Component

Mouse Tet1

Mus musculus ten-eleven translocation dioxygenase 1; distinct from human protein.

6 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

How nutrients influence it

Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.

How nutrients reach it in more than one step

Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.

Tracing routes…

What it does

Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.

Recorded relationships

What acts on it

  1. Ascorbate restored murine TET1-CD activity with ferric iron or under pH 8.0 conditions that rapidly oxidized Fe(II); iron-redox measurements support provision of reduced iron as the rescue mechanism.

    L-Ascorbate → Mouse Tet1 source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    true
    evidence_location
    Figure 1D–E; Figure S1A–C
    experimental_model
    Recombinant murine TET1 catalytic domain expressed in E. coli; methylated 86-mer DNA ELISA assay
    exposure
    1.5 µM TET1-CD, 0.5 µM DNA, 1 mM 2-oxoglutarate, 10 or 100 µM iron; sodium L-ascorbate 1 mM; pH 6.8 versus pH 8.0.
    limitations
    This does not directly measure free iron inside cells or establish a dietary iron/ascorbate requirement.
    nutrient_topic
    Vitamin C research collection; topical membership is not evidence of a direct dietary effect. · Vitamin C
    organism
    Mus musculus protein expressed in Escherichia coli
    plain_language
    Vitamin C helped restore the usable iron needed by this isolated DNA-modifying enzyme.
    primary_references
    [c-reg-hore] Retinol and ascorbate drive erasure of epigenetic memory and enhance reprogramming to naïve pluripotency by complementary mechanisms. (2016). https://pubmed.ncbi.nlm.nih.gov/27729528/ DOI: 10.1073/pnas.1608679113
    tissue_or_cell_type
    Cell-free

    Vitamin C: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1019–1031

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant murine TET1 catalytic domain expressed in E. coli; methylated 86-mer DNA ELISA assay · source_derived_draft · unverified_draft

    ### c-reg-tet-iron-reduction-rescue Ascorbate restored murine TET1-CD activity with ferric iron or under pH 8.0 conditions that rapidly oxidized Fe(II); iron-redox measurements support provision of reduced iron as the rescue mechanism. Condition category: normal nutrient_topic: Vitamin C research collection; topical membership is not evidence of a direct dietary effect. plain_language: Vitamin C helped restore the usable iron needed by this isolated DNA-modifying enzyme. organism: Mus musculus protein expressed in Escherichia coli tissue_or_cell_type: Cell-free experimental_model: Recombinant murine TET1 catalytic domain expressed in E. coli; methylated 86-mer DNA ELISA assay limitations: This does not directly measure free iron inside cells or establish a dietary iron/ascorbate requirement. exposure: 1.5 µM TET1-CD, 0.5 µM DNA, 1 mM 2-oxoglutarate, 10 or 100 µM iron; sodium L-ascorbate 1 mM; pH 6.8 versus pH 8.0. cross_nutrient: true evidence_location: Figure 1D–E; Figure S1A–C [c-reg-hore] Retinol and ascorbate drive erasure of epigenetic memory and enhance reprogramming to naïve pluripotency by complementary mechanisms. (2016). https://pubmed.ncbi.nlm.nih.gov/27729528/ DOI: 10.1073/pnas.1608679113
    Complete structured claim and evidence

  2. At pH 6.8 with sufficient Fe(II), murine TET1-CD remained active without ascorbate and adding ascorbate did not increase the measured activity; substrate-free preincubation also did not rapidly destroy activity.

    L-Ascorbate → Mouse Tet1 source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    true
    evidence_location
    Figure 1D; Figure S1B–D
    experimental_model
    Recombinant murine TET1 catalytic domain expressed in E. coli; methylated 86-mer DNA ELISA assay
    exposure
    1.5 µM TET1-CD, 0.5 µM DNA, 1 mM 2-oxoglutarate, 10 or 100 µM iron; sodium L-ascorbate 1 mM; pH 6.8 versus pH 8.0. Substrate-free preincubation up to 30 min.
    limitations
    A conditional biochemical null result; it does not negate ascorbate enhancement in cells or more oxidizing buffers.
    nutrient_topic
    Vitamin C research collection; topical membership is not evidence of a direct dietary effect. · Vitamin C
    organism
    Mus musculus protein expressed in Escherichia coli
    plain_language
    With usable iron maintained in this assay, the enzyme did not require extra vitamin C to keep working.
    primary_references
    [c-reg-hore] Retinol and ascorbate drive erasure of epigenetic memory and enhance reprogramming to naïve pluripotency by complementary mechanisms. (2016). https://pubmed.ncbi.nlm.nih.gov/27729528/ DOI: 10.1073/pnas.1608679113
    tissue_or_cell_type
    Cell-free

