CYP79B3 (At2g22330, Q501D8) curation notes

2026-10-03 — initial review (claude-code)

Sources: UniProt Q501D8, GOA (25 rows), Falcon deep research
(CYP79B3-deep-research-falcon.md), cached publications, and the completed
paralog review genes/ARATH/CYP79B2/CYP79B2-ai-review.yaml (kept strictly
consistent). Module: modules/camalexin_biosynthesis.yaml, annoton
cyp79b_activity (GO:0090489, ER membrane) — this review agrees.

Activity

• Hull et al. 2000 cloned CYP79B2 and CYP79B3 and showed both convert Trp to IAOx
  in E. coli membrane extracts PMID:10681464.
  Only the abstract is cached; deep research (Fig. 2C) confirms CYP79B3 was assayed
  directly, not by inference from CYP79B2.
• UniProt: EC 1.14.14.156, RHEA:33279, reaction uses reduced
  [NADPH--hemoprotein reductase] (flavoprotein donor) -> GO:0090489 sits under
  GO:0016712, not GO:0016709 (same correction as CYP79B2).
• No CYP79B3-specific kinetics or substrate panel; Phe/Tyr negative tests were done
  on CYP79B2 only (deep research).
• GOA has only an IEA for GO:0090489 on CYP79B3; there is no experimental MF row,
  although Hull 2000 is a direct assay. Proposed NEW GO:0090489 (IDA, PMID:10681464).

Pathways (shared IAOx branch point)

• Camalexin and indole glucosinolates: double mutant devoid of both; labelled IAOx
  is incorporated into camalexin PMID:15148388.
• Paralog difference: PMID:15148388. So CYP79B2
  is the main pathogen-induced contributor; CYP79B3 still catalyses the same step.
• IAA: PMID:12464638; root IAA synthesis
  reduced PMID:15772288. Minor route; non-core.
• CYP79B3-GUS in roots around lateral root primordia PMID:15772288.

Localization

• UniProt: single-pass membrane protein (TM 22-42), signal anchor typical of ER P450s.
• No direct CYP79B3 localization in the cache. Deep research notes an old N-terminal
  GUS fusion that went to plastids, contradicted by predictions and P450 biology, and
  unresolved. CYP79B2 colocalizes with ER CYP71A13 (Mucha 2019). Treated ER membrane
  as the location by family inference (IBA accepted) and chloroplast ISM as
  over-annotation (not REMOVE, since a plastid fusion report exists).
• CYP79B3 is NOT part of the ComplexPortal camalexin metabolon rows (no NAS rows for
  B3 in GOA), unlike CYP79B2.

Defence phenotypes (all double mutant, all upstream necessity)

• P. brassicae susceptibility PMID:20230487, mlo2 antifungal defence
  PMID:20023151, flg22 callose PMID:19095898, Pf.SS101 ISR PMID:23073694.
  Kept as non-core, matching CYP79B2. Did not add defense response to fungus:
  CYP79B3 makes a precursor; the antifungal work is done by camalexin and indole
  glucosinolate hydrolysis products (PAD3, PEN2, CYP81F2 sides).
• SAR (GO:0010112, IEP, Truman 2010, abstract only): indole compounds implicated in
  SAR PMID:20081042. An expression change does not show that a
  biosynthetic enzyme regulates SAR -> MARK_AS_OVER_ANNOTATED.
• Wounding (IEP, PMID:17675405): microarray list of JA-dependent wound-inducible
  genes; CYP79B3 not named in main text (presumably in supplementary list). Kept
  non-core; JA/wound inducibility of CYP79B3 is consistent with deep research
  (MeJA 3.5-fold induction, Mikkelsen 2003).
• Aphid (IEP, PMID:23144921): PMID:23144921. Non-core.