Journal article

Conserved Tao Kinase Activity Regulates Dendritic Arborization, Cytoskeletal Dynamics, and Sensory Function in Drosophila

Chun Hu, Alexandros K Kanellopoulos, Melanie Richter, Meike Petersen, Anja Konietzny, Federico M Tenedini, Nina Hoyer, Lin Cheng, Carole LC Poon, Kieran F Harvey, Sabine Windhorst, Jay Z Parrish, Marina Mikhaylova, Claudia Bagni, Froylan Calderon de Anda, Peter Soba

JOURNAL OF NEUROSCIENCE | SOC NEUROSCIENCE | Published : 2020

Abstract

Dendritic arborization is highly regulated and requires tight control of dendritic growth, branching, cytoskeletal dynamics, and ion channel expression to ensure proper function. Abnormal dendritic development can result in altered network connectivity, which has been linked to neurodevelopmental disorders, including autism spectrum disorders (ASDs). How neuronal growth control programs tune dendritic arborization to ensure function is still not fully understood. Using Drosophila dendritic arborization (da) neurons as a model, we identified the conserved Ste20-like kinase Tao as a negative regulator of dendritic arborization. We show that Tao kinase activity regulates cytoskeletal dynamics a..

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Grants

Awarded by NCCR


Awarded by Deutsche Forschungsgemeinschaft Emmy-Noether Programm


Awarded by National Health and Medical Research Council of Australia


Awarded by National Institutes of Health National Institute of Neurological-Disorders and Sroke


Awarded by Deutsche Forschungsgemeinschaft


Awarded by EU Joint Programme-Neurodegenerative Disease Research (JPND) (Bundesministerium fur Bildung und Forschung)


Awarded by Landesforschungsforderung Hamburg


Awarded by ERA-NET NEURON (Bundesministerium fur Bildung und Forschung)


Awarded by Deutsche Forschungsgemeinschaft priority program SPP1926


Awarded by Bloomington Stock Center (National Institutes of Health)


Awarded by SNSF


Funding Acknowledgements

A.K.K. and C.B. were supported by NCCR Synapsy 51NF40-158776 and SNSF 310030_182651/1. A.K.K. was supported by the Autism Speaks Meixner Postdoctoral Fellowship and Fondation Sophie Afenduli. A.K. and M.M. were supported by Deutsche Forschungsgemeinschaft Emmy-Noether Programm Grants Ml 1923/1-1 and FOR2419 MI 1923/2-1. C.L.C.P. and K.F.H. were supported by National Health and Medical Research Council of Australia Project Grants APP1103604 and APP1142469. K.F.H. is a National Health and Medical Research Council Senior Research Fellow (APP1078220). J.Z.P. was supported by National Institutes of Health National Institute of Neurological-Disorders andSroke R01 NS076614. M.R. and F.C.d.A. were supported by Deutsche Forschungsgemeinschaft FOR 2419, CA1495/1-1, and CA 1495/4-1 and EU Joint Programme-Neurodegenerative Disease Research (JPND) (Bundesministerium fur Bildung und Forschung, ED1806). F.C.d.A. and P.S. were supported by Landesforschungsforderung Hamburg LFF-FV27 and ERA-NET NEURON (Bundesministerium fur Bildung und Forschung, 01EW1410). C.H. and P.S. weresupported by Deutsche Forschungsgemeinschaft priority program SPP1926 (SO1337/2-1).Stocks used in this study were obtained from the Bloomington Stock Center (National Institutes of Health P40OD018537). Wethank Buzz Baum for Tao plasmids; Ralf Pflanz for Taoantibody; Veit Riechmann for Taoeta and UAS-Tao-HA flies; Zuoren Wang for ppk26 antibody; and Vittoria Mariano and Yuening Li for sharing preliminary data.