    Vitamin C: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1033–1045

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant murine TET1 catalytic domain expressed in E. coli; methylated 86-mer DNA ELISA assay · source_derived_draft · unverified_draft

    ### c-reg-tet-sufficient-ferrous-iron At pH 6.8 with sufficient Fe(II), murine TET1-CD remained active without ascorbate and adding ascorbate did not increase the measured activity; substrate-free preincubation also did not rapidly destroy activity. Condition category: normal nutrient_topic: Vitamin C research collection; topical membership is not evidence of a direct dietary effect. plain_language: With usable iron maintained in this assay, the enzyme did not require extra vitamin C to keep working. organism: Mus musculus protein expressed in Escherichia coli tissue_or_cell_type: Cell-free experimental_model: Recombinant murine TET1 catalytic domain expressed in E. coli; methylated 86-mer DNA ELISA assay limitations: A conditional biochemical null result; it does not negate ascorbate enhancement in cells or more oxidizing buffers. exposure: 1.5 µM TET1-CD, 0.5 µM DNA, 1 mM 2-oxoglutarate, 10 or 100 µM iron; sodium L-ascorbate 1 mM; pH 6.8 versus pH 8.0. Substrate-free preincubation up to 30 min. cross_nutrient: true evidence_location: Figure 1D; Figure S1B–D [c-reg-hore] Retinol and ascorbate drive erasure of epigenetic memory and enhance reprogramming to naïve pluripotency by complementary mechanisms. (2016). https://pubmed.ncbi.nlm.nih.gov/27729528/ DOI: 10.1073/pnas.1608679113
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Maternal vitamin C withdrawal increased Dazl-promoter methylation in female fetal germ cells, with reduced Dazl expression.

    L-Ascorbic acid → Mouse Dazl promoter demethylation source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    cross_nutrient
    true
    experimental_model
    Same-genotype nutritional comparison and bisulfite sequencing
    exposure
    Gulo-null dams: water vitamin C withdrawn 3-7 days before mating through E13.5; controls 3.3 g/L.
    limitations
    Methylation-expression association does not prove the sole causal mediator or impaired RA synthesis.
    nutrient_topic
    Vitamin A expansion research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
    organism
    Mus musculus
    plain_language
    Vitamin C shortage altered an epigenetic step in germ-cell development.
    primary_references
    [ditroia2019] Maternal vitamin C regulates reprogramming of DNA methylation and germline development. (2019). https://pubmed.ncbi.nlm.nih.gov/31485074/ DOI: 10.1038/s41586-019-1536-1
    tissue_or_cell_type
    female fetal germ cells
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Vitamin A expansion: reproduction, light-driven vision and shared mechanisms (2026-09-17) · lines 369–380

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Same-genotype nutritional comparison and bisulfite sequencing · source_derived_draft · unverified_draft

    ### va-repro-vitamin-c-demethylation Maternal vitamin C withdrawal increased Dazl-promoter methylation in female fetal germ cells, with reduced Dazl expression. Condition category: nutrient_deficiency nutrient_topic: Vitamin A expansion research collection; topical membership is not evidence of a direct dietary effect. plain_language: Vitamin C shortage altered an epigenetic step in germ-cell development. organism: Mus musculus tissue_or_cell_type: female fetal germ cells experimental_model: Same-genotype nutritional comparison and bisulfite sequencing limitations: Methylation-expression association does not prove the sole causal mediator or impaired RA synthesis. exposure: Gulo-null dams: water vitamin C withdrawn 3-7 days before mating through E13.5; controls 3.3 g/L. cross_nutrient: true [ditroia2019] Maternal vitamin C regulates reprogramming of DNA methylation and germline development. (2019). https://pubmed.ncbi.nlm.nih.gov/31485074/ DOI: 10.1038/s41586-019-1536-1
    Complete structured claim and evidence

