Related Experiment Video
Updated: Jun 25, 2026
08:43
Loss- and Gain-of-function Approach to Investigate Early Cell Fate Determinants in Preimplantation Mouse Embryos
Published on: June 6, 2016
Adaptive response in embryogenesis: vi. Comparative microarray analysis of gene expressions in mouse fetuses
1National Institute of Radiological Sciences, Anagawa, Inage-ku, Chiba, Japan.
International Journal of Radiation Biology
|February 12, 2009
Summary
Low-dose radiation exposure triggers a protective adaptive response (AR) in developing mouse fetuses. This study reveals molecular pathways, including p53 signaling, involved in this crucial radioresistance phenomenon.
Area of Science:
- Developmental Biology
- Radiation Biology
- Molecular Biology
Background:
- Sublethal ionizing radiation exposure can induce protective mechanisms against subsequent higher doses, a phenomenon known as radiation-induced adaptive response (AR).
- AR has been observed across various biological models, and its presence in mice during late organogenesis was previously established by our group.
- Understanding the molecular underpinnings of AR is crucial for assessing potential risks and benefits of radiation exposure during development.
Purpose of the Study:
- To investigate the molecular mechanisms responsible for radiation-induced adaptive response (AR) in mouse fetuses during late organogenesis.
- To identify specific gene modulations associated with AR in an in utero model.
- To explore the role of signal transduction and p53 pathways in AR induction.
Main Methods:
- Global transcriptome analysis using DNA microarrays was employed.
- Gene expression profiles were compared between adapted and non-adapted cells from whole mouse fetuses.
- Cells were collected following in utero exposure to a priming irradiation dose.
Main Results:
- AR-specific gene modulations were identified in the exposed mouse fetuses.
- Analysis suggested the involvement of signal transduction pathways in the adaptive response.
- Tumor protein (p53)-related pathways were implicated in the induction of AR.
Conclusions:
- The findings align with previous research indicating a dependence of AR on p53 activity.
- The identified gene modulations may influence subsequent fetal developmental processes.
- This study provides the first molecular-level report of AR-specific modulations in utero, offering a foundation for future research on AR and its potential long-term effects.
