Affinage

MTO1

5-taurinomethyluridine-[tRNA] synthase subunit MTO1, mitochondrial · UniProt Q9Y2Z2

Length
717 aa
Mass
80.0 kDa
Annotated
2026-06-10
30 papers in source corpus 17 papers cited in narrative 17 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 6/6 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

MTO1 encodes a mitochondrially targeted enzyme that catalyzes 5-carboxymethylaminomethylation (cmnm5/τm5) of the wobble uridine in mitochondrial tRNAs, a modification required for accurate and efficient mitochondrial translation (PMID:22608499). The human protein is a structural and functional homolog of yeast Mto1, complementing the respiratory-deficient phenotype of yeast mto1 mutants and confirming evolutionary conservation of its tRNA-modifying role (PMID:12011058, PMID:14522080). Mechanistically, this wobble-uridine modification is required for the structural integrity, steady-state stability, and aminoacylation of multiple mitochondrial tRNAs (tRNAGlu, tRNAGln, tRNALys, tRNATrp, tRNALeu(UUR)), and its loss destabilizes mitochondrial mRNAs and impairs synthesis of OXPHOS subunits (PMID:19460296, PMID:33836087). MTO1 acts within a heterodimeric complex with MSS1/GTPBP3 to optimize mitochondrial protein synthesis (PMID:9774408), and physically interacts with the mitochondrial poly(A) polymerase MTPAP, coupling tRNA modification to mRNA polyadenylation (PMID:33836087). Loss of function causes combined respiratory-chain deficiency, impaired mitochondrial translation, and hypertrophic cardiomyopathy with complex I deficiency in patients and animal models (PMID:22608499, PMID:23929671, PMID:25506927, PMID:33836087). Separately, the S. pombe ortholog Mto1 functions as a cytoplasmic microtubule nucleation factor that recruits the γ-tubulin complex to noncentrosomal MTOCs through its CM1 and MASC domains within an Mto1-Mto2 complex, and is negatively regulated by the ER protein Erg28 (PMID:19001497, PMID:20970338, PMID:41989917).

Mechanistic history

Synthesis pass · year-by-year structured walk · 13 steps
  1. 1998 High

    Established that Mto1 acts in concert with Mss1 in mitochondria to optimize mitochondrial protein synthesis, defining the founding biochemical partnership before its enzymatic role was known.

    Evidence Yeast pulse-labeling, respiratory enzyme assays, and genetic interaction with a paromomycin-resistance allele showing the Mto1·Mss1 heterodimer is required for COX1 processing and cytochrome oxidase synthesis

    PMID:9774408

    Open questions at the time
    • Did not identify the chemical modification catalyzed
    • Did not define which tRNAs are substrates
  2. 2002 Medium

    Showed human MTO1 is a functional ortholog by complementing yeast mto1 respiratory defects, extending the conserved mitochondrial role to humans.

    Evidence Yeast complementation with human MTO1 cDNA and sequence-based mitochondrial targeting inference

    PMID:12011058

    Open questions at the time
    • Mitochondrial localization inferred from sequence rather than directly demonstrated
    • Enzymatic activity not assayed directly
  3. 2003 Medium

    Confirmed conserved mitochondrial localization and function of the mammalian ortholog in mouse, reinforcing the cross-species tRNA-modification model.

    Evidence Subcellular fractionation of mouse Mto1 plus yeast complementation

    PMID:14522080

    Open questions at the time
    • Single-lab localization
    • No direct biochemical demonstration of modification activity
  4. 2009 High

    Defined the downstream consequences of MTO1 loss by showing tRNA modification is required for tRNA stability, aminoacylation, and mitochondrial mRNA stability, connecting modification to translational competence.

    Evidence Yeast MTO1 deletion analyzed by Northern blot of tRNA/mRNA levels and aminoacylation assays with genetic controls

    PMID:19460296

    Open questions at the time
    • Did not identify the precise chemical modification in human tRNAs
    • Mechanism linking modification loss to mRNA destabilization not resolved
  5. 2012 High

    Identified the specific catalytic activity (cmnm5 wobble-uridine modification) and established MTO1 as a human disease gene through patient mutations and rescue, the central mechanistic and clinical advance.

