Component
Sec-tRNA[Ser]Sec
The specialized transfer RNA carrying selenocysteine for UGA recoding.
6 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
A constrained Sec-tRNA supply can impair selenocysteine insertion at UGA in a transcript-dependent manner.
Experimental context and source evidence
- availability_state
- Selenium intake or availability becomes inadequate for the cellular context.
- experimental_scope
- Biochemical pathway and experimental shortage model; effects depend on transcript and tissue.
- limitations
- This is a conditional supply constraint, not a prediction that all selenoproteins fall equally. No validated plasma cutoff is assigned.
- trigger_kind
- nutrient_deficiency
Selenium deficiency: a mechanism-first reference · lines 35–45
Supplied selenium deficiency reference · supports · Supplied reference; verify the primary study and experimental context. · source_derived_draft · unverified_draft
Sec-tRNA^[Ser]Sec ↓ eEFSec ribosome reaches UGA ↓ SECIS + SECISBP2/SBP2 machinery ↓ SELENOCYSTEINE INSERTED SerRS charging tRNA^[Ser]Sec with serine is an obligatory biosynthetic step, not a mistake. SEPHS2 supplies selenophosphate, while PSTK and SEPSECS convert the serine-charged tRNA into Sec-tRNA^[Ser]Sec. UGA recoding is intrinsically less straightforward than ordinary amino-acid insertion and its efficiency varies substantially by transcript and cellular context. It should not be treated as a universal 5–10% process across all selenoprotein mRNAs.
Selenium deficiency: a mechanism-first reference · lines 783–790
Supplied selenium deficiency reference · supports · Supplied reference; verify the primary study and experimental context. · source_derived_draft · unverified_draft
selenium intake / availability ↓ │ ▼ central selenium metabolism and Sec-tRNA supply become constrained │ ├─ tRNA^[Ser]Sec modification can shift (including Um34 / FTSJ1 biology) ├─ SECIS-dependent UGA recoding changes ├─ selected transcripts can undergo stronger repression / NMD
Complete structured claim and evidenceSec-tRNA enables translation of SELENOK.
Experimental context and source evidence
- cell_type
- · T cell
- evidence_scope
- Source-derived draft; primary-source verification required
- organism
- · Human
Selenium in immune cells · lines 11–20
Selenium immune-cell mechanism draft · supports · Source draft; model details require primary-source verification · source_derived_draft · unverified_draft
# I. THE CLEANEST CHAIN — SELENOK → Ca²⁺ → NFAT → IL-2 This is the one to memorize. It's a direct, non-redox, molecule-by-molecule path from a selenium atom to a cytokine. ``` 1. Se → Sec-tRNA → SELENOK (ER membrane, single C-terminal Sec, tail in cytosol) 2. SELENOK binds ZDHHC6 (ER palmitoyl-S-acyltransferase, DHHC motif) → SELENOK is required as a COFACTOR to stabilize the palmitoyl-ZDHHC6 acyl-enzyme intermediate
Complete structured claim and evidence
What acts on it
When selenium availability falls, the Sec-tRNA supply can become constrained.
Experimental context and source evidence
- availability_state
- Selenium intake or availability becomes inadequate for the cellular context.
- experimental_scope
- Biochemical pathway and experimental shortage model; effects depend on transcript and tissue.
- limitations
- This is a conditional supply constraint, not a prediction that all selenoproteins fall equally. No validated plasma cutoff is assigned.
- trigger_kind
- nutrient_deficiency
Selenium deficiency: a mechanism-first reference · lines 783–790
Supplied selenium deficiency reference · supports · Supplied reference; verify the primary study and experimental context. · source_derived_draft · unverified_draft
selenium intake / availability ↓ │ ▼ central selenium metabolism and Sec-tRNA supply become constrained │ ├─ tRNA^[Ser]Sec modification can shift (including Um34 / FTSJ1 biology) ├─ SECIS-dependent UGA recoding changes ├─ selected transcripts can undergo stronger repression / NMD
Complete structured claim and evidencePathogenic SEPSECS impairment can disrupt Sec-tRNA synthesis.
Experimental context and source evidence
- availability_state
- Pathogenic SEPSECS impairment affecting Sec-tRNA synthesis.
