The GTPase-deficient Rab27A(Q78L) mutant inhibits melanosome transport in melanocytes through Trapping of Rab27A effector protein Slac2-a/Melanophilin in their cytosol: Development of a novel melanosome-targeting tag

Morié Ishida, Saki P. Arai, Norihiko Ohbayashi, Mitsunori Fukuda

    Research output: Contribution to journalArticlepeer-review

    9 Citations (Scopus)

    Abstract

    Background: A GTPase-deficient Rab27A(Q78L) mutation caused perinuclear melanosome aggregation by an unknown mechanism. Results: Forcible targeting of Rab27A(Q78L) to melanosomes by a novel melanosome-targeting tag restored peripheral melanosome distribution in Rab27A-deficient cells. Conclusion: The GTPase activity of Rab27A is required for its melanosome localization, not for melanosome transport. Significance: These findings provide new insights into the mechanism underlying the spatiotemporal regulation of Rab27A activity.

    Original languageEnglish
    Pages (from-to)11059-11067
    Number of pages9
    JournalJournal of Biological Chemistry
    Volume289
    Issue number16
    DOIs
    Publication statusPublished - 2014 Apr 18

    ASJC Scopus subject areas

    • Biochemistry
    • Molecular Biology
    • Cell Biology

    Fingerprint

    Dive into the research topics of 'The GTPase-deficient Rab27A(Q78L) mutant inhibits melanosome transport in melanocytes through Trapping of Rab27A effector protein Slac2-a/Melanophilin in their cytosol: Development of a novel melanosome-targeting tag'. Together they form a unique fingerprint.

    Cite this