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ULK1 negatively regulates Wnt signaling by phosphorylating Dishevelled

Hwang, Sun-Hong, Bang, Sunhoe, Kang, Kyung Shin, Kang, Deborah, Chung, Jongkyeong·2019·Biochemical and Biophysical Research Communications
DOI 10.1016/j.bbrc.2018.11.139
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Abstract

Wnt signaling pathway plays critical roles in body axes patterning, cell fate specification, cell proliferation, cell migration, stem cell maintenance, cancer development and etc. Deregulation of this pathway can be causative of cancer, metabolic disease and neurodegenerative disease such as Parkinson`s disease. Among the core components of Wnt signaling pathway, we discovered that Dishevelled (Dsh) interacts with ULK1 and is phosphorylated by ULK1. Unexpectedly, the knockdown of ULK1 elicited a marked increase in Wnt/β-catenin signaling. Multiple ULK1 phosphorylation sites existed on Dsh and many of them were located on the PDZ-DEP region. By using evolutionarily well conserved Drosophila Dsh, we found that S239, S247 and S254 in the PDZ-DEP region are involved in phosphorylation of Dsh by ULK1. Among these, S247 and S254 were conserved in human Dsh. When phospho-mimetic mutants (2D and 2E Dsh mutants) of these conserved residues were generated and expressed in the eyes of the fruit flies, the activity of Dsh was significantly decreased compared to wild type Dsh. Through additional alanine scanning, we further identified that S239, S247, S254, S266, S376, S554 and S555 on full length Dsh were phosphorylated by ULK1. In regards to the S266A mutation located in the PDZ domain among these phosphorylated residues, our results suggested that Dsh forms an SDS-resistant high molecular weight complex with β-catenin and TCF in the nucleus in an S266 phosphorylation-dependent manner.…

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Metadata

Authors
Hwang, S.-H., Bang, S., Kang, K. S., Kang, D., & Chung, J.
Venue
Biochemical and Biophysical Research Communications
Publisher
Elsevier BV
Published
2019-01
Volume
508
Issue
1
Pages
308-313
ISSN
0006-291X
DOI
10.1016/j.bbrc.2018.11.139
Cited by
13
References
2
Language
en
Licence
Funders
  • Ministry of Education
  • National Research Foundation of Korea
  • Ministry of Science, ICT and Future Planning
  • Ministry of Health and Welfare

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