Component

Embryonic neural tube closure

Developmental closure endpoint assessed in mouse embryos.

3 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. After maternal sodium formate treatment, 14 of 16 Slc25a32-null embryos completed neural tube closure in the reported nine-litter experiment.

    Formate → Embryonic neural tube closure source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    Connects a B2-related machinery defect to folate-dependent development through one-carbon availability.
    evidence_spans
    [{"source_bundle": "artifacts/riboflavin_metabolism_sources.json", "source_key": "PMC11072207", "locator": "HTML article p", "paragraph_index": 38, "char_start": 0, "char_end": 1062, "evidence_access": "full-text"}]
    experimental_model
    Slc25a32-null embryos and missense knock-in mice, isolated mitochondria and skeletal-muscle enzyme assays.
    exposure
    0.1 mol/L sodium formate in dam drinking water; 73 total embryos, nine litters.
    limitations
    Small animal intervention; incomplete rescue and no human treatment inference.
    nutrient_topic
    Riboflavin research collection; topical membership is not evidence of a direct dietary effect. · Riboflavin (vitamin B2)
    organism
    Mus musculus
    plain_language
    One-carbon supplementation partly bypassed a developmental consequence in this mouse model.
    primary_references
    [peng-2022-slc25a32] Mitochondrial FAD shortage in SLC25A32 deficiency affects folate-mediated one-carbon metabolism (2022). https://pubmed.ncbi.nlm.nih.gov/35727412/ DOI: 10.1007/s00018-022-04404-0
    tissue_or_cell_type
    E11.5 embryos
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Riboflavin: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 916–928

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Slc25a32-null embryos and missense knock-in mice, isolated mitochondria and skeletal-muscle enzyme assays. · source_derived_draft · unverified_draft

    ### b2-met-formate-embryo-neural-tube After maternal sodium formate treatment, 14 of 16 Slc25a32-null embryos completed neural tube closure in the reported nine-litter experiment. Condition category: machinery_impairment nutrient_topic: Riboflavin research collection; topical membership is not evidence of a direct dietary effect. plain_language: One-carbon supplementation partly bypassed a developmental consequence in this mouse model. organism: Mus musculus tissue_or_cell_type: E11.5 embryos experimental_model: Slc25a32-null embryos and missense knock-in mice, isolated mitochondria and skeletal-muscle enzyme assays. limitations: Small animal intervention; incomplete rescue and no human treatment inference. exposure: 0.1 mol/L sodium formate in dam drinking water; 73 total embryos, nine litters. cross_nutrient: Connects a B2-related machinery defect to folate-dependent development through one-carbon availability. evidence_spans: [{"source_bundle": "artifacts/riboflavin_metabolism_sources.json", "source_key": "PMC11072207", "locator": "HTML article p", "paragraph_index": 38, "char_start": 0, "char_end": 1062, "evidence_access": "full-text"}] [peng-2022-slc25a32] Mitochondrial FAD shortage in SLC25A32 deficiency affects folate-mediated one-carbon metabolism (2022). https://pubmed.ncbi.nlm.nih.gov/35727412/ DOI: 10.1007/s00018-022-04404-0
    Complete structured claim and evidence

  2. Blocking PKC beta I prevented the inositol-mediated reduction of neural tube defects in curly-tail mouse embryos.

    Mouse PKC beta I isoform → Embryonic neural tube closure source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/inositol-research/14613966.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "670b8f0a36bfbecfb417fe28f8748e65994ac47b153ffcf66c42c21e7489f9cc", "start_char": 0, "end_char": 1735, "text_sha256": "670b8f0a36bfbecfb417fe28f8748e65994ac47b153ffcf66c42c21e7489f9cc"}
    experimental_model
    Embryo culture with selective PKC inhibition
    exposure
    Inositol exposure in a folate-resistant neural-tube-defect model
    limitations
    Mechanistic mouse prevention does not establish human efficacy or permit replacing folic acid.
    nutrient_topic
    Inositol research collection; topical membership is not evidence of a direct dietary effect. · Inositol (stereoisomer family)
    organism
    Curly-tail mutant mice
    plain_language
    Adding inositol could not overcome failure of this downstream signaling step.
    primary_references
    [ino-p14613966] Specific isoforms of protein kinase C are essential for prevention of folate-resistant neural tube defects by inositol. (2004). https://pubmed.ncbi.nlm.nih.gov/14613966/ DOI: 10.1093/hmg/ddh003
    tissue_or_cell_type
    Neurulation-stage embryos and hindgut
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Inositol: synthesis, signaling, mineral interactions and conditional deficiency (2026-09-17) · lines 1367–1378

