Peroxiredoxin5 controls vertebrate ciliogenesis by modulating mitochondrial ROS
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- Peroxiredoxin5 controls vertebrate ciliogenesis by modulating mitochondrial ROS
- Ji, Yurim; Chae, Soomin; Lee, Hyun-Kyung; Park, Inji; Kim, Chowon; Ismail, Tayaba; Kim, Youni; Park, Jeen-Woo; Kwon, Oh-Shin; Kang, Beom-Sik; Lee, Dong-Seok; Bae, Jong-Sub; Kim, Sang-Hyun; Moon, Pyung-Gon; Baek, Moon-Chang; Park, Mae-Ja; Kil, In Sup; Rhee, Sue Goo; Kim, Joon; Huh, Yang Hoon; Shin, Jong-Yeon; Min, Kyoung-Jin; Kwon, Taeg Kyu; Jang, Dong Gil; Woo, Hyun Ae; Kwon, Taejoon; Park, Tae Joo; Lee, Hyun-Shik
- peroxiredoxin5; ROS; cilia; pyruvate kinase; mitochondria
- Issue Date
- MARY ANN LIEBERT INC
- ANTIOXIDANTS & REDOX SIGNALING, v., no., pp. -
- Aims: Peroxiredoxin5 (Prdx5) - a thioredoxin peroxidase is an antioxidant enzyme that is widely studied for its antioxidant properties and protective roles in neurological and cardiovascular disorders. The present study is aimed to investigate the functional significance of Prdx5 in mitochondria and to analyze its roles in ciliogenesis during the process of vertebrate development.
Results: We found that several Prdx genes were strongly expressed in multiciliated cells in developing Xenopus embryos, and their peroxidatic functions were crucial for normal cilia development. Depletion of Prdx5 increased levels of cellular ROS, consequently leading to mitochondrial dysfunction and abnormal cilia formation. Proteomic and transcriptomic approaches revealed that excessive ROS accumulation upon Prdx5 depletion subsequently reduced the expression level of pyruvate kinase (PK), a key metabolic enzyme in energy production. We further confirmed that the promotor activity of PK was significantly reduced upon Prdx5 depletion and that the reduction in PK expression and its promoter activity led to ciliary defects observed in Prdx5-depleted cells.
Innovation: Our data revealed the novel relationship between ROS and Prdx5 and the consequent effects of this interaction on vertebrate ciliogenesis. The normal process of ciliogenesis is interrupted by the Prdx5 depletion resulting in excessive ROS levels suggesting cilia as vulnerable targets of ROS.
Conclusion: Prdx5 play protective roles in mitochondria and is critical for normal cilia development by regulating the levels of ROS. The loss of Prdx5 is associated with excessive production of ROS resulting in mitochondrial dysfunction and aberrant ciliogenesis.
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