    Evidence Patient respiratory chain assays, lentiviral wild-type MTO1 rescue, yeast modeling, in vivo mtDNA pulse-labeling, and exome sequencing

    PMID:22608499

    Open questions at the time
    • Initially defined modification on three tRNAs
    • Structural basis of catalysis not resolved
  6. 2013 High

    Extended the disease-gene model with additional pathogenic missense mutations validated functionally, solidifying genotype-to-phenotype causality for combined respiratory deficiency.

    Evidence Recombinant yeast functional assays (growth, respiration, complex IV, mitochondrial protein synthesis) and patient fibroblast rescue with wild-type MTO1

    PMID:23929671

    Open questions at the time
    • Tissue-specificity of phenotype unexplained
    • Genotype-phenotype correlation across mutations incomplete
  7. 2014 Medium

    Demonstrated in vivo that MTO1 loss produces hypertrophic cardiomyopathy and complex I deficiency in mammals, establishing a faithful disease model.

    Evidence Gene-trap MTO1 mouse with cardiac morphology and respiratory chain enzyme assays

    PMID:25506927

    Open questions at the time
    • Single-lab model
    • Molecular reason for cardiac selectivity not addressed
  8. 2017 Medium

    Revealed that MTO1 expression is itself regulated by retrograde-signal-induced miRNAs, placing tRNA modification under mitochondria-to-nucleus feedback control.

    Evidence Cybrid models with miRNA overexpression/antagonist transfection and OXPHOS activity readouts

    PMID:28740091

    Open questions at the time
    • Direct miRNA-MTO1 transcript targeting not fully mapped
    • Single-lab cybrid system
  9. 2018 Medium

    Mapped the metabolic reprogramming downstream of MTO1 deficiency, distinguishing its HIF-PPARγ-UCP2-AMPK signature from that of GTPBP3 deficiency.

    Evidence Patient fibroblasts and siRNA knockdown with Western/activity assays for HIF-1, AMPK, PPARγ, UCP2 plus lipid droplet staining

    PMID:29348686

    Open questions at the time
    • Causal ordering within the signaling axis not established
    • Single-lab observation
  10. 2021 High

    Integrated the full mitochondrial mechanism in vivo by linking MTO1 to tRNA structure/aminoacylation, OXPHOS, cardiomyopathy, and a novel physical interaction with the poly(A) polymerase MTPAP coupling modification to mRNA polyadenylation.

    Evidence CRISPR/Cas9 zebrafish knockout with tRNA structural analysis, aminoacylation, polyadenylation assays, MTO1-MTPAP Co-IP, OXPHOS assays, and cardiac histology

    PMID:33836087

    Open questions at the time
    • MTO1-MTPAP interaction shown by Co-IP without reciprocal/structural validation
    • Mechanism by which MTO1 controls MTPAP expression unresolved
  11. 2010 High

    For the S. pombe ortholog, defined CM1 as the γ-tubulin-complex-binding/nucleation motif and MASC as the MTOC-targeting region, separating the nucleation and localization functions of cytoplasmic Mto1.

    Evidence In vivo domain mutagenesis, Co-IP, live imaging, microtubule nucleation assays, and genetic dependency analysis (Myp2, SIN components)

    PMID:19001497 PMID:20970338

    Open questions at the time
    • Relationship between fission-yeast cytoplasmic role and the conserved mitochondrial enzyme function unresolved
    • Structural basis of CM1-γ-TuC binding not determined
  12. 2020 Medium

    Broadened the cytoplasmic Mto1 roles to NE-based and astral microtubule nucleation and to interphase chromosome organization, cohesion, and DNA repair, showing nucleation activity has downstream chromosomal consequences.

    Evidence Fission yeast deletions with live-cell imaging, microtubule repolymerization, NE-tethering rescue, Rho1-GTP assays, DNA repair assays, and Rad21 ChIP

    PMID:31087092 PMID:31483748 PMID:32520628

    Open questions at the time
    • Single-lab observations
    • Direct mechanistic link between microtubule nucleation and cohesin loading not established
  13. 2026 High

    Identified Erg28 as a negative regulator that competes with γ-TuSC for the Mto1-Mto2 complex, defining a brake on noncentrosomal microtubule assembly.

