ArticleMolecular biology of the cell2023
Temporal control of contact site formation reveals a relationship between mitochondrial division and Num1-mediated mitochondrial tethering.
Article in Molecular biology of the cell, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
7 citing papers in PubMed, 8 citations in OpenAlex.
- The power of connections: Recent advances in understanding the regulation of mitochondrial dynamics by membrane contact sites.Current opinion in cell biology · 2025Review
- Emerging Approaches for Studying Lipid Dynamics, Metabolism, and Interactions in Cells.Annual review of biochemistry · 2025Review
- Mitochondria-plasma membrane contact sites regulate the ER-mitochondria encounter structure.Journal of cell science · 2025Article
- The photosensitive endoplasmic reticulum-chloroplast contact site.Journal of microscopy · 2025Article
- Significantly reduced, but balanced, rates of mitochondrial fission and fusion are sufficient to maintain the integrity of yeast mitochondrial DNA.Molecular biology of the cell · 2024Article
- Mitochondria-ER-PM contacts regulate mitochondrial division and PI(4)P distribution.The Journal of cell biology · 2024Article
- Mitochondria-Plasma Membrane Contact Sites: Emerging Regulators of Mitochondrial Form and Function.Contact (Thousand Oaks (Ventura County, Calif.))Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Mitochondrial division is critical for maintenance of mitochondrial morphology and cellular homeostasis. Previous studies have suggested that the mitochondria-ER-cortex anchor (MECA), a tripartite membrane contact site between mitochondria, the ER, and the plasma membrane, is involved in mitochondrial division. However, its role is poorly understood. We developed a system to control MECA formation and depletion, which allowed us to investigate the relationship between MECA-mediated contact sites and mitochondrial division. Num1 is the protein that mediates mitochondria-ER-plasma membrane tethering at MECA sites. Using both rapamycin-inducible dimerization and auxin-inducible degradation components coupled with Num1, we developed systems to temporally control the formation and depletion of the native contact site. Additionally, we designed a regulatable Num1-independant mitochondria-PM tether. We found that mitochondria-PM tethering alone is not sufficient to rescue mitochondrial division and that a specific feature of Num1-mediated tethering is required. This study demonstrates the utility of systems that regulate contact-site formation and depletion in studying the biological functions of membrane contact sites.
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Registered trials
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.