Component
Mouse histone H3K79 methyltransferase / Dot1l
Context-specific entity; species, compartment and exposure are stated on each claim.
1 recorded relationships. Experimental role, claim status and evidence remain attached to each record.
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.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
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.
What it acts on
T-cell Dot1l deletion removed H3K79me2 and prevented methionine supplementation from rescuing tumor-medium-induced apoptosis and impaired cytokine production.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_access
- Primary full text
- experimental_model
- Conditional mouse T-cell Dot1l knockout and culture add-back experiments.
- limitations
- Not a claim that dietary methionine deficiency causes DOT1L loss; gene loss and substrate shortage are distinct. Correction record: Author correction published online 12 December 2025 (2026 issue): Extended Data Fig. 1j originally duplicated the A375-supernatant flow-cytometry plot in the Sup+Ser condition; publisher replaced the representative image. This is a figure correction, not an opposing scientific finding. https://www.nature.com/articles/s41586-025-09845-8
- nutrient_topic
- L-Methionine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Methionine
- plain_language
- Supplying the nutrient failed when the downstream methyltransferase was absent.
- primary_references
- Cancer SLC43A2 alters T cell methionine metabolism and histone methylation. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32879489/ · DOI 10.1038/s41586-020-2682-1
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
L-Methionine: transport, methylation, sulfur metabolism and cross-nutrient mechanisms (2026-09-19) · lines 348–354
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Conditional mouse T-cell Dot1l knockout and culture add-back experiments. · source_derived_draft · unverified_draft
## methionine-dot1l-gate Supplying the nutrient failed when the downstream methyltransferase was absent. T-cell Dot1l deletion removed H3K79me2 and prevented methionine supplementation from rescuing tumor-medium-induced apoptosis and impaired cytokine production. Model: Conditional mouse T-cell Dot1l knockout and culture add-back experiments. Limitations: Not a claim that dietary methionine deficiency causes DOT1L loss; gene loss and substrate shortage are distinct. Correction record: Author correction published online 12 December 2025 (2026 issue): Extended Data Fig. 1j originally duplicated the A375-supernatant flow-cytometry plot in the Sup+Ser condition; publisher replaced the representative image. This is a figure correction, not an opposing scientific finding. https://www.nature.com/articles/s41586-025-09845-8 Evidence access: Primary full text Cancer SLC43A2 alters T cell methionine metabolism and histone methylation. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32879489/ · DOI 10.1038/s41586-020-2682-1
Complete structured claim and evidence
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.