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Light-mediated Reversible Modulation of the Mitogen-activated Protein Kinase Pathway during Cell Differentiation and Xenopus Embryonic Development
Published on: June 15, 2017
miR-3928 activates ATR pathway by targeting Dicer
Lei Chang1, Wentao Hu, Caiyong Ye
1Department of Space Radiobiology, Key Laboratory of Heavy Ion Radiation Biology and Medicine, Institute of Modern Physics, Chinese Academy of Sciences, Lanzhou, PR China.
RNA Biology
|August 28, 2012
Summary
This study reveals microRNA-3928 (miR-3928) regulates Dicer expression in response to ionizing radiation. MiR-3928 impacts DNA damage and cell cycle arrest via the ATR/Chk1 pathway.
Area of Science:
- Molecular Biology
- Cellular Biology
- Genetics
Background:
- MicroRNA (miRNA) expression changes under cellular stress, suggesting a role in stress response, but mechanisms remain unclear.
- Ionizing radiation is a significant exogenous stressor impacting cellular function and integrity.
Purpose of the Study:
- To elucidate the role and mechanism of miR-3928 in cellular response to ionizing radiation.
- To identify the regulatory network involving miR-3928 and its downstream targets.
Main Methods:
- Quantitative analysis of miR-3928 and Dicer expression in irradiated cells.
- Luciferase reporter assay to confirm direct binding of miR-3928 to Dicer mRNA.
- Assessment of DNA damage, ATR/Chk1 pathway activation, and cell cycle progression.
Main Results:
- miR-3928 expression increased and oscillated post-X-ray exposure, correlating with Dicer mRNA levels.
- miR-3928 directly targets Dicer mRNA, suppressing its expression and inhibiting miRNA maturation.
- Overexpression of miR-3928 induced DNA damage, activated ATR/Chk1, and caused G1 arrest.
Conclusions:
- miR-3928 is a key regulator in the cellular response to ionizing radiation.
- A novel miRNA regulatory network involving miR-3928, Dicer, and the ATR/Chk1 pathway is identified.
- miR-3928 plays a crucial role in managing Dicer expression and subsequent cellular stress responses.
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