    Evidence Co-IP (Erg28-Mto1/Mto2 and Erg28-γ-TuSC), in vitro microtubule assembly reconstitution, domain deletion mutagenesis, and live-cell microscopy

    PMID:41989917

    Open questions at the time
    • Whether an analogous regulator exists for mammalian MTO1 unknown
    • Structural basis of competitive binding not resolved

Open questions

Synthesis pass · forward-looking unresolved questions
  • It remains unresolved how the same gene symbol reconciles a conserved mitochondrial tRNA-modifying enzyme with the fission-yeast cytoplasmic microtubule nucleator, and whether these reflect orthologous functions or distinct proteins.
  • No experiment in the corpus bridges the mitochondrial enzymatic and cytoplasmic nucleation activities
  • Structural model of human MTO1 catalysis absent
  • Mechanism of cardiac-selective pathology unexplained

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140098 catalytic activity, acting on RNA 3 GO:0003723 RNA binding 2 GO:0008092 cytoskeletal protein binding 2 GO:0016740 transferase activity 1
Localization
GO:0005739 mitochondrion 3 GO:0005815 microtubule organizing center 3 GO:0005635 nuclear envelope 1
Pathway
R-HSA-1643685 Disease 3 R-HSA-392499 Metabolism of proteins 3 R-HSA-8953854 Metabolism of RNA 3
Partners
ERG28GTPBP3MTO2MTPAPMYP2
Complex memberships
MTO1-MSS1/GTPBP3 complexMto1-Mto2 complex

