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14-3-3 proteins regulate Tctp–Rheb interaction for organ growth in Drosophila

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  • Thao Phuong Le

    (Korea Advanced Institute of Science and Technology)

  • Linh Thuong Vuong

    (Korea Advanced Institute of Science and Technology
    Present address: Department of Developmental and Regenerative Biology and Graduate School of Biomedical Sciences, Icahn School of Medicine at Mount Sinai, New York, New York 10029, USA)

  • Ah-Ram Kim

    (Korea Advanced Institute of Science and Technology)

  • Ya-Chieh Hsu

    (Harvard University, Sherman Fairchild 358A)

  • Kwang-Wook Choi

    (Korea Advanced Institute of Science and Technology)

Abstract

14-3-3 family proteins regulate multiple signalling pathways. Understanding biological functions of 14-3-3 proteins has been limited by the functional redundancy of conserved isotypes. Here we provide evidence that 14-3-3 proteins regulate two interacting components of Tor signalling in Drosophila, translationally controlled tumour protein (Tctp) and Rheb GTPase. Single knockdown of 14-3-3ɛ or 14-3-3ζ isoform does not show obvious defects in organ development but causes synergistic genetic interaction with Tctp and Rheb to impair tissue growth. 14-3-3 proteins physically interact with Tctp and Rheb. Knockdown of both 14-3-3 isoforms abolishes the binding between Tctp and Rheb, disrupting organ development. Depletion of 14-3-3s also reduces the level of phosphorylated S6 kinase, phosphorylated Thor/4E-BP and cyclin E (CycE). Growth defects from knockdown of 14-3-3 and Tctp are suppressed by CycE overexpression. This study suggests a novel mechanism of Tor regulation mediated by 14-3-3 interaction with Tctp and Rheb.

Suggested Citation

  • Thao Phuong Le & Linh Thuong Vuong & Ah-Ram Kim & Ya-Chieh Hsu & Kwang-Wook Choi, 2016. "14-3-3 proteins regulate Tctp–Rheb interaction for organ growth in Drosophila," Nature Communications, Nature, vol. 7(1), pages 1-10, September.
    • Handle: RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms11501
    DOI: 10.1038/ncomms11501
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