14-3-3 proteins regulate Tctp–Rheb interaction for organ growth in Drosophila
Le, Thao Phuong
Vuong, Linh Thuong
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CitationLe, Thao Phuong, Linh Thuong Vuong, Ah-Ram Kim, Ya-Chieh Hsu, and Kwang-Wook Choi. 2016. “14-3-3 proteins regulate Tctp–Rheb interaction for organ growth in Drosophila.” Nature Communications 7 (1): 11501. doi:10.1038/ncomms11501. http://dx.doi.org/10.1038/ncomms11501.
Abstract14-3-3 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.
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