Gene Ontology annotation through association of InterPro records with GO terms

Annotation inferences using phylogenetic trees

The BBSome controls IFT assembly and turnaround in cilia.

The BBSome assembles IFT particles at the ciliary base and, after binding the anterograde IFT particle as a cargo, regulates IFT turnaround/recycling at the ciliary tip.

"the in vivo function for the BBSome is to regulate the assembly of the IFT particles at the ciliary base"
The BBSome binds the moving IFT particle as a cargo, not as an integral structural component.

"the BBSome binds to the IFT particle like a cargo but not a structural component"
Worm BBS-9 is a member of the BBSome, shown directly by BiFC coexistence of BBS-1 and BBS-9 in the same complex.

"fluorescence complementation can be observed in BBS-1"
BBS1, BBS7 and BBS9 lie close to each other in the BBSome, consistent with the worm BBS-1–BBS-9 interaction.

"consistent with the prediction that mammalian BBS1, 7, and 9 locate closely to each other in the BBSome"
A bbs-9 nonsense allele (Q171) separates IFT-A and IFT-B during anterograde transport, the canonical bbs-null IFT-uncoupling phenotype.

"encodes BBS-9 with a nonsense mutation at Q171 site"
When the BBSome is uncoupled from moving IFT, BBS-9 (with BBS-2/5/7/8) loses IFT movement and shows only dim ciliary staining, accumulating at the base.

"only showed very dim ciliary staining when compared to"
The BBSome shares coat features with COPI/COPII/clathrin and can directly recognize IFT cargo.

"shares the common structural features with COPI, COPII, and clathrin coats, and can directly recognize IFT cargos"

PMID:22022287

Mutations in a guanylate cyclase GCY-35/GCY-36 modify Bardet-Biedl syndrome-associated phenotypes in Caenorhabditis elegans.

The eight BBSome proteins function as a conserved complex regulating vesicular sorting/packaging, IFT, and cilium maintenance and function.

"eight function mostly as a conserved protein complex (BBSome)"
Loss of BBSome function in C. elegans causes cilium-dependent developmental and behavioral defects (small body size, developmental delay, exploration defects) that are modified by cGMP signalling (GCY-35/GCY-36, EGL-4).

"exploration defects exhibited by multiple bbs mutants"

PMID:30014846

Thioredoxin shapes the C. elegans sensory response to Pseudomonas produced nitric oxide.

bbs-9 null mutants are cilia-defective and fail to avoid NO and NO-producing P. aeruginosa, showing bbs-9 is required for cilium-dependent NO sensory behavior.

"Two cilia defective mutants, osm-12(n1606) null mutants and bbs-9(gk471) null mutants, were both defective in avoiding the lawn of PA14 and the NO donor"

PMID:26150102

BBS4 and BBS5 show functional redundancy in the BBSome to regulate the degradative sorting of ciliary sensory receptors.

The molecular activity by which the BBSome controls ciliary membrane protein homeostasis is stated by the field to remain unclear.

"the definite molecular activity of the BBSome in regulating the homoeostasis of ciliary membrane proteins remain unclear"

file:worm/bbs-9/bbs-9-deep-research-falcon.md

Deep research report on bbs-9 (Edison/falcon)

BBS-9 is the central structural hub of the BBSome, directly contacting more subunits than any other component; its GAE domain heterodimerizes with BBS1 and its C-terminal coiled-coil pairs with BBS2 to form the neck of the complex.

"BBS-9 directly contacts four to five other BBSome subunits, more than any other component"