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Rab38 and Rab32 control post-Golgi trafficking of melanogenic enzymes

Wasmeier, Christina, Romao, Maryse, Plowright, Lynn, Bennett, Dorothy C., Raposo, Graça, Seabra, Miguel C.·2006·The Journal of Cell Biology
DOI 10.1083/jcb.200606050PMC PMC2064568
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Abstract

Amutation in the small GTPase Rab38 gives rise to the mouse coat color phenotype “chocolate” (cht), implicating Rab38 in the regulation of melanogenesis. However, its role remains poorly characterized. We report that cht Rab38G19V is inactive and that the nearly normal pigmentation in cht melanocytes results from functional compensation by the closely related Rab32. In cht cells treated with Rab32-specific small interfering RNA, a dramatic loss of pigmentation is observed. In addition to mature melanosomes, Rab38 and Rab32 localize to perinuclear vesicles carrying tyrosinase and tyrosinase-related protein 1, consistent with a role in the intracellular sorting of these proteins. In Rab38/Rab32-deficient cells, tyrosinase appears to be mistargeted and degraded after exit from the trans-Golgi network (TGN). This suggests that Rab38 and Rab32 regulate a critical step in the trafficking of melanogenic enzymes, in particular, tyrosinase, from the TGN to melanosomes. This work identifies a key role for the Rab38/Rab32 subfamily of Rab proteins in the biogenesis of melanosomes and potentially other lysosome-related organelles.

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  • The phenotypes of rab32a and hps5 mutants suggest distinct contributions to crystal morphology and organelle maturation.

    “Notably, the phenotypes of rab32a and hps5 mutants suggest distinct contributions also to crystal morphology and organelle maturation, mirroring the specialized trafficking roles previously ascribed to these proteins in melanosomes (30, 41, 85, 90, 91).”

    From Lysosome-related organelles orchestrate guanine crystal formation in pigment cells (2026) · cites this paper as [41]

    The Results and Discussion describe Rab32/Rab38-dependent trafficking of melanogenic enzymes and a loss of mature, but not stage II, melanosomes in deficient cells. The Discussion also notes that different HPS mutants disrupt melanosome maturation at different stages. It does not examine rab32a or hps5 mutants, compare their phenotypes, or address crystal morphology; those specifics are not supported by this source. (LLM, conf=0.87)

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  • The partial reduction in crystal formation in rab32a and ap3m2 mutants is consistent with known redundancy and compensatory trafficking pathways in LRO biology.

    “The phenotypes we observed for rab32a and ap3m2 mutants show partial yet statistically significant reduction in crystal formation, a feature that is consistent with known redundancy and compensatory trafficking pathways in LRO biology (41, 48, 89).”

    From Lysosome-related organelles orchestrate guanine crystal formation in pigment cells (2026) · cites this paper as [41]

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Citations

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Metadata

Authors
Wasmeier, C., Romao, M., Plowright, L., Bennett, D. C., Raposo, G., & Seabra, M. C.
Affiliations
  • 1Molecular and Cellular Medicine, Division of Biomedical Sciences, Imperial College London, London SW7 2AZ, England, UK
  • 2Institut Curie, Centre National de la Recherche Scientifique, UMR144, Paris, Cedex 75005, France
  • 3Department of Basic Medical Sciences, St George's University of London, London SW17 0RE, England, UK
Venue
The Journal of Cell Biology
Publisher
Rockefeller University Press
Published
2006-10-16
Volume
175
Issue
2
Pages
271-281
ISSN
  • 1540-8140
  • 0021-9525
DOI
10.1083/jcb.200606050
PMC
PMC2064568
Cited by
275
References
2
Language
en

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