WDPCP is a CPLANE ciliary scaffold with an independent actin/septin/polarity role. Mouse microscopy and perturbation establish ciliary-base, cytoplasmic actin and focal-adhesion pools. Recombinant structural work demonstrates individual WDPCP phosphoinositide binding in its C-terminal tail. The full2016paper explicitly reports human WDPCP variants and relevant digit/tongue/palate phenotypes.
The horse N-terminal difference resembles the approximately35-residue human extension relative to mouse reported in the structure. The conserved scaffold supports broad ciliary/cytoskeletal predictions. A separate nine-residue deletion affects the lipid-binding tail; disorder does not imply that deletion is functionally irrelevant, and exact lipid affinity remains unresolved.
The reproducible alignment, source paths and hashes are in the paired comparison. Current UniProt sequences have not been proven identical to the original ProtNLM input sequences. Sequence anomalies are therefore recorded as model/transfer limitations, not as proven wrong-input pipeline errors.
Distinguish transition-zone/base localization from the axonemal shaft. Test the tail deletion before transferring quantitative phosphoinositide affinity.
Every seeded annotation receives a current assessment. UNDECIDED marks unresolved source-specific or biological evidence; these are initial reviews rather than a claim that every original experimental assay has been independently reproduced or verified. The human Edison report is retained as a research synthesis and source-finding aid; decisive YAML excerpts cite primary publications, source records or reproducible analysis. The validator advisory to cite the deep-research file is deliberately not satisfied by citing AI prose as biological proof.
ProtNLM2 files were not opened or used. Deep research: just deep-research-falcon HORSE WDPCP --fallback perplexity-lite
failed (Edison API "Failed to authenticate", 403; the perplexity-lite fallback also failed), so this
re-review uses the cached primary literature directly.
WDPCP-bioinformatics/rereview/RESULTS-rereview.md): A0A3Q2KRK8 is colinear withAll horse models, human, mouse, rat and Xenopus WDPCP are in PTHR13667:SF5. The PAINT node PTN001007408
(Eumetazoa) carries IBD for GO:0097541, GO:0044782, GO:0045184 and GO:0007399, but not plasma membrane,
axoneme, phosphatidylinositol binding or septin cytoskeleton organization (taken as deliberate).
genes/HORSE/WDPCP__A0A9L0T876). A0A9L0R7M2 is the more human-like full-length model and could be thegenes/human/WDPCP/, all rowsinterpro/panther/PTHR13667/PTHR13667-review.yaml places horse A0A3Q2KRK8 and human O95876 in SF5; nomodules/bbsome.yaml mentions WDPCP/BBS15 only as out of scope; no CPLANE module exists.The re-review had proposed NEW rows (GO:0097541, GO:0044782) on this benchmark accession because GOA propagates the
gene's annotations, including PAINT IBA rows, to one representative product per gene and not to
alternative transcript models. The same terms are already annotated in GOA on the canonical horse
product of this gene (WDPCP__A0A9L0T876, reviewed in genes/HORSE/WDPCP__A0A9L0T876/). Filling that propagation
convention on a second product of the same gene is not a curation gap, so the rows were withdrawn
for consistency across the cohort. The gene-level function is unchanged and is recorded on the
canonical product's review; this file's description and core functions still describe it.
The GO:0005930 axoneme row's reason still said the basal plate localization "is added as a NEW row below".
That row was withdrawn in PR #5303 because GOA carries it on the canonical product A0A9L0T876. The sentence
now says so.