{"gene":"KIF27","run_date":"2026-06-10T02:59:49","timeline":{"discoveries":[{"year":2004,"finding":"KIF27 was identified as the human ortholog of Drosophila Costal-2 (Cos2) by bioinformatics and phylogenetic analysis. KIF27 shares the same domain structure as Cos2, including a kinesin motor (KISc) domain, Ci-binding domain, and Smo-binding domain. KIF7 was identified as a paralog of KIF27 within the human genome.","method":"Bioinformatics/phylogenetic analysis; domain architecture comparison","journal":"International journal of oncology","confidence":"Low","confidence_rationale":"Tier 4 / Weak — computational prediction only, no experimental validation of interactions or function","pmids":["15547729"],"is_preprint":false},{"year":2005,"finding":"Mouse Fu (Stk36)-deficient mice do not exhibit embryonic phenotypes indicative of perturbed Hh signaling, suggesting that the Fu–Kif27/Kif7 complex does not have a conserved role in mammalian Hh signal transduction, in contrast to the Drosophila pathway.","method":"Gene-targeted knockout mouse; phenotypic analysis","journal":"Molecular and cellular biology","confidence":"Medium","confidence_rationale":"Tier 2 / Moderate — clean KO with defined phenotypic readout; negative result replicated in later studies","pmids":["16055716"],"is_preprint":false},{"year":2009,"finding":"Mouse Fu (Stk36) physically interacts with Kif27, a mammalian Cos2 orthologue. This interaction was identified by co-immunoprecipitation and links Fu to known structural components of the central pair apparatus of motile 9+2 cilia. Fu is essential for construction of the central pair apparatus and is linked to ciliogenesis rather than Hh signaling in mice.","method":"Co-immunoprecipitation; mouse knockout genetics; electron microscopy of cilia ultrastructure","journal":"Nature","confidence":"High","confidence_rationale":"Tier 2 / Strong — reciprocal Co-IP demonstrating physical interaction, combined with KO phenotypic analysis and ultrastructural evidence, replicated across multiple tissues","pmids":["19305393"],"is_preprint":false},{"year":2009,"finding":"In vitro analysis of mammalian Kif7 and Kif27 led to the conclusion that neither protein has a role in Hh signaling (negative result for Hh pathway function in mammals). Kif7 accumulates at the distal tip of primary cilia in a Hh-dependent manner and is required for Gli3 localization to cilia and processing of Gli3 to its repressor form.","method":"Kif7 knockout mice; immunofluorescence localization; Gli3 processing assays","journal":"Current biology : CB","confidence":"Medium","confidence_rationale":"Tier 2 / Moderate — KO mouse with defined molecular phenotype (Gli3 processing); KIF27 negative result for Hh signaling is from in vitro analysis cited within this paper","pmids":["19592253"],"is_preprint":false},{"year":2009,"finding":"In planarians, RNAi knockdown of Cos2/Kif27/Kif7 orthologs does not result in detectable Hh signaling defects but is essential for ciliogenesis, establishing a mechanistic link between Kif27-family proteins and cilia function independent of Hh signaling.","method":"RNA interference in planarians; phenotypic analysis of cilia and Hh pathway readouts","journal":"Science (New York, N.Y.)","confidence":"Medium","confidence_rationale":"Tier 2 / Moderate — RNAi loss-of-function with specific cellular phenotypes (ciliogenesis vs. Hh signaling) assessed separately","pmids":["19933103"],"is_preprint":false},{"year":2011,"finding":"Kif27 knockout mice develop autosomal recessive congenital hydrocephalus, and the pathogenic mechanism is attributed to dysfunctional motile cilia, placing KIF27 as an essential component of motile ciliogenesis in vivo.","method":"Gene knockout mouse; neuropathological and histological analysis; ciliary function assessment","journal":"Veterinary pathology","confidence":"Medium","confidence_rationale":"Tier 2 / Moderate — KO mouse with defined organismal phenotype attributed to ciliary dysfunction; single