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AIMP3 Deletion Induces Acute Radiation Syndrome-like Phenotype in Mice
Doyeun Kim1, Sunmi Kim2, Youngsun Oh1
1Medicinal Bioconvergence Research Center, College of Pharmacy, Seoul National University, Seoul, Korea.
Abstract:
Genomes are mostly protected from constant DNA-damaging threats, either internal or external, which ultimately sustain the organism. Herein, we report that AIMP3, a previously demonstrated tumour suppressor, plays an essential role in maintaining genome integrity in adult mice. Upon induction of the temporal systemic deletion of AIMP3 by tamoxifen in adult mice, the animals developed an acute radiation syndrome-like phenotype, typified by scleroderma, hypotrophy of haematopoietic cells and organs, and intestinal failure. Induction of γH2AX, an early marker of DNA double-strand breaks, was observed in the spleen, intestine, and the highly replicating embryonic cortex. In addition, sub-lethal irradiation of AIMP3 mKO mice dramatically affected organ damage and survival. Using isolated MEFs from conditional KO mice or AIMP3 knockdown cells, we confirmed the presence of spontaneously occurring DNA double-strand breaks by COMET assay and γH2AX induction. Furthermore, γH2AX removal was delayed, and homologous DNA repair activity was significantly reduced. Reduction of RPA foci formation and subsequent Rad51 foci formation probably underlie the significant reduction in homologous recombination activity in the absence of AIMP3. Together, our data demonstrate that AIMP3 plays a role in genome stability through the DNA repair process.
Insights
The tumor suppressor AIMP3 is crucial for maintaining genome integrity in adult mice. Its absence leads to DNA damage and radiation-like symptoms, highlighting AIMP3
Area of Science:
- Genetics
- Molecular Biology
- Cell Biology
Background:
- Genomes face constant DNA damage threats.
- AIMP3 is a known tumor suppressor.
- Maintaining genome integrity is vital for organism survival.
Purpose of the Study:
- To investigate the role of AIMP3 in maintaining genome integrity in adult mice.
- To understand the consequences of AIMP3 deletion on DNA repair and organism health.
Main Methods:
- Temporal systemic deletion of AIMP3 in adult mice using tamoxifen.
- Induction of DNA double-strand breaks marker γH2AX.
- Sub-lethal irradiation of AIMP3 knockout mice.
- Analysis of DNA repair in AIMP3-deficient cells (MEFs, knockdown cells) using COMET assay, γH2AX removal assessment, RPA, and Rad51 foci formation.
Main Results:
- AIMP3 deletion induced an acute radiation syndrome-like phenotype, including scleroderma, organ atrophy, and intestinal failure.
- Increased DNA double-strand breaks (γH2AX induction) were observed in multiple tissues.
- AIMP3 deficiency impaired DNA repair, evidenced by delayed γH2AX removal and reduced homologous recombination activity.
- Reduced RPA and Rad51 foci formation indicated compromised DNA repair pathways.
Conclusions:
- AIMP3 plays an essential role in maintaining genome stability in adult mice.
- AIMP3 is critical for efficient DNA double-strand break repair, particularly homologous recombination.
- AIMP3 deficiency significantly impacts organismal health and survival due to impaired genome maintenance.
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