  2. Maternal vitamin C deficiency delayed female fetal meiotic progression, with reduced STRA8 expression.

    L-Ascorbic acid → Mouse fetal ovarian meiotic progression source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    cross_nutrient
    true
    experimental_model
    Nutrient withdrawal with histology and meiotic staging
    exposure
    Withdrawal before mating through E13.5; same-genotype supplemented controls; staging at E14.5.
    limitations
    The individual SYCP3-positive protein fraction was not significantly reduced; this is not an A-C supplementation trial.
    nutrient_topic
    Vitamin A expansion research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
    organism
    Mus musculus
    plain_language
    A second nutrient shortage affected the germ-cell program also studied in vitamin A biology.
    primary_references
    [ditroia2019] Maternal vitamin C regulates reprogramming of DNA methylation and germline development. (2019). https://pubmed.ncbi.nlm.nih.gov/31485074/ DOI: 10.1038/s41586-019-1536-1
    tissue_or_cell_type
    female fetal ovary
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Vitamin A expansion: reproduction, light-driven vision and shared mechanisms (2026-09-17) · lines 382–393

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Nutrient withdrawal with histology and meiotic staging · source_derived_draft · unverified_draft

    ### va-repro-vitamin-c-meiotic-delay Maternal vitamin C deficiency delayed female fetal meiotic progression, with reduced STRA8 expression. Condition category: nutrient_deficiency nutrient_topic: Vitamin A expansion research collection; topical membership is not evidence of a direct dietary effect. plain_language: A second nutrient shortage affected the germ-cell program also studied in vitamin A biology. organism: Mus musculus tissue_or_cell_type: female fetal ovary experimental_model: Nutrient withdrawal with histology and meiotic staging limitations: The individual SYCP3-positive protein fraction was not significantly reduced; this is not an A-C supplementation trial. exposure: Withdrawal before mating through E13.5; same-genotype supplemented controls; staging at E14.5. cross_nutrient: true [ditroia2019] Maternal vitamin C regulates reprogramming of DNA methylation and germline development. (2019). https://pubmed.ncbi.nlm.nih.gov/31485074/ DOI: 10.1038/s41586-019-1536-1
    Complete structured claim and evidence

  3. Adding L-ascorbic acid 2-phosphate to mouse ESC medium rapidly increased global DNA 5hmC and promoter-associated 5hmC, preceding later methylcytosine loss.

    L-Ascorbic acid 2-phosphate → DNA 5-hydroxymethylcytosine residues source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    false
    evidence_location
    Figures 1–2
    experimental_model
    Mouse Oct4-GiP ESCs in feeder-free 2i/LIF medium; DNA dot blot and hydroxymethyl-DNA immunoprecipitation
    exposure
    100 µg/mL L-ascorbic acid 2-phosphate (A8960), medium replaced daily; 12-h and 72-h sampling.
    limitations
    5hmC abundance alone is not proof of completed demethylation; cultured ESCs are not adult human tissues.
    nutrient_topic
    Vitamin C research collection; topical membership is not evidence of a direct dietary effect. · Vitamin C
    organism
    Mus musculus
    plain_language
    A stable vitamin C derivative increased an early DNA-demethylation intermediate in cultured mouse stem cells.
    primary_references
    [c-reg-blaschke] Vitamin C induces Tet-dependent DNA demethylation and a blastocyst-like state in ES cells. (2013). https://pubmed.ncbi.nlm.nih.gov/23812591/ DOI: 10.1038/nature12362
    tissue_or_cell_type
    Embryonic stem cells

    Vitamin C: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 977–989

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mouse Oct4-GiP ESCs in feeder-free 2i/LIF medium; DNA dot blot and hydroxymethyl-DNA immunoprecipitation · source_derived_draft · unverified_draft

