D14 (AtD14, At3g03990, UniProt Q9SQR3) curation notes
Context: reviewed as part of the strigolactone_signaling_shoot_branching module (D14 receptor ->
SCF(MAX2) -> SMXL6/7/8 degradation -> BRC1). Falcon deep research was attempted but all providers
failed, so these notes are built from cached publications.
Identity
- UniProt Q9SQR3 (D14_ARATH, 267 aa), alpha/beta hydrolase, catalytic triad S97/D218/H247.
- Arabidopsis ortholog of rice D14; paralog KAI2 mediates karrikin responses
PMID:22357928.
Receptor function
- SL induces open-to-closed transition and D14-D3/MAX2-ASK1 complex
PMID:27479325.
- Catalytically dead AtD14 D218A still complements atd14 -> intact SL binding may suffice
PMID:30643123.
- GR24-enhanced interaction with SMXL6/7 (Y2H, co-IP) PMID:26546446.
- Nuclear D14 binds SMXL7 and MAX2 SL-dependently PMID:27317673.
Hydrolase
Localisation / feedback
- Nucleus + cytoplasm, overlapping MAX2; local action; SL-induced MAX2-dependent degradation PMID:24610723.
Curation decisions
- GO:1901601 strigolactone biosynthetic process: IBA REMOVE (receptor clade, d14 is SL-insensitive);
IMP (PMID:22422982) also REMOVE on the same biology. Full text is not open access (Europe PMC: no PMC
copy; science.org returns 403), so the assay could not be read; the same paper's IMP secondary shoot
formation row suggests it was a branching phenotype, which reflects SL insensitivity, not biosynthesis.
D14 does none of the work of SL formation (D27/CCD7/CCD8/MAX1 do), so the term is contradicted
regardless of evidence code. (Changed from MARK_AS_OVER_ANNOTATED after PR #4383 review.)
- GO:0010223 secondary shoot formation -> MODIFY to GO:2000032 regulation of secondary shoot formation.
- protein binding to SMXLs/MAX2 -> MODIFY to GO:0038023 signaling receptor activity; HT HIPP26 -> REMOVE.
- NEW: GO:0038023 signaling receptor activity; GO:0052689 carboxylic ester hydrolase activity.
- Proposed term: strigolactone receptor activity (child of GO:0038023, analogous to GO:0038198 auxin receptor activity).