Mouse loss-of-function, rescue and microscopy connect CC2D2A to mother-centriole appendages, ciliary assembly and transition-zone elaboration. Loss disrupts cilia-dependent Shh signaling and embryonic laterality/neural development. These developmental roles arise through ciliary organization.
Horse N-terminal deletions align within the human predicted disordered1–241region, while the long coiled-coil/C2 architecture is retained. This supports broad ciliary/developmental transfer. Renal tubule ciliation defects alone do not resolve the more specific kidney-development claim, which remains UNC.
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.
Confirm the horse transcript model and distinguish renal morphogenesis from renal cilia/homeostasis. A calcium-binding molecular activity should not be invented solely from the C2 domain label.
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 output was not opened or used. Deep research (just deep-research-falcon HORSE CC2D2A --fallback perplexity-lite) failed: falcon "Failed to authenticate" and perplexity returned HTTP 401 insufficient quota. The review uses cached primary literature instead (PMID:24947469, PMID:21725307 and PMID:21422230 with full text; PMID:22179047 abstract only).
CC2D2A-bioinformatics/compare_sequences_rereview.py → RESULTS-rereview.md / results-rereview.json aligns all of them, plus mouse Q8CFW7, to human Q9P2K1 (1620 aa). The existing RESULTS.md was not modified.existing_annotations are all NEW.interpro/panther/PTHR20837/PTHR20837-review.yaml lists A0A5F5PJ44 as an SF7 representative, which agrees with this review.PTHR20837-paint.tsv, node PTN000464650 (taxon 2759) carries ciliary transition zone, protein localization to ciliary transition zone and non-motile cilium assembly. Horse is inside that clade, so these three are added as NEW with IBA, mirroring the horse canonical model.Rewrote the description, which now covers the domain architecture, MKS-module role and gene-model identity. Added four NEW rows. Changed core_function process from cilium assembly to non-motile cilium assembly. Added references PMID:21725307, PMID:22179047, PMID:21422230, the PAINT tsv, the horse UniProt record and RESULTS-rereview.md. All existing references were kept.
A0A5F5PUW7, the gene-centric canonical horse CC2D2A model (same gene). No review exists in the repo. Its folder would be genes/HORSE/CC2D2A__A0A5F5PUW7. The human ortholog Q9P2K1 already has a complete review (genes/human/CC2D2A, every annotation actioned).
The re-review had proposed NEW rows (GO:0035869, GO:1904491, GO:1905515, GO:0036038) 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 (CC2D2A__A0A5F5PUW7, reviewed in genes/HORSE/CC2D2A__A0A5F5PUW7/). 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.