Effects on vesicular transport pathways at the late endosome in cells with limited very long-chain fatty acids

HANDLE オープンアクセス

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

  • Journal of Lipid Research

    Journal of Lipid Research 54 (3), 831-842, 2013-03

    American Society for Biochemistry and Molecular Biology

詳細情報 詳細情報について

  • CRID
    1050564288966732160
  • NII論文ID
    120005228358
  • HANDLE
    2115/52255
  • ISSN
    00222275
  • 本文言語コード
    en
  • 資料種別
    journal article
  • データソース種別
    • IRDB
    • CiNii Articles

問題の指摘

ページトップへ