Evidence

Reading pass · 17 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1998 Yeast Mto1p and Mss1p form a heterodimer complex in mitochondria; in a paromomycin-resistant background, the Mto1p·Mss1p complex is required for processing the COX1 mitochondrial transcript and for synthesis of cytochrome oxidase subunit 1. The complex is proposed to optimize mitochondrial protein synthesis, possibly by a proofreading mechanism. In vivo pulse-labeling, respiratory phenotype analysis, visible absorption spectroscopy, respiratory enzyme activity assays, genetic interaction with paromomycin-resistance allele The Journal of biological chemistry High 9774408
2002 Human MTO1 encodes a mitochondrially targeted protein that is a structural and functional homolog of yeast Mto1; human MTO1 cDNA complements the respiratory-deficient phenotype of yeast mto1 cells carrying the paromomycin-resistance (PR) 15S rRNA mutation, establishing functional conservation in mitochondrial tRNA modification. Yeast complementation assay, cDNA cloning, subcellular localization inference from sequence analysis The Journal of biological chemistry Medium 12011058
2003 Mouse Mto1 localizes to mitochondria and functionally complements yeast mto1 respiratory-deficient cells carrying the PR rRNA mutation, confirming its conserved role in mitochondrial tRNA modification. Subcellular fractionation/localization, yeast complementation assay Biochimica et biophysica acta Medium 14522080
2009 Deletion of yeast MTO1 decreases steady-state levels of multiple mitochondrial tRNAs (tRNALys, tRNAGlu, tRNAGln, tRNALeu, tRNAGly, tRNAArg, tRNAPhe), reduces aminoacylation of tRNALys, tRNALeu, and tRNAArg, and decreases steady-state levels of mitochondrial mRNAs (COX1, COX2, COX3, ATP6, ATP9), demonstrating that MTO1-dependent tRNA modification is required for mitochondrial tRNA and mRNA stability and tRNA charging. Northern blot (steady-state tRNA and mRNA levels), aminoacylation assay, genetic interaction analysis with 15S rRNA C1409G mutation Mitochondrion High 19460296
2012 Human MTO1 catalyzes 5-carboxymethylaminomethylation (cmnm5) of the wobble uridine base in three mitochondrial tRNAs; pathogenic MTO1 mutations in patients cause variably combined reduction in mtDNA-dependent respiratory chain activities in muscle and fibroblasts, and wild-type MTO1 cDNA corrects the respiratory defect in mutant cells. Equivalent yeast mutations phenocopy the patient respiratory deficiency and impair in vivo mtDNA translation. Patient cell respiratory chain enzyme assays, wild-type MTO1 rescue (lentiviral cDNA expression), yeast mto1 mutant complementation, in vivo mtDNA translation (pulse-labeling), exome sequencing to identify mutations American journal of human genetics High 22608499
2013 Novel missense MTO1 mutations cause combined mitochondrial respiratory chain (MRC) deficiency with impaired mitochondrial protein synthesis; pathogenic role validated in recombinant yeast by oxidative growth, respiratory activity, mitochondrial protein synthesis, and complex IV activity assays. Wild-type MTO1 expression rescues the respiratory defect in patient fibroblasts. Yeast recombinant model (oxidative growth, respiratory activity, complex IV assay, mitochondrial protein synthesis), patient fibroblast rescue with wt MTO1, exome sequencing Human mutation High 23929671
2008 In fission yeast S. pombe, Mto1 contains a conserved CM1 region (short N-terminal motif) required for cytoplasmic microtubule nucleation and interaction with the γ-tubulin complex (γ-TuC); CM1 mutations abolish γ-TuC binding and microtubule nucleation without affecting Mto1 localization or Mto2 binding. A separate non-CM1 region is required for Mto2 binding and also contributes to γ-TuC association. Mto1 and Mto2 form a complex (Mto1/2) independent of γ-TuC, and each can weakly associate with γ-TuC in the absence of the other. In vivo mutagenesis, co-immunoprecipitation, live-cell imaging/localization, microtubule nucleation assays (fission yeast genetics) Journal of cell science High 19001497
2010 Fission yeast Mto1 contains a conserved C-terminal MASC sequence required for targeting to multiple distinct MTOCs; different MASC subregions target Mto1 to different MTOCs. Mto1 targeting to the cell equator during division requires direct interaction with unconventional type II myosin Myp2. Targeting to the spindle pole body during mitosis depends on SIN components Sid4 and Cdc11. In vivo mutagenesis, live-cell imaging, co-immunoprecipitation (Mto1-Myp2 interaction), genetic dependency analysis (SIN pathway) Current biology : CB High 20970338
2014 MTO1-deficient mice (generated by gene trap mutagenesis) develop hypertrophic cardiomyopathy and complex I deficiency with mitochondrial dysfunction in cardiac tissue, mirroring the human disease phenotype. Gene trap mouse model, cardiac morphology, respiratory chain enzyme activity assays (complex I), mitochondrial functional analysis PloS one Medium 25506927
