SCR (SCARECROW) curation notes — Arabidopsis thaliana, UniProt Q9M384, AT3G54220

Overview

SCR is a plant-specific GRAS-family transcriptional regulator. Core role: with the mobile
GRAS factor SHORT-ROOT (SHR), it controls the asymmetric (formative) cell division that
generates the cortex and endodermis, and it specifies/maintains the root quiescent centre (QC)
and surrounding stem-cell niche. It acts in a nuclear SHR–SCR heterodimer that recruits
BIRD/IDD zinc-finger transcription factors (JKD, MGP, NUC) to control ground-tissue patterning.

Molecular function — DNA binding vs coregulator

Key point for MF curation: GRAS proteins including SHR–SCR are best characterised as transcription
cofactors that act through DNA-binding partners (BIRD/IDD zinc fingers), not as direct
sequence-specific DNA binders.

Implication: The MF annotations GO:0003700 (DNA-binding transcription factor activity, ISS/IMP)
and GO:0043565 (sequence-specific DNA binding, IDA from PMID:17446396) likely over-state a direct
DNA-binding activity for SCR. SCR/SHR bind target promoters (e.g. MGP, NUC, CYCD6;1) but the
structural and biochemical evidence (PMID:28211915) argues this is indirect, via BIRD/IDD partners.
The IDA "sequence-specific DNA binding" from PMID:17446396 (the SHR-sequestration paper, abstract
does not describe an EMSA/DNA-binding assay for SCR itself) is questionable; best treated as
over-annotation rather than core direct activity. The ISS GO:0003700 calls (PMID:11118137 genome-wide
TF survey; PMID:8756724 original cloning) derive from family/sequence classification of GRAS as
"putative transcription factors," appropriate as a broad classification but better expressed as
transcription regulator / coregulator given current evidence.

Asymmetric cell division and radial patterning (core BP)

QC / stem-cell niche

Protein interactions (replace bare "protein binding")

Maintenance of protein location in nucleus (SHR sequestration)

Gravitropism (shoot)

Leaf bundle sheath / redox

Localization

Domain architecture (UniProt)

Deep research synthesis (Falcon / Edison Scientific)

The Falcon deep-research report (file:ARATH/SCR/SCR-deep-research-falcon.md) corroborates and
slightly extends the existing review; it introduced no contradictions and no UNDECIDED items needed
resolving. Key corroborated points:
- Core MF/BP: SCR is a putative transcriptional regulator required for the formative periclinal
division generating cortex and endodermis [falcon "SCR is a putative transcriptional regulator/transcription factor required for the asymmetric periclinal division that generates cortex and endodermis."]; in scr the division fails and a single heterogeneous ground-tissue layer forms [falcon "In scr mutants, the second asymmetric division fails and a single heterogeneous ground-tissue layer forms instead of separate cortex and endodermis"], establishing normal radial organization [falcon "generating separate cortex and endodermis layers and thus normal radial organization"].
- SHR interaction / nuclear sequestration: confirms direct SHR–SCR interaction and SCR confining SHR
to nuclei [falcon "Reviews further emphasize SCR’s direct interaction with SHR and SCR’s role in confining SHR to nuclei"; "restricting SHR to the nucleus and coordinating downstream patterning and stem cell niche functions"; "SCR co-localizes with SHR in nuclei in primordia, and supports direct SHR–SCR interaction in these contexts"].
- In vivo complexes: FRET-FLIM JKD-YFP + SCR-RFP lifetime reduction up to 0.17 ± 0.02 ns supports
SCR–JKD complex formation [falcon "coexpression of JKD-YFP with SCR-RFP reduced fluorescence lifetime by up to 0.17 ± 0.02 ns, supporting close interaction/complex formation in meristem peripheral/primordia regions"].
- Gravitropism (non-core): amyloplasts in scr fail to sediment, explaining impaired shoot gravitropism
[falcon "amyloplasts in scr do not sediment in response to gravity"].
- New (untracked) context: the report highlights an expanded SAM role (Bahafid et al. 2023, eLife;
PMID not in current GOA) where SCR within the SHR network is needed for normal auxin-maxima
formation and lateral organ initiation, and regulation of CYCD6;1. This is consistent with SCR's
patterning role but does not map to a verifiable new GO term from the existing GOA/UniProt set, so
no NEW annotation was added on this basis.

No new GO ID verifiable from GOA/UniProt warranted a NEW annotation; the GRAS-cofactor mechanism
remains captured by the existing proposed_new_terms entry.

Action summary rationale

PR #1417 review follow-up (ai4c-agent)