report","pmids":["21746835"],"is_preprint":false},{"year":2013,"finding":"Fu (Stk36) physically associates with Kif27 at the base of motile cilia and with known central pair components Spag16 and Pcdp1 in oviductal epithelium. Fu-deficient mouse oviducts show defects in central pair construction and cilia orientation, placing Kif27 as part of a complex required for central pair apparatus assembly.","method":"Co-immunoprecipitation; immunofluorescence localization; Fu-deficient mouse oviduct analysis","journal":"Developmental dynamics : an official publication of the American Association of Anatomists","confidence":"Medium","confidence_rationale":"Tier 2 / Moderate — Co-IP and localization with functional KO phenotype, single lab replicating earlier findings in a new tissue","pmids":["23907739"],"is_preprint":false},{"year":2014,"finding":"Kif27 is detected in the manchette of spermatids, and Fu (Stk36) interacts with Kif27 in the context of spermatogenesis. Conditional inactivation of Fu in male germ cells causes infertility with abnormal sperm head shaping and periaxonemal structure defects, placing Kif27 as part of the Fu-containing complex in spermatid head shaping structures.","method":"Co-immunoprecipitation; immunofluorescence localization in manchette; conditional KO mouse","journal":"Developmental biology","confidence":"Medium","confidence_rationale":"Tier 2 / Moderate — Co-IP and localization data with conditional KO phenotype; Kif27 role is inferred from its interaction and co-localization with Fu rather than direct Kif27 KO","pmids":["24525297"],"is_preprint":false},{"year":2016,"finding":"Sequence similarities between KIF21A, KIF7, and KIF27 in the regulatory domain suggest a conserved autoinhibitory mechanism (antiparallel coiled-coil regulatory domain inhibiting the motor domain) shared among kinesin-4 family members. The KIF21A regulatory domain interacts with the KIF21B motor domain, and analogous sequences in KIF27 suggest this regulation is conserved.","method":"Crystal structure of KIF21A regulatory domain; domain-interaction assay; sequence conservation analysis with KIF27","journal":"Scientific reports","confidence":"Low","confidence_rationale":"Tier 3 / Weak — structural data is for KIF21A; KIF27 involvement is inferred from sequence similarity without direct experimental validation in KIF27","pmids":["27485312"],"is_preprint":false},{"year":2018,"finding":"KIF27 is a slow and processive kinesin whose mechanochemical behavior arises from a slow ATPase rate and high affinity for both ATP and microtubules. KIF27 can influence microtubule dynamics. Unlike KIF7 (immotile due to inability to release ADP upon microtubule binding), KIF27 moves slowly and processively but cannot cooperate for fast processive transport in teams. Neither KIF7 nor KIF27 functions as a transporter; instead they are proposed to act as microtubule-based tethers of signaling complexes.","method":"In vitro single-molecule motility assays; microtubule dynamics assays; ATPase kinetics; mutagenesis-guided mechanistic analysis","journal":"The Journal of cell biology","confidence":"High","confidence_rationale":"Tier 1 / Strong — reconstituted in vitro with multiple orthogonal biochemical and biophysical assays (motility, ATPase, microtubule dynamics) providing direct mechanistic characterization","pmids":["29351996"],"is_preprint":false},{"year":2025,"finding":"KIF27 localizes to the transition zone (TZ) of motile cilia and forms a cytoskeletal scaffold that promotes TZ integrity. Loss of KIF27 causes specific defects in axonemal structure and disrupts cilia beating, leading to a primary ciliary dyskinesia (PCD)-like phenotype. The motile properties of KIF27 are dispensable for its function in cilia assembly; instead, KIF27 acts as a microtubule scaffold to regulate TZ architecture and enable correct ciliary incorporation of motility-generating proteins. KIF27 interactors at the TZ were identified by proteomics.","method":"Mouse