ArticleBiochimica et biophysica acta. Molecular basis of disease2021
SUMOylation of mitofusins: A potential mechanism for perinuclear mitochondrial congression in cells treated with mitochondrial stressors.
Article in Biochimica et biophysica acta. Molecular basis of disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 15 citations in OpenAlex.
- Herpes simplex virus 1 subverts the mitochondrial network to support the infection: A lesson on mitochondrial versatility.bioRxiv : the preprint server for biology · 2026Article
- SUMOylation in Mitochondrial Quality Control: Mechanisms and Implications for Neurodegenerative Disease.Molecular neurobiology · 2026Review
- Reprogramming of bacterial virulence by lysine acetylation.Nature communications · 2026Article
- Organelle regulation of SUMOylation: regulatory mechanisms and therapeutic application.Journal of advanced research · 2026Review
- Hypoxia Affects Mitochondrial Stress and Facilitates Tumor Metastasis of Colorectal Cancer Through Slug SUMOylation.Current molecular medicine · 2025Article
- Host SUMOylation in bacterial infections and immune defense mechanisms.Frontiers in microbiology · 2025Review
- ULP-2 SUMO protease regulates UPRFree radical biology & medicine · 2024Article
- Mechanisms of Modulation of Mitochondrial Architecture.Biomolecules · 2023Review
- SUMOylation targeting mitophagy in cardiovascular diseases.Journal of molecular medicine (Berlin, Germany) · 2022Review
- SUMOylation and Major Depressive Disorder.International journal of molecular sciences · 2022Review
- Downregulation of SUMO2 inhibits hepatocellular carcinoma cell proliferation, migration and invasion.FEBS open bio · 2021Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Depolarized/damaged mitochondria aggregate at the perinuclear region prior to mitophagy in cells treated with mitochondrial stressors. However, the cellular mechanism(s) by which damaged mitochondria are transported and remain aggregated at the perinuclear region is unknown. Here, we demonstrate that mitofusins (Mfn1/2) are post-translationally modified by SUMO2 (Small Ubiquitin-related Modifier 2) in Human embryonic kidney 293 (Hek293) cells treated with protonophore CCCP and proteasome inhibitor MG132, both known mitochondrial stressors. SUMOylation of Mfn1/2 is not for their proteasomal degradation but facilitate mitochondrial congression at the perinuclear region in CCCP- and MG132-treated cells. Additionally, congressed mitochondria (mito-aggresomes) colocalize with LC3, ubiquitin, and SUMO2 in CCCP-treated cells. Knowing that SUMO functions as a "molecular glue" to facilitate protein-protein interactions, we propose that SUMOylation of Mfn1/2 may congress, glues, and confines damaged mitochondria to the perinuclear region thereby, protectively quarantining them from the heathy mitochondrial network until their removal via mitophagy in cells.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.