PBL27 (At5g18610, Q1PDV6) curation notes

Sources used

• Falcon deep research: PBL27-deep-research-falcon.md (used for orientation; claims below traced to cached primary papers).
• PMID:24750441 (Shinya et al. 2014, Plant J) - abstract only cached.
• PMID:27679653 (Yamada et al. 2016, EMBO J) - full text cached.
• PMID:31524595 (Liu et al. 2019, eLife) - full text cached (newly fetched).
• PMID:29907700 (Rao et al. 2018, Plant Physiol) and PMID:29871986 (Bi et al. 2018, Plant Cell) - abstract only (newly fetched); both PMIDs resolved from DOIs via NCBI esearch.
• PMID:32385340 (Uemura et al. 2020, Commun Biol) - full text cached.
• PMID:14506206 (Nuhse et al. 2003) - abstract only; plasma membrane phosphoproteomics (HDA).

Identity

RLCK subfamily VII (VII-1) member, PBS1-like; Arabidopsis homologue of rice OsRLCK185.
UniProt: palmitoylation at Cys-4/Cys-7 (by similarity) anchors it at the plasma membrane;
catalytic activity (Ser and Thr, EC 2.7.11.1) with ECO:0000269 from PMID:27679653.

Chitin -> MAPK branch

• PBL27 is "an immediate downstream component of the chitin receptor CERK1" and CERK1
  "preferentially phosphorylated PBL27 in comparison to BIK1" PMID:24750441.
• Knockout suppresses chitin-induced MPK3/6 activation, callose deposition and resistance
  to fungal and bacterial infection; flg22 contribution "very limited" PMID:24750441.
• "PBL27 phosphorylates MAPKKK5 in a CERK1‐dependent manner." PMID:27679653
• "PBL27 directly phosphorylated only the C‐terminal domain of MAPKKK5" PMID:27679653;
  phosphosites S617, S622, S658, S660, T677, S685; "The S622A mutation strongly reduces
  phosphorylation by PBL27." -> Ser and Thr substrate residues: protein Ser/Thr kinase.
• Interacts with MAPKKK5 at the PM: "PBL27 interacts with MAPKKK5 at the PM where CERK1 and
  PBL27 form the complex" PMID:27679653; weaker interaction with MAPKKK3 (Y2H) PMID:27679653.
• PBL27 Alternaria phenotype is cited, not re-tested, in PMID:27679653 ("As reported
  previously, lyk5, cerk1, and pbl27 mutations reduce resistance to the fungal pathogen
  Alternaria brassicicola").

Dispute

• Rao et al. 2018: "RLCK VII-4 members were required for the chitin-triggered activation of
  MAPK" PMID:29907700. Per deep research (full text not cached), the pbl27 allele and an
  rlck vii-1 quintuple mutant did not show reduced chitin MAPK activation.
• Bi et al. 2018: RLCK VII members "directly phosphorylate MAPKKK5 Ser-599, which is required
  for pattern-triggered MPK3/6 activation" PMID:29871986; PBL27 is not the dominant
  MAPKKK5 kinase in their hands (deep research; full text not cached).
• Conclusion: biochemical activity (MAPKKK5 phosphorylation) is solid; quantitative genetic
  requirement for MAPK activation is contested and likely redundant with RLCK VII-4.
  Keep the GOA IMP MAPK row (curators read full text) but flag the dispute.

Guard-cell branch (SLAH3)

• "PBL27 has the capacity to phosphorylate SLAH3, of which S127 and S189 are required to
  activate SLAH3." PMID:31524595
• "We conclude that PBL27 is the primary kinase that directly phosphorylates SLAH3 for the
  release of anions and functions in an activation status-dependent manner regulated by
  CERK1." PMID:31524595
• "consistently stomata of pbl27 mutants showed no closure to chitin either" PMID:31524595
• pbl27 does not affect chitin ROS burst; PBL27 does not interact with RBOHD PMID:31524595,
  consistent with the BIK1-type branch handling ROS.
• Not in GOA -> NEW GO:0090333 regulation of stomatal closure. PBL27 performs the
  phosphorylation step that activates the channel (participation), and the comparator RLCK
  BIK1 carries regulation of stomatal movement for its OSCA1.3 phosphorylation.

Herbivore branch (HAK1)

• AtHAK1 (At1g06840) interacts with PBL27 (AlphaScreen, BiFC, co-IP) PMID:32385340;
  pbl27 and hak1 reduce Fr-alpha-induced ethylene/PDF1.2 and herbivore resistance. No
  substrate shown downstream. Non-core; not proposed as NEW.

Other

• ALR1/PSKR1 phosphorylation in aluminium signalling (Xu 2025, Nature Plants) mentioned only
  in deep research; not cached, not used for annotation.

Decisions summary

• Protein kinase rows accepted; IDA generic kinase -> MODIFY to Ser/Thr kinase.
• protein binding rows (CERK1 x3, MAPKKK3, MAPKKK5, HAK1): MARK_AS_OVER_ANNOTATED, consistent
  with BIK1 review; interactions are enzyme-substrate relations captured by the kinase MF.
• innate immune response (IMP) -> MODIFY to GO:0002752 cell surface pattern recognition
  receptor signaling pathway (PBL27 is a relay kinase in the CERK1 PRR pathway; matches
  module and CERK1 review).
• Defence response to fungus/bacteria and regulation-of-defence rows: KEEP_AS_NON_CORE
  (phenotype-level; necessity rather than mechanism).