genetics (KO); high-resolution imaging; in situ cryo-electron tomography; single-molecule motility assays; proteomics","journal":"Proceedings of the National Academy of Sciences of the United States of America","confidence":"High","confidence_rationale":"Tier 1 / Strong — multiple orthogonal methods including cryo-ET structural analysis, KO mouse genetics with defined phenotype, single-molecule motility assays, and proteomics in a single rigorous study","pmids":["41400996"],"is_preprint":false},{"year":2025,"finding":"KIF27 promotes the integrity of the transition zone (TZ), a diffusion barrier at the cilium base. Loss of KIF27 results in defects in axonemal structure and cilia beating recapitulating primary ciliary dyskinesia. KIF27's motile properties are dispensable for this function; it acts as a microtubule scaffold to regulate TZ architecture and enable ciliary incorporation of motility-generating proteins. (Preprint version of PMID:41400996, confirms same findings prior to peer review.)","method":"Mouse genetics; single-molecule motility assays; proteomics; high-resolution imaging; in situ cryo-tomography","journal":"bioRxiv","confidence":"High","confidence_rationale":"Tier 1 / Strong — same study as PMID:41400996 with multiple orthogonal experimental methods; preprint predating the published version","pmids":[],"is_preprint":true}],"current_model":"KIF27 is a kinesin-4 family motor protein that functions primarily as a microtubule-associated scaffold at the ciliary transition zone to promote motile cilia assembly and structural integrity, acting through physical interactions with Fu (Stk36) and central pair apparatus components rather than through its motile properties, and does not play a significant role in mammalian Hedgehog signal transduction despite being a structural ortholog of the Drosophila Hh pathway component Costal-2."},"narrative":{"mechanistic_narrative":"KIF27 is a kinesin-4 family motor protein that functions as a microtubule-based scaffold for the assembly and structural integrity of motile cilia rather than as a transporter [PMID:29351996, PMID:41400996]. Although originally identified by phylogenetics as the human ortholog of Drosophila Costal-2 (Cos2), sharing its kinesin motor, Ci-binding, and Smo-binding domain architecture and being paralogous to KIF7 [PMID:15547729], mammalian KIF27 does not contribute to Hedgehog signal transduction; loss-of-function across mouse, planarian, and in vitro systems consistently fails to perturb Hh pathway readouts while disrupting ciliogenesis [PMID:19592253, PMID:19933103]. Biochemically, KIF27 is a slow, processive motor with a low ATPase rate and high affinity for ATP and microtubules, can influence microtubule dynamics, and does not cooperate for fast team-based transport, consistent with a role as a microtubule-based tether of signaling complexes rather than a cargo-moving motor [PMID:29351996]. KIF27 physically associates with the kinase Fu (Stk36) at the base of motile cilia, linking it to central pair apparatus components including Spag16 and Pcdp1, and Fu/KIF27 complexes are required for central pair construction and cilia orientation in oviductal epithelium [PMID:19305393, PMID:23907739]. KIF27 localizes to the ciliary transition zone, where it forms a cytoskeletal scaffold that maintains transition zone architecture and enables correct ciliary incorporation of motility-generating proteins; its motile properties are dispensable for this function [PMID:41400996]. Consistent with this structural role, Kif27-knockout mice develop autosomal recessive congenital hydrocephalus from dysfunctional motile cilia, and KIF27 loss produces axonemal defects and disrupted ciliary beating recapitulating a primary ciliary dyskinesia-like phenotype [PMID:21746835, PMID:41400996].","teleology":[{"year":2004,"claim":"Established KIF27's identity and domain architecture by defining it as the human Costal-2 ortholog, framing the hypothesis that it might function in