Peroxiredoxin5 Controls Vertebrate Ciliogenesis by Modulating Mitochondrial Reactive Oxygen Species

Yurim Ji, Soomin Chae, Hyun Kyung Lee, Inji Park, Chowon Kim, Tayaba Ismail, Youni Kim, Jeen Woo Park, Oh Shin Kwon, Beom Sik Kang, Dong Seok Lee, Jong Sup Bae, Sang Hyun Kim, Pyung Gon Moon, Moon Chang Baek, Mae Ja Park, In Sup Kil, Sue Goo Rhee, Joon Kim, Yang Hoon HuhJong Yeon Shin, Kyoung Jin Min, Taeg Kyu Kwon, Dong Gil Jang, Hyun Ae Woo, Taejoon Kwon, Tae Joo Park, Hyun Shik Lee

Research output: Contribution to journalArticlepeer-review

9 Scopus citations


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. This study is aimed at investigating the functional significance of Prdx5 in mitochondria and at analyzing 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 reactive oxygen species (ROS), consequently leading to mitochondrial dysfunction and abnormal cilia formation. Proteomic and transcriptomic approaches revealed that excessive ROS accumulation on 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 on 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 and suggesting cilia as vulnerable targets of ROS. Conclusion: Prdx5 plays 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.

Original languageEnglish
Pages (from-to)1731-1745
Number of pages15
JournalAntioxidants and Redox Signaling
Issue number14
StatePublished - May 2019

Bibliographical note

Publisher Copyright:
© Copyright 2019, Mary Ann Liebert, Inc.


  • ROS
  • cilia
  • mitochondria
  • peroxiredoxin5
  • pyruvate kinase


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