternal obesity

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Area of Science:

Developmental Biology
Reproductive Biology
Skeletal Muscle Physiology

Background:

Myogenic cell migration is crucial for embryonic limb muscle formation.
Maternal obesity (MO) is known to negatively impact prenatal skeletal muscle development.
The specific effects of MO on embryonic myogenic cell migration remain largely unexamined.

Purpose of the Study:

To investigate the impact of maternal obesity on myogenic cell migration during embryonic limb development.
To identify molecular pathways and genes affected by maternal obesity in migrating myogenic cells.

Main Methods:

Utilized C57BL/6 mouse embryos at embryonic day 13.5 (E13.5).
Employed the GeoMx DSP platform to analyze gene expression in specific regions of the embryonic limb.
Performed Gene Ontology (GO) enrichment analysis and analyzed signaling pathways.

Main Results:

Maternal obesity led to the down-regulation of 2224 genes in E13.5 embryonic limbs.
GO analysis indicated that MO inhibited crucial migration-related biological processes.
Key signaling pathways (HGF, FGF, Wnt, GTPase) and myogenic migration genes (Pax3, Gab1, Pxn, Tln2, Arpc) were suppressed in the MO group, particularly in the limb.
Myogenic differentiation genes were also down-regulated in MO limbs.

Conclusions:

Maternal obesity significantly impedes myogenic cell migration and differentiation in the developing embryonic limb.
This molecular disruption provides a mechanistic explanation for impaired fetal muscle development and potential long-term muscle function deficits in offspring of obese mothers.