Hedgehog signaling like its Drosophila counterpart.","evidence":"Bioinformatics and phylogenetic analysis with domain architecture comparison","pmids":["15547729"],"confidence":"Low","gaps":["Computational prediction only with no experimental validation of interactions or function","Hh-pathway role inferred from Drosophila ortholog, not tested in mammals","No localization or biochemical data"]},{"year":2005,"claim":"Tested whether the Fu–Kif27/Kif7 module conserves a Hh signaling role in mammals, and found it does not, redirecting attention away from canonical Hh function.","evidence":"Stk36 (Fu)-deficient knockout mouse with phenotypic analysis","pmids":["16055716"],"confidence":"Medium","gaps":["Negative result for Hh does not define the alternative function","Does not directly assay KIF27 loss","No mechanistic readout for cilia at this stage"]},{"year":2009,"claim":"Connected KIF27 to ciliogenesis by demonstrating a physical interaction with Fu and linking the complex to the central pair apparatus of motile cilia rather than Hh signaling.","evidence":"Co-immunoprecipitation, mouse knockout genetics, and electron microscopy of cilia ultrastructure (Fu); parallel Kif7 KO and planarian RNAi establishing cilia-not-Hh roles","pmids":["19305393","19592253","19933103"],"confidence":"High","gaps":["KIF27's direct contribution separated from Fu and from KIF7 not fully resolved","Mechanism of central pair assembly by the complex undefined","No structural detail of the interaction"]},{"year":2011,"claim":"Demonstrated that KIF27 is required in vivo for motile cilia function by showing its loss causes congenital hydrocephalus, establishing an organismal phenotype.","evidence":"Kif27 knockout mouse with neuropathological/histological analysis and ciliary function assessment","pmids":["21746835"],"confidence":"Medium","gaps":["Single report","Molecular basis of the ciliary defect not resolved","Does not distinguish scaffolding from motor activity"]},{"year":2013,"claim":"Defined the molecular context of KIF27 at the cilium base by placing it in a Fu complex with central pair components Spag16 and Pcdp1 required for central pair construction and cilia orientation.","evidence":"Co-immunoprecipitation, immunofluorescence localization, and Fu-deficient oviduct analysis","pmids":["23907739"],"confidence":"Medium","gaps":["Whether KIF27 directly binds Spag16/Pcdp1 versus via Fu unclear","Single-lab extension to a new tissue","Stoichiometry and assembly order of the complex unknown"]},{"year":2014,"claim":"Extended the Fu–KIF27 association to spermatogenesis, localizing KIF27 to the spermatid manchette and implicating the complex in sperm head shaping.","evidence":"Co-immunoprecipitation, immunofluorescence in the manchette, and conditional Fu KO mouse","pmids":["24525297"],"confidence":"Medium","gaps":["KIF27 role inferred from interaction/co-localization, not direct Kif27 KO in germ cells","Functional necessity of KIF27 in manchette untested","Mechanism linking complex to head shaping undefined"]},{"year":2018,"claim":"Resolved KIF27's mechanochemistry, showing it is a slow processive motor unable to transport in teams, supporting a tethering role rather than cargo transport.","evidence":"In vitro single-molecule motility, microtubule dynamics, and ATPase kinetics with mutagenesis","pmids":["29351996"],"confidence":"High","gaps":["Tethering model not yet demonstrated in cilia in vivo","Identity of tethered signaling complexes not established here","Relationship of motility to ciliary function untested"]},{"year":2025,"claim":"Established KIF27 as a transition-zone microtubule scaffold whose motility is dispensable, defining the mechanism by which it maintains TZ architecture and enables incorporation of motility proteins.","evidence":"Kif27 KO mouse genetics, high-resolution imaging, in situ cryo-electron tomography, single-molecule motility assays, and proteomics","pmids":["41400996"],"confidence":"High","gaps":["Specific TZ interactors and how they are recruited not fully detailed in this summary","How scaffolding regulates motility-protein incorporation mechanistically unresolved","Human disease genetics for KIF27-associated PCD not established in the corpus"]},{"year":null,"claim":"How KIF27 scaffolding activity is molecularly coupled to transition-zone assembly and to the gating/incorporation of axonemal motility components remains to be defined, as does any direct link to human ciliopathy.","evidence":"","pmids":[],"confidence":"High","gaps":["No structural model of the KIF27 scaffold at the TZ","TZ interactor network only partially characterized","No timeline evidence for KIF27 mutations in human disease"]}],"mechanism_profile":{"molecular_activity":[{"term_id":"GO:0140657","term_label":"ATP-dependent activity","supporting_discovery_ids":[9]},{"term_id":"GO:0008092","term_label":"cytoskeletal protein binding","supporting_discovery_ids":[9,10]},{"term_id":"GO:0005198","term_label":"structural molecule activity","supporting_discovery_ids":[10]}],"localization":[{"term_id":"GO:0005929","term_label":"cilium","supporting_discovery_ids":[2,6,10]},{"term_id":"GO:0005856","term_label":"cytoskeleton","supporting_discovery_ids":[10]}],"pathway":[{"term_id":"R-HSA-1852241","term_label":"Organelle biogenesis and maintenance","supporting_discovery_ids":[5,10]}],"complexes":["central pair apparatus","transition zone"],"partners":["STK36","SPAG16","PCDP1"],"other_free_text":[]}},"prefetch_data":{"uniprot":{"accession":"Q86VH2","full_name":"Kinesin-like protein KIF27","aliases":[],"length_aa":1401,"mass_kda":160.3,"function":"Plays an essential role in motile ciliogenesis","subcellular_location":"Cytoplasm, cytoskeleton; Cell projection, cilium","url":"https://www.uniprot.org/uniprotkb/Q86VH2/entry"},"depmap":{"release":"DepMap","has_data":true,"is_common_essential":false,"resolved_as":"","url":"https://depmap.org/portal/gene/KIF27","classification":"Not Classified","n_dependent_lines":80,"n_total_lines":1208,"dependency_fraction":0.06622516556291391},"opencell":{"profiled":false,"resolved_as":"","ensg_id":"","cell_line_id":"","localizations":[],"interactors":[],"url":"https://opencell.sf.czbiohub.org/search/KIF27","total_profiled":1310},"omim":[{"mim_id":"611254","title":"KINESIN FAMILY MEMBER 7; KIF7","url":"https://www.omim.org/entry/611254"},{"mim_id":"611253","title":"KINESIN FAMILY MEMBER 27; KIF27","url":"https://www.omim.org/entry/611253"},{"mim_id":"607652","title":"SERINE/THREONINE PROTEIN KINASE 36; STK36","url":"https://www.omim.org/entry/607652"},{"mim_id":"607035","title":"SUFU NEGATIVE REGULATOR OF HEDGEHOG SIGNALING; SUFU","url":"https://www.omim.org/entry/607035"},{"mim_id":"600725","title":"SONIC HEDGEHOG SIGNALING MOLECULE; SHH","url":"https://www.omim.org/entry/600725"}],"hpa":{"profiled":true,"resolved_as":"","reliability":"","locations":[],"tissue_specificity":"Tissue enhanced","tissue_distribution":"Detected in all","driving_tissues":[{"tissue":"testis","ntpm":24.5}],"url":"https://www.proteinatlas.org/search/KIF27"},"hgnc":{"alias_symbol":["DKFZp434D0917"],"prev_symbol":[]},"alphafold":{"accession":"Q86VH2","domains":[{"cath_id":"3.40.850.10","chopping":"5-199_206-350","consensus_level":"medium","plddt":85.0948,"start":5,"end":350},{"cath_id":"1.10.287,1.10.287","chopping":"697-889","consensus_level":"medium","plddt":83.1194,"start":697,"end":889},{"cath_id":"1.10.287","chopping":"931-1104","consensus_level":"medium","plddt":84.6846,"start":931,"end":1104},{"cath_id":"1.20.5","chopping":"1107-1161","consensus_level":"medium","plddt":86.6142,"start":1107,"end":1161}],"viewer_url":"https://alphafold.ebi.ac.uk/entry/Q86VH2","model_url":"https://alphafold.ebi.ac.uk/files/AF-Q86VH2-F1-model_v6.cif","pae_url":"https://alphafold.ebi.ac.uk/files/AF-Q86VH2-F1-predicted_aligned_error_v6.png","plddt_mean":69.25},"mouse_models":{"mgi_url":"https://www.informatics.jax.org/marker/summary?nomen=KIF27","jax_strain_url":"https://www.jax.org/strain/search?query=KIF27"},"sequence":{"accession":"Q86VH2","fasta_url":"https://rest.uniprot.org/uniprotkb/Q86VH2.fasta","uniprot_url":"https://www.uniprot.org/uniprotkb/Q86VH2/entry","alphafold_viewer_url":"https://alphafold.ebi.ac.uk/entry/Q86VH2"}},"corpus_meta":[{"pmid":"19933103","id":"PMC_19933103","title":"Planarian