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Regulatory role of Wdr24 in autophagy activity during zebrafish embryogenesis

Authors
  • Kim, Yong-Il1
  • Nam, In-Koo2
  • Um, Jae-Young3
  • Choe, Seong-Kyu1
  • 1 Wonkwang University School of Medicine, Department of Microbiology, Iksan, 54538, Republic of Korea , Iksan (South Korea)
  • 2 Gwangju Institute of Science & Technology, Department of Biomedical Science & Engineering, Institute of Integrated Technology, Gwangju, 61005, Republic of Korea , Gwangju (South Korea)
  • 3 Kyung Hee University, College of Korean Medicine, Basic Research Laboratory for Comorbidity Regulation, Graduate School, Seoul, 02447, Republic of Korea , Seoul (South Korea)
Type
Published Article
Journal
Molecular & Cellular Toxicology
Publisher
The Korean Society of Toxicogenomics and Toxicoproteomics
Publication Date
Dec 28, 2018
Volume
15
Issue
1
Pages
85–92
Identifiers
DOI: 10.1007/s13273-019-0010-3
Source
Springer Nature
Keywords
License
Yellow

Abstract

BackgroundsTOR and autophagy are essential pathways to mediate anabolic and catabolic reactions, respectively, in response to various nutritional stimuli. Vertebrate development requires such reactions to achieve the common goal of generating an independent organism from a single fertilized egg.MethodsUsing the zebrafish as an animal model, we characterized the role of Wdr24, a component of the GATOR2 complex that reportedly activates TORC1.ResultsSequence analysis and subcellular localization of zebrafish Wdr24 suggested functional resemblance to its mammalian counterpart. We found that wdr24 expression commences during early embryogenesis, implicating its requirement. Accordingly, wdr24 knockdown induced defective embryogenesis accompanied by massive cell death. The developmental defects induced by wdr24 knockdown were attributable, at least in part, to dysregulated autophagy, which could be partially restored by wdr24 overexpression.ConclusionThese findings suggest that a conserved role of Wdr24 may be a critical part of the cellular metabolism in different species.

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