2018 MTO1 deficiency in human fibroblasts activates HIF-1, downregulates PPARγ and UCP2, and inactivates AMPK, uncoupling glycolysis from oxidative phosphorylation and causing lipid droplet accumulation; this metabolic reprogramming through the HIF-PPARγ-UCP2-AMPK axis is distinct from that triggered by GTPBP3 deficiency (which activates AMPK and increases UCP2/PPARγ). Patient fibroblast analysis, siRNA-mediated MTO1 silencing, Western blot and activity assays for HIF-1, AMPK, PPARγ, UCP2, fatty acid oxidation assays, lipid droplet staining Scientific reports Medium 29348686
2021 Mto1 deficiency in zebrafish (CRISPR/Cas9 knockout) causes: (1) perturbed tRNA structure and reduced stability of tRNAGln, tRNALys, tRNATrp, tRNALeu(UUR); (2) global decrease in aminoacylation of mitochondrial tRNAs with taurine modification; (3) altered polyadenylation of cox1, cox3, and nd1 mRNAs via decreased expression of MTPAP; (4) MTO1 physically interacts with MTPAP (poly(A) polymerase) as shown by immunoprecipitation; (5) impaired mitochondrial translation and reduced OXPHOS complex activities; and (6) heart development defects and hypertrophic cardiomyopathy. CRISPR/Cas9 knockout zebrafish, tRNA structural analysis (S1 nuclease digestion), aminoacylation assays, mRNA polyadenylation analysis, co-immunoprecipitation (MTO1-MTPAP), OXPHOS complex activity assays, cardiac histology Nucleic acids research High 33836087
2015 Deletion of MTO1 in yeast carrying the mitochondrial 15S rRNA C1477G mutation (equivalent to human A1555G) suppresses aminoglycoside sensitivity and partially compensates for the energy deficit by upregulating key glycolytic genes (HXK2, PFK1, PYK1), indicating MTO1 acts as a modifier of the neomycin-sensitive phenotype through regulation of mitochondrial tRNA modification and compensatory glycolysis. Yeast genetics (null mutation analysis), growth assays under aminoglycoside treatment, RT-PCR for glycolytic gene expression, mitochondrial function assays PloS one Medium 25898254
2017 Expression of MTO1 (along with TRMU and GTPBP3) is regulated by specific miRNAs induced by mitochondria-to-nucleus retrograde signals (ROS and Ca2+) in cybrid models of mtDNA diseases; transfection of mutant cybrids with miRNA antagonists improves cell energetic state, demonstrating that miRNA-mediated modulation of MTO1 expression affects mitochondrial tRNA modification status and OXPHOS function. Cybrid cell models, miRNA overexpression/antagonist transfection, OXPHOS activity assays, ROS/Ca2+ pathway analysis Scientific reports Medium 28740091
2019 In fission yeast, Mto1 and Alp7 interdependently localize to the nuclear envelope (NE) in cells without microtubules; Alp14 localizes to the NE in an Alp7- and Mto1-dependent manner. Artificial tethering of Mto1 to the NE in alp7-deleted cells partially restores microtubule generation from the NE, demonstrating that Mto1 recruitment to the NE is a limiting step for NE-based microtubule nucleation. Live-cell fluorescence microscopy, microtubule repolymerization assay, artificial NE-tethering experiment, genetic deletion analysis Journal of molecular cell biology Medium 31087092
2019 In fission yeast, loss of Mto1 leads to defects in DNA repair, reduced homologous recombination efficiency, abnormal DNA repair factory dynamics, impaired sister chromatid pairing, and reduced Rad21 cohesin binding along chromosomal arms; this links cytoplasmic microtubule nucleation by Mto1 to chromosomal organization, cohesion, and DNA repair during interphase. Genetic deletion (mto1Δ), DNA repair assays, live-cell imaging of repair foci, ChIP for Rad21 cohesin Molecular biology of the cell Medium 31483748
2020 In fission yeast, Mto1 (together with Mto2 and γ-tubulin) regulates astral microtubule nucleation at the spindle pole body; deletion of Mto1 reduces astral microtubule number, elevates Rho1-GTP at the division site, and, in combination with a bgs1 mutation, causes defective cytokinetic furrow ingression. Genetic deletion analysis, live-cell imaging of microtubules and division site, Rho1-GTP assay, double-mutant epistasis Molecular biology of the cell Medium 32520628
2026 The ER transmembrane protein Erg28 physically interacts with both the Mto1-Mto2 complex and the γ-tubulin small complex (γ-TuSC), significantly attenuating γ-TuSC binding to the Mto1-Mto2 complex; Erg28 inhibits Mto1-Mto2/γ-TuSC-mediated microtubule assembly in vitro; the cytosolic N-terminal region of Erg28 is required for this inhibitory activity; erg28 deletion causes excessive microtubule assembly and nuclear shape deformation. Co-immunoprecipitation (Erg28-Mto1/Mto2, Erg28-γ-TuSC), in vitro microtubule assembly assay, domain deletion mutagenesis, live-cell microscopy Cell reports High 41989917

