Effects on vesicular transport pathways at the late endosome in cells with limited very long-chain fatty acids
抄録
Very long-chain fatty acids (VLCFAs), fatty acids with chain length of > 20, possess a wide range of biological functions. However, their roles at the molecular level remain largely unknown. In the presented study, we screened for multicopy suppressors that rescued temperature-sensitive growth of VLCFA-limited yeast cells, and identified the VPS21 gene, encoding a Rab GTPase, as such a suppressor. When the vps21Δ mutation was introduced into a deletion mutant of the SUR4 gene, which encodes a VLCFA elongase, a synthetic growth defect was observed. Endosome-mediated vesicular trafficking pathways, including endocytosis and the CPY pathway, were severely impaired in sur4Δ vps21Δ double mutants, while the AP-3 pathway that bypasses the endosome was unaffected. In addition, the sur4Δ mutant also exhibited a synthetic growth defect when combined with the deletion of VPS3, which encodes a subunit of the CORVET (class C core vacuole/endosome tethering) complex that tethers transport vesicles to the late endosome/multivesicular body (MVB). These results suggest that requirement of VLCFAs is especially high in the endosomal pathways, of all the intracellular trafficking pathways.
収録刊行物
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- Journal of Lipid Research
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Journal of Lipid Research 54 (3), 831-842, 2013-03
American Society for Biochemistry and Molecular Biology
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詳細情報 詳細情報について
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- CRID
- 1050564288966732160
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- NII論文ID
- 120005228358
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- HANDLE
- 2115/52255
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- ISSN
- 00222275
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- 本文言語コード
- en
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- 資料種別
- journal article
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- データソース種別
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- IRDB
- CiNii Articles