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Updated: Mar 12, 2026

Author Spotlight: A Selective Luciferase-Based Assay for Monitoring ATG4B 27 Activity in Cells
Published on: June 30, 2023
RecQL4 regulates autophagy and apoptosis in U2OS cells
1a Key Laboratory of Genomic and Precision Medicine, China Gastrointestinal Cancer Research Center, Beijing Institute of Genomics, Chinese Academy of Sciences, Beijing, China; University of Chinese Academy of Sciences, Beijing, China.
Abstract:
RecQL4, one of the 5 human RecQ helicases, is a key mediator of genomic stability and its deficiency can cause premature aging phenotypes. Here, by using CRISPR/Cas and RNAi technology, we demonstrated that autophagy level was elevated in both RecQL4 knockdown and knockout cells compared with those of the control cells. Surprisingly, mitochondrial content was increased and LC3 co-localization with mitochondria was partially lost in RecQL4 knockout cells compared with the control cells, suggesting that RecQL4 deficiency impaired mitophagic processes in U2OS cells. Furthermore, we found that knockout of RecQL4 destabilized PINK1. In addition, RecQL4 knockout cells were more susceptible to apoptosis under mitochondrial stress than the control cells. In conclusion, our findings indicated a novel role of RecQL4 in the regulation of autophagy/mitophagy in U2OS cells.
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