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MFF budding from mitochondria regulates melanosome size and maturation

ABSTRACT: Melanosomes are lysosome-related organelles that produce and accumulate melanin. Their biogenesis begins with the trafficking of melanogenic proteins from the endo-lysosomal system into non-pigmented vacuoles derived from endosomes. Subsequently, melanosome maturation is regulated by their association with mitochondria and requires the export and recycling of unneeded cargo via tubular carriers and fission, the mechanisms of which are unknown. Here we show that the outer mitochondrial membrane protein mitochondrial fission factor (MFF) is actively released from mitochondria to melanosomes. We found MFF on melanosomes at different stages of maturation and early melanosome fission sites. Upon downregulation of MFF, but not DRP1, early melanosomes enlarged, intracellular melanin accumulated and melanosome lumen catabolism increased. The MFF interactome in melanocytes posited a role for a complex network of cytoskeletal factors in its activity. Inhibition of actin nucleation was sufficient to restore the effects of MFF silencing on melanosomes. Our data unveil an extramitochondrial role for MFF in the regulation of melanosome morphology and maturation that, independently of DRP1, is supported by actin polymerization and nucleation factors.

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ORGANISM(S): Homo Sapiens (human) Mus Musculus (mouse)

TISSUE(S): Melanocyte, Cell Culture

SUBMITTER: Marta Giacomello

LAB HEAD: Marta Giacomello

PROVIDER: PXD052198 | Pride | 2026-03-20

REPOSITORIES: Pride

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Project description:Purpose:to verify Drp1-mediated biological pathways under physiological and ischemia conditions.Methods:C57BL/6 mice and Drp1 knockdown mice were used for ischemia treatment. Right femoral arteries were catheterized with polyethylene catheters for bleeding 50% of total blood volume (≈7% of weight). The ischemia time started to calculate after the model was established. A laparotomy was then carried out to obtain superior mesenteric artery tissues (SMAs) for transcriptome analysis. Series-Cluster analysis was performed to identify the global trends of mitochondrial DEGs after Drp1 knockdown. Gene ontology (GO) analysis was performed to facilitate elucidating the biological process (BP), molecular function (MF) and cellular component (CC) of unique genes in the significant or representative profiles. Results:In addition to its traditional roles in GTPase regulation and mitochondrial fission, Drp1 may also regulate actin cytoskeleton and the movement of microtubules. Besides, Drp1 may participate in the regulation of morphology and functions of other organelles, including endoplasmic reticulum, peroxisome, phagolysosome, etc. As for general organ functions, Drp1 may regulate vascular constriction and dilation. These consequences indicated the important role of Drp1 in ischemia-induced cellular regulation. Conclusions: Drp1 deficiency proves the important role of Drp1 in ischemia-induced biomedical processes through multiple potential fission-independent manners. Methods:C57BL/6 mice and Drp1 knockdown mice were used for ischemia treatment. Right femoral arteries were catheterized with polyethylene catheters for bleeding 50% of total blood volume (≈7% of weight). The ischemia time started to calculate after the model was established. A laparotomy was then carried out to obtain superior mesenteric artery tissues (SMAs) for transcriptome analysis. Series-Cluster analysis was performed to identify the global trends of mitochondrial DEGs after Drp1 knockdown. Gene ontology (GO) analysis was performed to facilitate elucidating the biological process (BP), molecular function (MF) and cellular component (CC) of unique genes in the significant or representative profiles. Results:In addition to its traditional roles in GTPase regulation and mitochondrial fission, Drp1 may also regulate actin cytoskeleton and the movement of microtubules. Besides, Drp1 may participate in the regulation of morphology and functions of other organelles, including endoplasmic reticulum, peroxisome, phagolysosome, etc. As for general organ functions, Drp1 may regulate vascular constriction and dilation. These consequences indicated the important role of Drp1 in ischemia-induced cellular regulation. Conclusions: Drp1 deficiency proves the important role of Drp1 in ischemia-induced biomedical processes through multiple potential fission-independent manners.

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MFF budding from mitochondria regulates melanosome size and maturation

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