# Heat Shock Differentially Compromises Embryonic Development and Gene Expression in a Mouse Embryoid Body Model System

## TL;DR

This study uses mouse embryoid bodies to model how heat stress affects early embryo development, finding that heat shock delays gene expression and increases cell death.

## Contribution

The study introduces mouse embryoid bodies as a novel in vitro model to investigate heat stress effects on peri- and post-implantation embryo development.

## Key findings

- Heat shock delays the expression of germ layer marker genes in mouse embryoid bodies.
- Heat shock increases cell death and expression of heat shock proteins in mouse embryoid bodies.
- Mouse embryoid bodies closely mimic in vivo embryos in germ layer marker expression profiles.

## Abstract

High environmental temperatures can negatively affect embryo development in animals. In this study, we used mouse embryoid bodies (mEBs) grown from embryonic stem cells to model early embryo development in the laboratory. Mouse EBs developed in a way similar to real mouse embryos during the peri- and post-implantation stages. When exposed to heat shock (39 °C or 41 °C), mEBs showed delayed expression of key genes for the three germ layers and increased cell death. Heat shock also triggered the production of heat shock proteins, which help protect cells from heat stress. Mouse EBs can be used to study how heat stress affects early embryo development and may help improve animal reproduction under high-temperature conditions.

This study established an in vitro model to investigate peri- and post-implantation embryo development under heat shock conditions. In Experiment 1, we compared the gene expression profiles of the three germ layers in in vivo mouse embryos with those of mEBs derived from mouse embryonic stem cells. mEBs (Days 1–5) closely resembled developing E5.5–E6.5 embryos, expressing key germ layer markers: nestin (ectoderm), flk-1 (mesoderm), and ttr (endoderm). In Experiment 2, mEBs were randomly allocated to one of the following treatments: a control group (37 °C) or a heat shock group (39 °C or 41 °C) for 12 h or 24 h. Timing of germ layer marker expression, including ttr, was delayed by 1–2 days in the heat-shocked groups compared with the control group. Morphological analysis of mEBs revealed that the peripheral cell layer exhibited signs of disassembly or degeneration and became increasingly apoptotic under heat shock conditions. Additionally, these mEBs showed increased expression of heat shock proteins 70 and 72 in response to elevated temperatures and prolonged heat shock durations. Mouse EBs closely mimic in vivo-developing embryos in their germ layer marker expression profiles. In vitro heat shock delays germ layer marker gene expression and induces heat shock protein 72 expression in mEBs.