ArticleJournal of cell science2022
Loss of Num1-mediated cortical dynein anchoring negatively impacts respiratory growth.
Article in Journal of cell science, 2022. 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed, 7 citations in OpenAlex.
- Mitochondrial anchor protein Num11 is key to pathogenicity ofVirulence · 2025Article
- Mitochondria-plasma membrane contact sites regulate the ER-mitochondria encounter structure.Journal of cell science · 2025Article
- A role for mitochondria-ER crosstalk in amyotrophic lateral sclerosis 8 pathogenesis.Life science alliance · 2025Article
- Mitochondria-ER-PM contacts regulate mitochondrial division and PI(4)P distribution.The Journal of cell biology · 2024Article
- Mitochondrial Protease Oct1p Regulates Mitochondrial Homeostasis and Influences Pathogenicity through Affecting Hyphal Growth and Biofilm Formation Activities inJournal of fungi (Basel, Switzerland) · 2024Article
- Temporal control of contact site formation reveals a relationship between mitochondrial division and Num1-mediated mitochondrial tethering.Molecular biology of the cell · 2023Article
- 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
8 authors at 3 institutions in 1 country.
Funding
Abstract
Num1 is a multifunctional protein that both tethers mitochondria to the plasma membrane and anchors dynein to the cell cortex during nuclear inheritance. Previous work has examined the impact loss of Num1-based mitochondrial tethering has on dynein function in Saccharomyces cerevisiae; here, we elucidate its impact on mitochondrial function. We find that like mitochondria, Num1 is regulated by changes in metabolic state, with the protein levels and cortical distribution of Num1 differing between fermentative and respiratory growth conditions. In cells lacking Num1, we observe a reproducible respiratory growth defect, suggesting a role for Num1 in not only maintaining mitochondrial morphology, but also function. A structure-function approach revealed that, unexpectedly, Num1-mediated cortical dynein anchoring is important for normal growth under respiratory conditions. The severe respiratory growth defect in Δnum1 cells is not specifically due to the canonical functions of dynein in nuclear migration but is dependent on the presence of dynein, as deletion of DYN1 in Δnum1 cells partially rescues respiratory growth. We hypothesize that misregulated dynein present in cells that lack Num1 negatively impacts mitochondrial function resulting in defects in respiratory growth.
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What OpenQuestion holds
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.