AIMP3 Deletion Induces Acute Radiation Syndrome-like Phenotype in Mice

Doyeun Kim, Sunmi Kim, Youngsun Oh, Songhwa Park, Yoon Jeon, Hongtae Kim, Ho Lee, Sunghoon Kim

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8 Citations (Scopus)


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.

Original languageEnglish
Article number15025
JournalScientific reports
Issue number1
Publication statusPublished - 2018 Dec 1

Bibliographical note

Funding Information:
This work was supported by the Global Frontier Project grant (NRF-M3A6A4-2010-0029785) of National Research Foundation funded by the Ministry of Science and ICT (MSIT) of Korea. We wish to express thanks to the staff and crew of the Seoul National University AMS Facility(NCIRF) for their untiring efforts and perseverance.

Publisher Copyright:
© 2018, The Author(s).

All Science Journal Classification (ASJC) codes

  • General


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