    ### c-reg-esc-hydroxymethylation Adding L-ascorbic acid 2-phosphate to mouse ESC medium rapidly increased global DNA 5hmC and promoter-associated 5hmC, preceding later methylcytosine loss. Condition category: normal nutrient_topic: Vitamin C research collection; topical membership is not evidence of a direct dietary effect. plain_language: A stable vitamin C derivative increased an early DNA-demethylation intermediate in cultured mouse stem cells. organism: Mus musculus tissue_or_cell_type: Embryonic stem cells experimental_model: Mouse Oct4-GiP ESCs in feeder-free 2i/LIF medium; DNA dot blot and hydroxymethyl-DNA immunoprecipitation limitations: 5hmC abundance alone is not proof of completed demethylation; cultured ESCs are not adult human tissues. exposure: 100 µg/mL L-ascorbic acid 2-phosphate (A8960), medium replaced daily; 12-h and 72-h sampling. cross_nutrient: false evidence_location: Figures 1–2 [c-reg-blaschke] Vitamin C induces Tet-dependent DNA demethylation and a blastocyst-like state in ES cells. (2013). https://pubmed.ncbi.nlm.nih.gov/23812591/ DOI: 10.1038/nature12362
    Complete structured claim and evidence

  4. After vitamin C derivative treatment, numerous mouse ESC promoters lost methylcytosine; imprinted regions and IAP retroelements were relatively resistant, so the effect was not indiscriminate erasure of genomic methylation.

    L-Ascorbic acid 2-phosphate → Gene-promoter DNA methylation source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    false
    evidence_location
    Figure 2; resistant-region analysis
    experimental_model
    Mouse Oct4-GiP ESCs in feeder-free 2i/LIF medium; DNA dot blot and hydroxymethyl-DNA immunoprecipitation; mC-DIP sequencing/qPCR and bisulfite validation
    exposure
    100 µg/mL L-ascorbic acid 2-phosphate (A8960), medium replaced daily; 12-h and 72-h sampling.
    limitations
    Locus-selective cell-culture result; promoter demethylation did not automatically activate every affected gene.
    nutrient_topic
    Vitamin C research collection; topical membership is not evidence of a direct dietary effect. · Vitamin C
    organism
    Mus musculus
    plain_language
    Vitamin C changed selected DNA methylation patterns in these cells; protected regions retained their marks.
    primary_references
    [c-reg-blaschke] Vitamin C induces Tet-dependent DNA demethylation and a blastocyst-like state in ES cells. (2013). https://pubmed.ncbi.nlm.nih.gov/23812591/ DOI: 10.1038/nature12362
    tissue_or_cell_type
    Embryonic stem cells

    Vitamin C: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 991–1003

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mouse Oct4-GiP ESCs in feeder-free 2i/LIF medium; DNA dot blot and hydroxymethyl-DNA immunoprecipitation; mC-DIP sequencing/qPCR and bisulfite validation · source_derived_draft · unverified_draft

    ### c-reg-esc-promoter-demethylation After vitamin C derivative treatment, numerous mouse ESC promoters lost methylcytosine; imprinted regions and IAP retroelements were relatively resistant, so the effect was not indiscriminate erasure of genomic methylation. Condition category: normal nutrient_topic: Vitamin C research collection; topical membership is not evidence of a direct dietary effect. plain_language: Vitamin C changed selected DNA methylation patterns in these cells; protected regions retained their marks. organism: Mus musculus tissue_or_cell_type: Embryonic stem cells experimental_model: Mouse Oct4-GiP ESCs in feeder-free 2i/LIF medium; DNA dot blot and hydroxymethyl-DNA immunoprecipitation; mC-DIP sequencing/qPCR and bisulfite validation limitations: Locus-selective cell-culture result; promoter demethylation did not automatically activate every affected gene. exposure: 100 µg/mL L-ascorbic acid 2-phosphate (A8960), medium replaced daily; 12-h and 72-h sampling. cross_nutrient: false evidence_location: Figure 2; resistant-region analysis [c-reg-blaschke] Vitamin C induces Tet-dependent DNA demethylation and a blastocyst-like state in ES cells. (2013). https://pubmed.ncbi.nlm.nih.gov/23812591/ DOI: 10.1038/nature12362
    Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

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