ArticleScientific reports2017
ROS induced distribution of mitochondria to filopodia by Myo19 depends on a class specific tryptophan in the motor domain.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed.
- Mitochondria are absent from microglial processes performing surveillance, chemotaxis, and phagocytic engulfment.Nature communications · 2025Article
- Compositionally unique mitochondria in filopodia support cellular migration.Current biology : CB · 2025Article
- Mitochondrial fission process 1 protein: a comprehensive review of its core roles in mitochondrial dynamics, disease, and therapeutic targets.Frontiers in cell and developmental biology · 2025Review
- MYO19 is associated with tumor progression, immune evasion, ferroptosis-related signatures in lung squamous cell carcinoma.Frontiers in oncology · 2025Article
- Ceramide-mediated orchestration of oxidative stress response through filopodia-derived small extracellular vesicles.Journal of extracellular vesicles · 2024Article
- Compositionally unique mitochondria in filopodia support cellular migration.bioRxiv : the preprint server for biology · 2024Article
- Loss of Myo19 increases metastasis by enhancing microenvironmental ROS gradient and chemotaxis.EMBO reports · 2024Article
- The multiple links between actin and mitochondria.Nature reviews. Molecular cell biology · 2023Review
- Mitochondrial regulation of local supply of energy in neurons.Current opinion in neurobiology · 2023Review
- Myo19 tethers mitochondria to endoplasmic reticulum-associated actin to promote mitochondrial fission.Journal of cell science · 2023Article
- Ensembles of human myosin-19 bound to calmodulin and regulatory light chain RLC12B drive multimicron transport.The Journal of biological chemistry · 2023Article
- Mechanical instability generated by Myosin 19 contributes to mitochondria cristae architecture and OXPHOS.Nature communications · 2022Article
- Mitochondria-associated myosin 19 processively transports mitochondria on actin tracks in living cells.The Journal of biological chemistry · 2022Article
- Migrasomes: From Biogenesis, Release, Uptake, Rupture to Homeostasis and Diseases.Oxidative medicine and cellular longevity · 2022Review
- The asymmetric Pitx2 gene regulates gut muscular-lacteal development and protects against fatty liver disease.Cell reports · 2021Article
- 17q12 Recurrent Deletions and Duplications: Description of a Case Series with Neuropsychiatric Phenotype.Genes · 2021Article
- Motor proteins at the mitochondria-cytoskeleton interface.Journal of cell science · 2021Review
- The Functions, Methods, and Mobility of Mitochondrial Transfer Between Cells.Frontiers in oncology · 2021Review
- The MyMOMA domain of MYO19 encodes for distinct Miro-dependent and Miro-independent mechanisms of interaction with mitochondrial membranes.Cytoskeleton (Hoboken, N.J.) · 2020Article
- Altered mitochondrial trafficking as a novel mechanism of cancer metastasis.Cancer reports (Hoboken, N.J.) · 2020Review
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The role of the actin cytoskeleton in relation to mitochondria function and dynamics is only recently beginning to be recognized. Myo19 is an actin-based motor that is bound to the outer mitochondrial membrane and promotes the localization of mitochondria to filopodia in response to glucose starvation. However, how glucose starvation induces mitochondria localization to filopodia, what are the dynamics of this process and which enzymatic adaptation allows the translocation of mitochondria to filopodia are not known. Here we show that reactive oxygen species (ROS) mimic and mediate the glucose starvation induced phenotype. In addition, time-lapse fluorescent microscopy reveals that ROS-induced Myo19 motility is a highly dynamic process which is coupled to filopodia elongation and retraction. Interestingly, Myo19 motility is inhibited by back-to-consensus-mutation of a unique residue of class XIX myosins in the motor domain. Kinetic analysis of the purified mutant Myo19 motor domain reveals that the duty ratio (time spent strongly bound to actin) is highly compromised in comparison to that of the WT motor domain, indicating that Myo19 unique motor properties are necessary to propel mitochondria to filopodia tips. In summary, our study demonstrates the contribution of actin-based motility to the mitochondrial localization to filopodia by specific cellular cues.
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