Source papers

Stage 0 corpus · 30 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2012 Mutations of the mitochondrial-tRNA modifier MTO1 cause hypertrophic cardiomyopathy and lactic acidosis. American journal of human genetics 153 22608499
2002 Isolation and characterization of the putative nuclear modifier gene MTO1 involved in the pathogenesis of deafness-associated mitochondrial 12 S rRNA A1555G mutation. The Journal of biological chemistry 131 12011058
2018 Circular RNA‑MTO1 suppresses breast cancer cell viability and reverses monastrol resistance through regulating the TRAF4/Eg5 axis. International journal of oncology 113 30015883
1998 MTO1 codes for a mitochondrial protein required for respiration in paromomycin-resistant mutants of Saccharomyces cerevisiae. The Journal of biological chemistry 80 9774408
2013 MTO1 mutations are associated with hypertrophic cardiomyopathy and lactic acidosis and cause respiratory chain deficiency in humans and yeast. Human mutation 69 23929671
2004 Phenotype of non-syndromic deafness associated with the mitochondrial A1555G mutation is modulated by mitochondrial RNA modifying enzymes MTO1 and GTPBP3. Molecular genetics and metabolism 58 15542390
2008 Two distinct regions of Mto1 are required for normal microtubule nucleation and efficient association with the gamma-tubulin complex in vivo. Journal of cell science 49 19001497
2010 Fission yeast Mto1 regulates diversity of cytoplasmic microtubule organizing centers. Current biology : CB 48 20970338
2019 A regulatory circuit of circ-MTO1/miR-17/QKI-5 inhibits the proliferation of lung adenocarcinoma. Cancer biology & therapy 46 30975029
2017 The genotypic and phenotypic spectrum of MTO1 deficiency. Molecular genetics and metabolism 28 29331171
2020 Circular RNA MTO1 suppresses tumorigenesis of gastric carcinoma by sponging miR-3200-5p and targeting PEBP1. Molecular and cellular probes 27 32194149
2021 Ablation of Mto1 in zebrafish exhibited hypertrophic cardiomyopathy manifested by mitochondrion RNA maturation deficiency. Nucleic acids research 26 33836087
2018 Defects in the mitochondrial-tRNA modification enzymes MTO1 and GTPBP3 promote different metabolic reprogramming through a HIF-PPARγ-UCP2-AMPK axis. Scientific reports 26 29348686
2020 Circular RNA MTO1 Inhibits the Proliferation and Invasion of Ovarian Cancer Cells Through the miR-182-5p/KLF15 Axis. Cell transplantation 25 32731816
2014 MTO1-deficient mouse model mirrors the human phenotype showing complex I defect and cardiomyopathy. PloS one 25 25506927
2020 Circular RNA MTO1 inhibits gastric cancer progression by elevating PAWR via sponging miR-199a-3p. Cell cycle (Georgetown, Tex.) 23 33089757
2015 Optic neuropathy, cardiomyopathy, cognitive disability in patients with a homozygous mutation in the nuclear MTO1 and a mitochondrial MT-TF variant. American journal of medical genetics. Part A 23 26061759
2009 Mutation in MTO1 involved in tRNA modification impairs mitochondrial RNA metabolism in the yeast Saccharomyces cerevisiae. Mitochondrion 18 19460296
2003 Identification and characterization of mouse MTO1 gene related to mitochondrial tRNA modification. Biochimica et biophysica acta 17 14522080
2013 Nuclear-encoded mitochondrial MTO1 and MRPL41 are regulated in an opposite epigenetic mode based on estrogen receptor status in breast cancer. BMC cancer 15 24160266
2017 microRNA-mediated differential expression of TRMU, GTPBP3 and MTO1 in cell models of mitochondrial-DNA diseases. Scientific reports 9 28740091
2016 The homozygous R504C mutation in MTO1 gene is responsible for ONCE syndrome. Clinical genetics 9 27256614
2019 Alp7-Mto1 and Alp14 synergize to promote interphase microtubule regrowth from the nuclear envelope. Journal of molecular cell biology 8 31087092
2020 Microtubule nucleation promoters Mto1 and Mto2 regulate cytokinesis in fission yeast. Molecular biology of the cell 7 32520628
2022 Clinical and genetic analysis of combined oxidative phosphorylation defificiency-10 caused by MTO1 mutation. Clinica chimica acta; international journal of clinical chemistry 6 34990597
2019 Effects of the microtubule nucleator Mto1 on chromosomal movement, DNA repair, and sister chromatid cohesion in fission yeast. Molecular biology of the cell 5 31483748
2015 MTO1 worked as a modifier in the aminoglycosides sensitivity of yeast carrying a mitochondrial 15S rRNA C1477G mutation. PloS one 4 25898254
2021 A novel compound heterozygous mutation of the MTO1 gene associated with complex oxidative phosphorylation deficiency type 10. Clinica chimica acta; international journal of clinical chemistry 1 34547275
2026 The endoplasmic reticulum protein Erg28 restrains Mto1-Mto2-γ-TuSC-mediated microtubule assembly. Cell reports 0 41989917
2025 Circular RNAs MTO1 and ZNF292 as potential diagnostic biomarkers in HIV patients treated with antiretroviral therapy. Molecular biology reports 0 40694227

Missed literature

Know a paper Affinage missed for MTO1? Flag it for the maintainers and the community.

No submissions yet.