ArticleDevelopmental cell2016
Polo Kinase Phosphorylates Miro to Control ER-Mitochondria Contact Sites and Mitochondrial Ca(2+) Homeostasis in Neural Stem Cell Development.
Article in Developmental cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers, 2 of them syntheses that pooled it.
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
71 citing papers in PubMed, 2 syntheses or guidelines pooled it, 111 citations in OpenAlex.
- MAM kinases: physiological roles, related diseases, and therapeutic perspectives-a systematic review.Cellular & molecular biology letters · 2025Pooled it
- Inter-organellar Communication in Parkinson's and Alzheimer's Disease: Looking Beyond Endoplasmic Reticulum-Mitochondria Contact Sites.Frontiers in neuroscience · 2022Pooled it
- Chloroplast Stress Signals Orchestrate Epidermis-Specific Remodeling of Mitochondria and ER Under High Light.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Review
- A dual-purification system to isolate mitochondrial subpopulations.Journal of cell science · 2025Article
- Restoration of Miro1's N-terminal GTPase function alleviates prenatal stress-induced mitochondrial fission via Drp1 modulation.Cell communication and signaling : CCS · 2025Article
- Article
- The inter-organelle cross-talk finely orchestrated in the amyloidogenic processing of amyloid precursor protein in dendritic arborization neurons ofTheranostics · 2025Article
- Research advances on CaMKs-mediated neurodevelopmental injury.Archives of toxicology · 2024Review
- Review
- Mitochondrial Differentiation during Spermatogenesis: Lessons fromInternational journal of molecular sciences · 2024Review
- Interaction between the mitochondrial adaptor MIRO and the motor adaptor TRAK.The Journal of biological chemistry · 2023Article
- The mechanism of biomineralization: Progress in mineralization from intracellular generation to extracellular deposition.The Japanese dental science review · 2023Review
- Loss of the mitochondrial protein SPD-3 elevates PLK-1 levels and dysregulates mitotic events.Life science alliance · 2023Article
- Alpha synuclein modulates mitochondrial CaNPJ Parkinson's disease · 2023Article
- Genome-wide kinase-MAM interactome screening reveals the role of CK2A1 in MAM CaProceedings of the National Academy of Sciences of the United States of America · 2023Article
- MIRO-1 interacts with VDAC-1 to regulate mitochondrial membrane potential in Caenorhabditis elegans.EMBO reports · 2023Article
- Optogenetic cleavage of the Miro GTPase reveals the direct consequences of real-time loss of function in Drosophila.PLoS biology · 2023Article
- Yeast NDI1 reconfigures neuronal metabolism and prevents the unfolded protein response in mitochondrial complex I deficiency.PLoS genetics · 2023Article
- Compartment specific mitochondrial dysfunction in Drosophila knock-in model of ALS reversed by altered gene expression of OXPHOS subunits and pro-fission factor Drp1.Molecular and cellular neurosciences · 2023Article
11 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Mitochondria play central roles in buffering intracellular Ca²⁺ transients. While basal mitochondrial Ca²⁺ (Ca²⁺ mito) is needed to maintain organellar physiology, Ca²⁺ mito overload can lead to cell death. How Ca²⁺ mito homeostasis is regulated is not well understood. Here we show that Miro, a known component of the mitochondrial transport machinery, regulates Drosophila neural stem cell (NSC) development through Ca²⁺ mito homeostasis control, independent of its role in mitochondrial transport. Miro interacts with Ca²⁺ transporters at the ER-mitochondria contact site (ERMCS). Its inactivation causes Ca²⁺ mito depletion and metabolic impairment, whereas its overexpression results in Ca²⁺ mito overload, mitochondrial morphology change, and apoptotic response. Both conditions impaired NSC lineage progression. Ca²⁺ mito homeostasis is influenced by Polo-mediated phosphorylation of a conserved residue in Miro, which positively regulates Miro localization to, and the integrity of, ERMCS. Our results elucidate a regulatory mechanism underlying Ca²⁺ mito homeostasis and how its dysregulation may affect NSC metabolism/development and contribute to disease.
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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.