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Kctd10 regulates heart morphogenesis by repressing the transcriptional activity of Tbx5a in zebrafish

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  • Xiangjun Tong

    (Key Laboratory of Cell Proliferation and Differentiation of Ministry of Education, College of Life Sciences, Peking University)

  • Yao Zu

    (Key Laboratory of Cell Proliferation and Differentiation of Ministry of Education, College of Life Sciences, Peking University)

  • Zengpeng Li

    (State Key Laboratory Breeding Base of Marine Genetic Resources, Third Institute of Oceanography, State Oceanic Administration)

  • Wenyuan Li

    (Key Laboratory of Cell Proliferation and Differentiation of Ministry of Education, College of Life Sciences, Peking University)

  • Lingxiao Ying

    (Key Laboratory of Cell Proliferation and Differentiation of Ministry of Education, College of Life Sciences, Peking University)

  • Jing Yang

    (Key Laboratory of Cell Proliferation and Differentiation of Ministry of Education, College of Life Sciences, Peking University)

  • Xin Wang

    (Key Laboratory of Cell Proliferation and Differentiation of Ministry of Education, College of Life Sciences, Peking University)

  • Shuonan He

    (Key Laboratory of Cell Proliferation and Differentiation of Ministry of Education, College of Life Sciences, Peking University)

  • Da Liu

    (Key Laboratory of Cell Proliferation and Differentiation of Ministry of Education, College of Life Sciences, Peking University)

  • Zuoyan Zhu

    (Key Laboratory of Cell Proliferation and Differentiation of Ministry of Education, College of Life Sciences, Peking University)

  • Jianming Chen

    (State Key Laboratory Breeding Base of Marine Genetic Resources, Third Institute of Oceanography, State Oceanic Administration)

  • Shuo Lin

    (Cell and Developmental Biology, University of California Los Angeles)

  • Bo Zhang

    (Key Laboratory of Cell Proliferation and Differentiation of Ministry of Education, College of Life Sciences, Peking University)

Abstract

The T-box transcription factor Tbx5 (Tbx5a in zebrafish) plays a crucial role in the formation of cardiac chambers in a dose-dependent manner. Its deregulation leads to congenital heart disease. However, little is known regarding its regulation. Here we isolate a zebrafish mutant with heart malformations, called 34c. The affected gene is identified as kctd10, a member of the potassium channel tetramerization domain (KCTD)-containing family. In the mutant, the expressions of the atrioventricular canal marker genes, such as tbx2b, hyaluronan synthase 2 (has2), notch1b and bmp4, are changed. The knockdown of tbx5 rescues the ectopic expression of has2, and knockdown of either tbx5a or has2 alleviates the heart defects. We show that Kctd10 directly binds to Tbx5 to repress its transcriptional activity. Our results reveal a new essential factor for cardiac development and suggest that KCTD10 could be considered as a new causative gene of congenital heart disease.

Suggested Citation

  • Xiangjun Tong & Yao Zu & Zengpeng Li & Wenyuan Li & Lingxiao Ying & Jing Yang & Xin Wang & Shuonan He & Da Liu & Zuoyan Zhu & Jianming Chen & Shuo Lin & Bo Zhang, 2014. "Kctd10 regulates heart morphogenesis by repressing the transcriptional activity of Tbx5a in zebrafish," Nature Communications, Nature, vol. 5(1), pages 1-10, May.
    • Handle: RePEc:nat:natcom:v:5:y:2014:i:1:d:10.1038_ncomms4153
    DOI: 10.1038/ncomms4153
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