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- Title
Role of the Drosophila YATA protein in the proper subcellular localization of COPI revealed by in vivo analysis.
- Authors
Maiko Saito; Minoru Nakayama; Kyota Fujita; Atsuko Uchida; Hiroyuki Yano; Satoshi Goto; Hitoshi Okazawa; Masaki Sone
- Abstract
yata mutants of Drosophila melanogaster exhibit phenotypes including progressive brain shrinkage, developmental abnormalities and shortened lifespan, whereas in mammals, null mutations of the yata ortholog Scyl1 result in motor neuron degeneration. yata mutation also causes defects in the anterograde intracellular trafficking of a subset of proteins including APPL, which is the Drosophila ortholog of mammalian APP, a causative molecule in Alzheimer's disease. SCYL1 binds and regulates the function of coat protein complex I (COPI) in secretory vesicles. Here, we reveal a role for the Drosophila YATA protein in the proper localization of COPI. Immunohistochemical analyses performed using confocal microscopy and structured illumination microscopy showed that YATA colocalizes with COPI and GM130, a cis-Golgi marker. Analyses using transgenically expressed YATA with a modified N-terminal sequence revealed that the N-terminal portion of YATA is required for the proper subcellular localization of YATA. Analysis using transgenically expressed YATA proteins in which the C-terminal sequence was modified revealed a function for the C-terminal portion of YATA in the subcellular localization of COPI. Notably, when YATA was mislocalized, it also caused the mislocalization of COPI, indicating that YATA plays a role in directing COPI to the proper subcellular site. Moreover, when both YATA and COPI were mislocalized, the staining pattern of GM130 revealed Golgi with abnormal elongated shapes. Thus, our in vivo data indicate that YATA plays a role in the proper subcellular localization of COPI.
- Subjects
DROSOPHILA; MOTOR neuron diseases; DROSOPHILA melanogaster; SECRETORY granules; MOTOR neurons; HUMAN abnormalities
- Publication
Genes & Genetic Systems, 2020, Vol 95, Issue 6, p303
- ISSN
1341-7568
- Publication type
Article
- DOI
10.1266/ggs.20-00027