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

Thao Phuong Le, Linh Thuong Vuong, Ah-Ram Kim, Ya-Chieh Hsu and Kwang-Wook Choi ()
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Thao Phuong Le: Korea Advanced Institute of Science and Technology
Linh Thuong Vuong: Korea Advanced Institute of Science and Technology
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

Nature Communications, 2016, vol. 7, issue 1, 1-10

Abstract: 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.

Date: 2016
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DOI: 10.1038/ncomms11501

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