Component
Human RNA methyltransferase / METTL16
Context-specific entity; species, compartment and exposure are stated on each claim.
2 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
Methionine-starvation-induced SAM depletion increased MAT2A expression through METTL16-dependent splicing involving a conserved 3-prime-UTR hairpin.
Experimental context and source evidence
- availability_state
- nutrient_deficiency Imported condition classification; unverified.
- evidence_access
- Primary abstract
- experimental_model
- Human MAT2A reporter/cell and RNA-biochemistry experiments.
- limitations
- Increased transcript processing does not replace the missing methionine substrate.
- nutrient_topic
- L-Methionine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Methionine
- plain_language
- Low methyl-donor availability can increase production capacity through RNA processing.
- primary_references
- The U6 snRNA m6A Methyltransferase METTL16 Regulates SAM Synthetase Intron Retention. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28525753/ · DOI 10.1016/j.cell.2017.05.003
- trigger_kind
- nutrient_deficiency Imported condition classification; unverified.
L-Methionine: transport, methylation, sulfur metabolism and cross-nutrient mechanisms (2026-09-19) · lines 260–266
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human MAT2A reporter/cell and RNA-biochemistry experiments. · source_derived_draft · unverified_draft
## methionine-mettl16-feedback Low methyl-donor availability can increase production capacity through RNA processing. Methionine-starvation-induced SAM depletion increased MAT2A expression through METTL16-dependent splicing involving a conserved 3-prime-UTR hairpin. Model: Human MAT2A reporter/cell and RNA-biochemistry experiments. Limitations: Increased transcript processing does not replace the missing methionine substrate. Evidence access: Primary abstract The U6 snRNA m6A Methyltransferase METTL16 Regulates SAM Synthetase Intron Retention. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28525753/ · DOI 10.1016/j.cell.2017.05.003
Complete structured claim and evidenceMETTL16 was identified as a SAM-dependent U6 snRNA m6A methyltransferase.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Human RNA methylation/biochemical study.
- limitations
- No claim that every splicing event is controlled by dietary methionine.
- nutrient_topic
- L-Methionine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Methionine
- plain_language
- The same enzyme also modifies RNA used in splicing.
- primary_references
- The U6 snRNA m6A Methyltransferase METTL16 Regulates SAM Synthetase Intron Retention. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28525753/ · DOI 10.1016/j.cell.2017.05.003
L-Methionine: transport, methylation, sulfur metabolism and cross-nutrient mechanisms (2026-09-19) · lines 268–274
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human RNA methylation/biochemical study. · source_derived_draft · unverified_draft
## methionine-mettl16-u6 The same enzyme also modifies RNA used in splicing. METTL16 was identified as a SAM-dependent U6 snRNA m6A methyltransferase. Model: Human RNA methylation/biochemical study. Limitations: No claim that every splicing event is controlled by dietary methionine. Evidence access: Primary abstract The U6 snRNA m6A Methyltransferase METTL16 Regulates SAM Synthetase Intron Retention. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28525753/ · DOI 10.1016/j.cell.2017.05.003
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.