- experimental_scope
- Rare human genetic disorders and the defined Sec-tRNA biosynthetic pathway.
- limitations
- This is not ordinary selenium dietary deficiency. SEPSECS being the SLA/LP autoantigen does not make autoimmune hepatitis a selenium-deficiency disease.
- trigger_kind
- machinery_impairment
Selenium deficiency: a mechanism-first reference · lines 23–43
Supplied selenium deficiency reference · supports · Supplied reference; verify the primary study and experimental context. · source_derived_draft · unverified_draft
Selenocysteine (Sec) is unusual because it is synthesized on its own tRNA rather than existing as a large free amino-acid pool. There is no dedicated Sec-tRNA synthetase. Instead, two biosynthetic branches converge: Serine + tRNA^[Ser]Sec ↓ SerRS Ser-tRNA^[Ser]Sec ↓ PSTK PSer-tRNA^[Ser]Sec ────────────────────────┐ │ Selenide + ATP │ ↓ SEPHS2 │ selenophosphate ───────────────────────────┤ ↓ SEPSECS Sec-tRNA^[Ser]Sec ↓ eEFSec ribosome reaches UGA ↓ SECIS + SECISBP2/SBP2 machinery ↓ SELENOCYSTEINE INSERTED SerRS charging tRNA^[Ser]Sec with serine is an obligatory biosynthetic step, not a mistake. SEPHS2 supplies selenophosphate, while PSTK and SEPSECS convert the serine-charged tRNA into Sec-tRNA^[Ser]Sec.
Selenium deficiency: a mechanism-first reference · lines 541–545
Supplied selenium deficiency reference · supports · Supplied reference; verify the primary study and experimental context. · source_derived_draft · unverified_draft
SEPSECS Sec-tRNA synthesis defect Pontocerebellar hypoplasia spectrum
Complete structured claim and evidencePLP-dependent SEPSECS converts phosphoseryl-tRNA Sec to Sec-tRNA through phosphate elimination and selenium donation from selenophosphate, not incorporation of intact selenophosphate.
Experimental context and source evidence
- cell_type
- Purified enzyme/tRNA
- experimental_model
- Human enzyme/tRNA crystallography and biochemical assays
- limitations
- Not a measurement of dietary intake effects.
- organism
- Homo sapiens
Selenium: literature corrections and mechanism additions · lines 1154–1164
Metabolic Ledger literature curation, 17 September 2026; primary papers linked individually · supports · Human enzyme/tRNA crystallography and biochemical assays · secondary_verified · secondary_verified
## sepsecs-chemistry SEPSECS uses selenium from the donor to finish the tRNA-bound amino acid. PLP-dependent SEPSECS converts phosphoseryl-tRNA Sec to Sec-tRNA through phosphate elimination and selenium donation from selenophosphate, not incorporation of intact selenophosphate. Organism: Homo sapiens Cell type: Purified enzyme/tRNA Experimental model: Human enzyme/tRNA crystallography and biochemical assays Limitations: Not a measurement of dietary intake effects. Primary reference: [The human SepSecS–tRNASec complex reveals mechanism of selenocysteine formation](https://pubmed.ncbi.nlm.nih.gov/19608919/)
Complete structured claim and evidenceSelenium availability supports the specialized Sec-tRNA pool.
Experimental context and source evidence
- cell_type
- · T cell
- evidence_scope
- Source-derived draft; primary-source verification required
- organism
- · Human
Selenium in immune cells · lines 11–20
Selenium immune-cell mechanism draft · supports · Source draft; model details require primary-source verification · source_derived_draft · unverified_draft
# I. THE CLEANEST CHAIN — SELENOK → Ca²⁺ → NFAT → IL-2 This is the one to memorize. It's a direct, non-redox, molecule-by-molecule path from a selenium atom to a cytokine. ``` 1. Se → Sec-tRNA → SELENOK (ER membrane, single C-terminal Sec, tail in cytosol) 2. SELENOK binds ZDHHC6 (ER palmitoyl-S-acyltransferase, DHHC motif) → SELENOK is required as a COFACTOR to stabilize the palmitoyl-ZDHHC6 acyl-enzyme intermediate
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.