BZR1 (BRASSINAZOLE-RESISTANT 1; Q8S307; AT1G75080) — curation notes

Identity / family

Core molecular function — sequence-specific DNA-binding TF / repressor

Process — BR signaling pathway (core)

Regulation / localization (PTM-driven)

Protein interactions (the GO:0005515 IPI annotations)

All of these are generic "protein binding" (GO:0005515) IPI annotations from IntAct/TAIR. They are real interactions but uninformative as MF terms; the informative functions are captured by DNA binding / repressor activity / TF binding / dimerization:
- PMID:17681130 — 14-3-3 (GRF6/P48349) and ASK7/Q39011. Regulatory (14-3-3 sequestration).
- PMID:22307275 — BIN2/ASK7 (Q39011); BR regulates stomatal development via GSK3-mediated MAPK inhibition. Kinase-substrate.
- PMID:22820377 — DELLAs RGL1 (Q9C8Y3), GAI (Q9LQT8), RGA (Q9SLH3); BR/GA/phytochrome common transcription module. BZR1 interacts with DELLA proteins (GA signaling).
- PMID:22820378 — PIF1 (Q8GZM7), PIF4 (Q8W2F3); BZR1-PIF4 integrate BR and environmental signals, bind ~2000 common targets, synergistic PMID:22820378. → DNA-binding TF binding.
- PMID:28650476 — CrY2H-seq interactome: RGL1, TCP15 (Q9C9L2), TCP21 (Q9FTA2), GAI, TCP13 (Q9S7W5). High-throughput.
- PMID:32612234 — phytohormone protein network (large-scale Y2H): BEL1, At3g51180, TCP15, At5g47790, ANAC094, HHO3, TCP21, MYB21, GAI, MGH6.1, TCP16, TCP3, TCP13, RGA. Many TFs.
- PMID:37335918 — BLISTER (BLI, AT3G23980) interacts with BIN2 and BZR1; BLI cooperates with BZR1 to activate BR-responsive genes in skotomorphogenesis.
- PMID:21258370 — PP2A B' subunits (O04375, O04376, Q9LU89, Q8LF36). Phosphatase-substrate.
- PMID:25663622 — BSS1/BOP1 (AT3G57130) complex; BSS1 sequesters BZR1.

Note: Many partners are DNA-binding TFs (PIF1/PIF4, TCP3/13/15/16/21, MYB21, DELLAs are not classic DNA binders but PIFs/TCPs/MYB are) → supports GO:0140297 DNA-binding transcription factor binding as a NEW informative MF.

Biological processes (downstream / developmental — generally non-core developmental outputs of the BR pathway)

Deep research synthesis (Falcon / Edison Scientific, 2026-06-06)

The Falcon deep research report (file:ARATH/BZR1/BZR1-deep-research-falcon.md) corroborates and extends the existing review. Key points used as supported_by evidence:
- Core MF/activator-repressor role: "It binds BRRE/E-box-associated promoters and can activate or repress BR-responsive genes controlling growth and BR homeostasis" — supports GO:0003700 and the regulation-of-transcription terms.
- BR signaling pathway role: BZR1 "acts as a principal nuclear effector of the BR receptor-initiated signaling cascade" — supports GO:0009742.
- Localization switch: "phosphorylated forms are biased toward cytoplasmic sequestration, while dephosphorylated forms accumulate in the nucleus and drive transcriptional outputs"; and "BIN2-phosphorylated BZR1 is retained more in the cytoplasm through 14-3-3 association, whereas dephosphorylated BZR1 accumulates in the nucleus to regulate transcription" — supports nucleus (core) and cytosol (non-core, inactive exported pool).
- Signal integration: reviews "emphasize BZR1 as an integration node for light, auxin, GA, ethylene, and stress signaling" — supports GO:0140297 (DNA-binding TF binding) NEW term.

New mechanistic detail not previously captured (recorded here, not added as GO annotations because no new verifiable GO ID is warranted):
- 14-3-3 recognition is structurally defined: minimal phosphomotif at BZR1 residues 169–175 (RISNpSAP) centered on pSer173, binding 14-3-3κ with KD ~0.5 µM, 2:2 stoichiometry, complex lifetime ~1 s (Obergfell et al. 2024, Plant & Cell Physiology; doi:10.1093/pcp/pcae112-era / bioRxiv 2023.10.13.562204).
- Auxin promotes BZR1 nuclear accumulation via MPK3/MPK6-dependent phosphorylation/destabilization of GRF4 (a 14-3-3) at S248 (Yu et al. 2023, Science Advances, doi:10.1126/sciadv.ade2493).
- BIN2 proximity network (TurboID + phosphoproteomics): 482 BIN2-proximal proteins, BZR1 recovered as a canonical BIN2 substrate (Kim et al. 2023, Plant Cell, doi:10.1093/plcell/koad013).
- BZR1 family is redundant and indispensable for BR signaling (Chen et al. 2019, Mol Plant).

No UNDECIDED annotations existed; none required resolution. No new GO annotation was added from the deep research because the new mechanistic findings (14-3-3 KD, auxin/MPK crosstalk, BIN2 network) concern upstream regulation rather than a new verifiable BZR1 GO molecular function/process/component not already represented.

Curation reasoning summary