GSTF6 (At1g02930, P42760) — curation notes
Identity
- Phi-class glutathione S-transferase, 208 aa, GST N-terminal (2-83) and C-terminal (89-208) domains; EC 2.5.1.18 (UniProt P42760).
- Synonyms ERD11, GST1, and (historically) AtGSTF3. Caution: in current Arabidopsis GST nomenclature GSTF3 is a different locus (At2g02930); the deep research flags this [file:ARATH/GSTF6/GSTF6-deep-research-falcon.md "“GSTF3” is an ambiguous historical alias"]. This matters for the Dixon et al. 2011 ligand-binding annotations (below).
- Tandem duplicate of GSTF7 PMID:15159623.
Expression
Biochemistry
- Recombinant GSTF6 is soluble and catalyses GSH conjugation PMID:12090627.
- CDNB activity reported as very low (0.87 nmol/min/mg; Wangwattana 2008, no PMID, via deep research). Physiological substrate(s) unknown.
Camalexin
- Su et al. 2011 [PMID:21239642 "GSTF6 overexpression increased and GSTF6-knockout reduced camalexin production"; "Arabidopsis GSTF6 expressed in yeast cells catalyzed GSH(IAN) formation"].
- Full text (PMC3051237, read via WebFetch, not cached, so not quoted in YAML): knockout effect ~27-28% reduction; overexpression +10-30%; GFP-expressing control yeast also formed GSH(IAN), GSTF6 adding only 40-61% more. So the yeast assay shows enhancement over a substantial non-GSTF6 background (spontaneous or endogenous yeast GST).
- Reviews repeat GSTF6 as the conjugating enzyme PMID:21712415, PMID:23449503.
- Counterevidence (Mucha 2019, PMID:31511315; full text not cached; via deep research): gstf2 gstf3 gstf6 triple knockout and quadruple knockdown had no significant camalexin change after AgNO3; GSTF6 did not boost camalexin in N. benthamiana reconstruction; 41/54 Arabidopsis GSTs supported GS-IAN formation with CYP71A13 in yeast. Activated intermediate (indole cyanohydrin) can react spontaneously with GSH. [file:ARATH/GSTF6/GSTF6-deep-research-falcon.md "Such findings point to enzyme redundancy, spontaneous chemistry, host-dependent effects, or spatial organization, rather than unique GSTF6 substrate specificity"].
- GSTU4 (not GSTF6) is the GST physically recruited to the P450 metabolon, and it is NOT a pathway enzyme PMID:31511315. Do not transfer metabolon membership to GSTF6.
- GOA has no camalexin biosynthesis annotation for GSTF6 (QuickGO, checked 2026-10-03), while CYP71A13, CYP71B15, GGP1 carry GO:0010120. The ComplexPortal camalexin metabolon (CPX-2833) does not include GSTF6.
- Decision: no NEW GO:0010120. Evidence is contributory/partially redundant and contested; module records GSTF6 as "implicated". Raised as a suggested question.
Localization
- No targeting peptide; predicted cytosolic PMID:21712415. Cytosolic SEC proteome (PMID:25293756) agrees.
- Organelle/wall/vacuole/PD/extracellular HDA hits are best read as contamination of an abundant soluble protein (e.g. PD proteome "still has a significant number (35%) of putative cytoplasmic contaminants" PMID:21533090).
- Stress granule (Kosmacz 2019) — kept as non-core.
Ligand binding (Dixon et al. 2011, PMID:21631432)
- Abstract reports camalexin and quercetin-3-O-rhamnoside binding by GSTF2; heterocycle binding by "GSTF2 and GSTF3". GSTF6 is not named in the abstract and the full text is paywalled (403). Could be a GSTF3/GSTF6 alias issue, but I cannot verify -> UNDECIDED.
Not anthocyanin carrier
- gstf6-1 has no anthocyanin defect; TT19 binds C3G 8.4x better (deep research; Wangwattana 2008, Sun 2012).
2026-10-15 journal: QuickGO record for the PMID:21631432 rows (PR #5026 follow-up)
- Query (re-run 2026-10-15): QuickGO REST,
https://www.ebi.ac.uk/QuickGO/services/annotation/search?reference=PMID:21631432&limit=200 (Accept: application/json) returned 4 annotations, all IDA enables, assigned by TAIR: GSTF2 (P46422) GO:2001147 camalexin binding and GO:2001227 quercitrin binding; GSTF6 (P42760) the same two terms. Nothing for GSTF3 (Q9SLM6, At2g02930). This fits the abstract's "GSTF2 and GSTF3" being mapped to P42760 via its legacy alias AtGSTF3. Both GSTF6 rows remain UNDECIDED (full text not readable), with a question to TAIR. GSTF6's own role in camalexin biosynthesis (GS-IAN formation) means camalexin binding is not biologically implausible; the concern is the name mapping.