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Embryo culture with selective PKC inhibition · source_derived_draft · unverified_draft

    ### ino-ntd-pkc-beta Blocking PKC beta I prevented the inositol-mediated reduction of neural tube defects in curly-tail mouse embryos. Condition category: machinery_impairment nutrient_topic: Inositol research collection; topical membership is not evidence of a direct dietary effect. plain_language: Adding inositol could not overcome failure of this downstream signaling step. organism: Curly-tail mutant mice tissue_or_cell_type: Neurulation-stage embryos and hindgut experimental_model: Embryo culture with selective PKC inhibition limitations: Mechanistic mouse prevention does not establish human efficacy or permit replacing folic acid. exposure: Inositol exposure in a folate-resistant neural-tube-defect model evidence_span: {"source_cache": "artifacts/inositol-research/14613966.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "670b8f0a36bfbecfb417fe28f8748e65994ac47b153ffcf66c42c21e7489f9cc", "start_char": 0, "end_char": 1735, "text_sha256": "670b8f0a36bfbecfb417fe28f8748e65994ac47b153ffcf66c42c21e7489f9cc"} [ino-p14613966] Specific isoforms of protein kinase C are essential for prevention of folate-resistant neural tube defects by inositol. (2004). https://pubmed.ncbi.nlm.nih.gov/14613966/ DOI: 10.1093/hmg/ddh003
    Complete structured claim and evidence

  3. PKC gamma activity was also required for inositol prevention of neural tube defects in this mouse model.

    Mouse PKC gamma → Embryonic neural tube closure source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/inositol-research/14613966.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "670b8f0a36bfbecfb417fe28f8748e65994ac47b153ffcf66c42c21e7489f9cc", "start_char": 0, "end_char": 1735, "text_sha256": "670b8f0a36bfbecfb417fe28f8748e65994ac47b153ffcf66c42c21e7489f9cc"}
    experimental_model
    Embryo culture with selective PKC inhibition
    exposure
    Inositol exposure in a folate-resistant neural-tube-defect model
    limitations
    Mechanistic mouse prevention does not establish human efficacy or permit replacing folic acid.
    nutrient_topic
    Inositol research collection; topical membership is not evidence of a direct dietary effect. · Inositol (stereoisomer family)
    organism
    Curly-tail mutant mice
    plain_language
    A second PKC isoform was separately required.
    primary_references
    [ino-p14613966] Specific isoforms of protein kinase C are essential for prevention of folate-resistant neural tube defects by inositol. (2004). https://pubmed.ncbi.nlm.nih.gov/14613966/ DOI: 10.1093/hmg/ddh003
    tissue_or_cell_type
    Neurulation-stage embryos and hindgut
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Inositol: synthesis, signaling, mineral interactions and conditional deficiency (2026-09-17) · lines 1380–1391

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Embryo culture with selective PKC inhibition · source_derived_draft · unverified_draft

    ### ino-ntd-pkc-gamma PKC gamma activity was also required for inositol prevention of neural tube defects in this mouse model. Condition category: machinery_impairment nutrient_topic: Inositol research collection; topical membership is not evidence of a direct dietary effect. plain_language: A second PKC isoform was separately required. organism: Curly-tail mutant mice tissue_or_cell_type: Neurulation-stage embryos and hindgut experimental_model: Embryo culture with selective PKC inhibition limitations: Mechanistic mouse prevention does not establish human efficacy or permit replacing folic acid. exposure: Inositol exposure in a folate-resistant neural-tube-defect model evidence_span: {"source_cache": "artifacts/inositol-research/14613966.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "670b8f0a36bfbecfb417fe28f8748e65994ac47b153ffcf66c42c21e7489f9cc", "start_char": 0, "end_char": 1735, "text_sha256": "670b8f0a36bfbecfb417fe28f8748e65994ac47b153ffcf66c42c21e7489f9cc"} [ino-p14613966] Specific isoforms of protein kinase C are essential for prevention of folate-resistant neural tube defects by inositol. (2004). https://pubmed.ncbi.nlm.nih.gov/14613966/ DOI: 10.1093/hmg/ddh003
    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.

    Evidence, AI assistance and curation standards