See1 (UMAG_02239; UniProt A0A0D1C8C8) - curation notes

Sources

Primary (and essentially only) experimental paper: Redkar et al. 2015 Plant Cell, PMID:25888589 (full text cached).
Falcon deep research (See1-deep-research-falcon.md): confirms identity (um02239 = see1) and that no newer
primary See1 mechanism has been published; Sts2/UMAG_05318 (2023) is a distinct effector.

157-aa precursor with N-terminal secretion signal (residues 1-21; constructs use See1 22-157)
PMID:25888589.
No catalytic domain or conserved family established (deep research).

Fungal-delivered See1-3xHA (immunogold TEM): PMID:25888589;
PMID:25888589.
Secreted mCherry control stayed at the interface - argues translocation is See1-specific.
Bombardment: PMID:25888589; cell-to-cell
spread seen only in overexpression, PMID:25888589
Conclusion: all three GOA CC terms (extracellular region, host cell cytoplasm, host cell nucleus) are supported.
Extracellular region is the transit compartment (biotrophic interface); site of action is host cytoplasm/nucleus.

Organ-specific: required for seedling-leaf tumours, not tassel tumours
PMID:25888589.
DNA synthesis reactivation: PMID:25888589
EdU: 67.5% (SG200) vs 7.3% (Δsee1) of colonized cells at 4 dpi; Δtin3 (another small-tumour mutant) retained ~44%,
so the defect is not a trivial consequence of small tumours.
GO:0141017 "effector-mediated induction of cell cycle reactivation in host" - definition (QuickGO): symbiont process
in which a secreted molecule reactivates the host cell cycle, resulting in DNA synthesis and host cell division,
contributing to vegetative tumour formation. Essentially tailored to this paper; correct symbiont-side term. ACCEPT.
Mechanism: interacts with ZmSGT1 (Y2H, in planta co-IP, BiFC in cytoplasm and nucleus)
PMID:25888589;
PMID:25888589
Downstream steps unresolved PMID:25888589
Immune modulation is only proposed ("Hijacking of SGT1 may contribute to the deactivation of immune responses.") -
not sufficient for a NEW suppression-of-host-immunity term.

No GO MF term fits: the only known activity is binding SGT1 and blocking its phosphorylation. "protein binding" is
excluded by policy; no evidence of kinase-inhibitor activity on the MAPK itself (direct inhibition not shown), so
"protein kinase inhibitor activity" / "molecular function inhibitor" would over-interpret. Leave MF unset in
core_functions.

See1's single BP annotation already uses a symbiont-side effector term (GO:0141017), backed by IDA on the effector
itself (knockout + complementation + EdU), not IEA. No plant-side defense terms present. CC annotations use
host-* terms correctly. Comparable to CMU1 (symbiont-side GO:0140502).