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

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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 14-3-3 epsilon or 14-3-3 zeta 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
Publisher
NATURE PUBLISHING GROUP
Issue Date
2016-05
Language
English
Article Type
Article
Keywords

CONTROLLED TUMOR PROTEIN; MEDIATED PHOSPHORYLATION; GENE-EXPRESSION; CELL-GROWTH; TSC2; TARGET; GTPASE; AKT; 14-3-3-PROTEINS; ACTIVATION

Citation

NATURE COMMUNICATIONS, v.7

ISSN
2041-1723
DOI
10.1038/ncomms11501
URI
http://hdl.handle.net/10203/209319
Appears in Collection
BS-Journal Papers(저널논문)
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