Journal article

A Hippo-like Signaling Pathway Controls Tracheal Morphogenesis in Drosophila melanogaster

Carole LC Poon, Weijie Liu, Yanjun Song, Marta Gomez, Yavuz Kulaberoglu, Xiaomeng Zhang, Wenjian Xu, Alexey Veraksa, Alexander Hergovich, Amin Ghabrial, Kieran F Harvey

DEVELOPMENTAL CELL | CELL PRESS | Published : 2018

Abstract

Hippo-like pathways are ancient signaling modules first identified in yeasts. The best-defined metazoan module forms the core of the Hippo pathway, which regulates organ size and cell fate. Hippo-like kinase modules consist of a Sterile 20-like kinase, an NDR kinase, and non-catalytic protein scaffolds. In the Hippo pathway, the upstream kinase Hippo can be activated by another kinase, Tao-1. Here, we delineate a related Hippo-like signaling module that Tao-1 regulates to control tracheal morphogenesis in Drosophila melanogaster. Tao-1 activates the Sterile 20-like kinase GckIII by phosphorylating its activation loop, a mode of regulation that is conserved in humans. Tao-1 and GckIII act ups..

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Grants

Awarded by National Health and Medical Research Council


Awarded by National Institutes of Health


Awarded by National Health and Medical Research Council of Australia


Awarded by American Cancer Society (ACS)


Awarded by Wellcome Trust


Awarded by BBSRC


Awarded by NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES


Funding Acknowledgements

We thank P. Adler, V. Riechmann, N. Tapon, E. Knust, the Vienna Drosophila RNAi Center, the Australian Drosophila Research Support Facility (www.ozdros.com), the Bloomington Drosophila Stock Center, and the Developmental Studies Hybridoma Bank for D. melanogaster stocks and antibodies. We thank the Centre for Advanced Histology and Microscopy at the Peter MacCallum Cancer Centre. H. Zhao provided help with SAINT analysis. K.F.H. is a National Health and Medical Research Council Senior Research Fellow (1078220). A. V. was supported by a grant from the National Institutes of Health (GM123136). Y.K. was sponsored by the Ministry of National Education (The Republic of Turkey). This research was supported by the Peter MacCallum Cancer Foundation and grants from the National Health and Medical Research Council of Australia (K.F.H. - 1032251 and C.L.C.P. - 1142469), the Company of Biologists (Development Journal) Travelling Fellowship (C.L.C.P.) (Harvey laboratory), the National Institutes of Health (1R01GM089782), the American Cancer Society (ACS) (RSG 124720) (Ghabrial laboratory), the Wellcome Trust (090090/Z/09/Z), and BBSRC (BB/I021248/1) (Hergovich laboratory).