Pi-ta (ORYSJ, UniProt Q84UB1) curation notes

2026-10-10 Identity of the UniProt record

Q84UB1 is an unreviewed TrEMBL entry (928 aa) translated from EMBL AY196754
(AAO45178.1), submitted by Jia, Bryan, Farrall & Valent, cv. Tsuyake
(japonica). The GenBank product name is lower-case "pi-ta protein".
Residue 918 of Q84UB1 is Ser (C-terminal ...LPWLLSLPSMHLQPDLMIV). The
resistant Pi-ta allele from Bryan et al. 2000 is Q9AY26 (EMBL AF207842,
taxon 4530 Oryza sativa), which has Ala918 (...LPWLLSLPAMHLQPDLMIV).
Checked by fetching both FASTA sequences from UniProt REST.
So Q84UB1 is the product of a susceptible pi-ta(-) allele. Bryan et al.:
PMID:11090207
Gramene attached the same IMP defense response (PMID:11090207) and the same
IEA set to both Q84UB1 and Q9AY26. GO annotation is gene-level, so this is not
a mistake as such, but it means the reviewed record is the allele that the
original paper showed does not trigger resistance.
Locus: LOC_Os12g18360 (per deep research; PTR is LOC_Os12g18729, a separate
ARM-repeat gene).

Rx_N coiled-coil (13-114), NB-ARC (214-385), winged helix (477-548), two
R13L4/SHOC2-like LRR blocks (597-857). CC-NB-LRR (CNL). PANTHER
PTHR23155:SF1094.
Walker A GSGGVGKTT (P-loop, ~236-244), kinase-2 FIIIEDLW, GLPL GGLPLAI
are present in the sequence, so the NB-ARC nucleotide pocket looks intact.
No nucleotide binding has been measured for Pi-ta.

Map-based cloning; PMID:11090207
Transient co-expression assay: PMID:11090207 and the Ser918 allele does not.
Direct binding: PMID:10921881 and PMID:10921881
Localisation was never measured; "putative cytoplasmic" is inferred from
architecture PMID:10921881.
US germplasm association study PMID:18943978 (abstract only): Pi-ta marker
co-segregates with resistance to races IB-49 and IC-17. Linkage only; does not
separate Pi-ta from linked Ptr.

Zhao et al. 2018 cloned Ptr, an ARM-repeat protein next to Pi-ta:
PMID:29795191 At the time Ptr was
framed as acting together with Pi-ta.
Xiao et al. 2024 (abstract only in cache): PMID:38834685 PtrB confers
"Pi-ta" resistance, PtrA confers Pi-ta2 resistance. Deep research reports that
they could not reproduce the yeast two-hybrid interaction and that four
independent NLR pi-ta mutants in IR64 stayed resistant
[file:ORYSJ/Pi-ta/Pi-ta-deep-research-falcon.md].
Contrary data: He et al. 2022 (full text) knocked out the Fuhui 2663 allele:
PMID:36050368 Only
two lines, one isolate (KJ201), AVR status of KJ201 not tested, and no
complementation reported. Off-target edits or effects on the linked Ptr
region were not excluded.

The NLR's role in AVR-Pita recognition is directly contradicted by the
locus-resolved 2024 genetics. Any defense role for this NLR now rests on one
small knockout study. The physiological function of the NLR is therefore
unresolved.
ADP binding (NB-ARC, intact P-loop) is the only activity that can be inferred
with confidence, and it is a family-level structural inference.
defense response to bacterium (ARBA): no bacterial data for Pi-ta at all.
Remove.
plant-type hypersensitive response and innate immune response-activating signaling pathway (ARBA): generic NLR propagation; the
only Pi-ta-specific support (Bryan 2000 transient assay, Jia 2000 binding) is
disputed. Over-annotated.
IMP defense response (Bryan 2000): the curator read the full text; the
claim is now disputed by PMID:38834685 but partly supported by PMID:36050368.
Initially marked UNDECIDED; changed to KEEP_AS_NON_CORE so that it agrees
with the IEA row for the same term. It is not removed (deference to the
curator plus the 2022 knockout) and not treated as core.
No NEW terms: no Pi-ta-specific activity or location has been measured.

Q3 necessity vs participation: here even necessity is in doubt. The
"Pi-ta" resistance phenotype maps to Ptr, so a fungal-defense annotation on
the NLR may be attached to the wrong gene of the chr12 cluster.
Q5 sensor/helper NLR pairs: Pi-ta is not part of a known NLR pair. Whether
PTR and the Pi-ta NLR interact at all is not known.