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

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.

journal_name

Nat Commun

journal_title

Nature communications

authors

Le TP,Vuong LT,Kim AR,Hsu YC,Choi KW

doi

10.1038/ncomms11501

subject

Has Abstract

pub_date

2016-05-06 00:00:00

pages

11501

issn

2041-1723

pii

ncomms11501

journal_volume

7

pub_type

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