Hh signaling regulates regeneration polarity and links Hh pathway evolution to cilia.","date":"2009","source":"Science (New York, N.Y.)","url":"https://pubmed.ncbi.nlm.nih.gov/19933103","citation_count":199,"is_preprint":false},{"pmid":"19592253","id":"PMC_19592253","title":"The mammalian Cos2 homolog Kif7 plays an essential role in modulating Hh signal transduction during development.","date":"2009","source":"Current biology : CB","url":"https://pubmed.ncbi.nlm.nih.gov/19592253","citation_count":189,"is_preprint":false},{"pmid":"17089004","id":"PMC_17089004","title":"Hedgehog signaling pathway and gastrointestinal stem cell signaling network (review).","date":"2006","source":"International journal of molecular medicine","url":"https://pubmed.ncbi.nlm.nih.gov/17089004","citation_count":156,"is_preprint":false},{"pmid":"16258256","id":"PMC_16258256","title":"Hedgehog signaling pathway and gastric cancer.","date":"2005","source":"Cancer biology & therapy","url":"https://pubmed.ncbi.nlm.nih.gov/16258256","citation_count":148,"is_preprint":false},{"pmid":"19305393","id":"PMC_19305393","title":"Fused has evolved divergent roles in vertebrate Hedgehog signalling and motile ciliogenesis.","date":"2009","source":"Nature","url":"https://pubmed.ncbi.nlm.nih.gov/19305393","citation_count":120,"is_preprint":false},{"pmid":"21746835","id":"PMC_21746835","title":"Congenital hydrocephalus in genetically engineered mice.","date":"2011","source":"Veterinary pathology","url":"https://pubmed.ncbi.nlm.nih.gov/21746835","citation_count":115,"is_preprint":false},{"pmid":"16328026","id":"PMC_16328026","title":"WNT antagonist, SFRP1, is Hedgehog signaling target.","date":"2006","source":"International journal of molecular medicine","url":"https://pubmed.ncbi.nlm.nih.gov/16328026","citation_count":100,"is_preprint":false},{"pmid":"20635334","id":"PMC_20635334","title":"Hedgehog signaling update.","date":"2010","source":"American journal of medical genetics. 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KIF27 shares the same domain structure as Cos2, including a kinesin motor (KISc) domain, Ci-binding domain, and Smo-binding domain. KIF7 was identified as a paralog of KIF27 within the human genome.\",\n      \"method\": \"Bioinformatics/phylogenetic analysis; domain architecture comparison\",\n      \"journal\": \"International journal of oncology\",\n      \"confidence\": \"Low\",\n      \"confidence_rationale\": \"Tier 4 / Weak — computational prediction only, no experimental validation of interactions or function\",\n      \"pmids\": [\"15547729\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2005,\n      \"finding\": \"Mouse Fu (Stk36)-deficient mice do not exhibit embryonic phenotypes indicative of perturbed Hh signaling, suggesting that the Fu–Kif27/Kif7 complex does not have a conserved role in mammalian Hh signal transduction, in contrast to the Drosophila pathway.\",\n      \"method\": \"Gene-targeted knockout mouse; phenotypic analysis\",\n      \"journal\": \"Molecular and cellular biology\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 2 / Moderate — clean KO with defined phenotypic readout; negative result replicated in later studies\",\n      \"pmids\": [\"16055716\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2009,\n      \"finding\": \"Mouse Fu (Stk36) physically interacts with Kif27, a mammalian Cos2 orthologue. This interaction was identified by co-immunoprecipitation and links Fu to known structural components of the central pair apparatus of motile 9+2 cilia. Fu is essential for construction of the central pair apparatus and is linked to ciliogenesis rather than Hh signaling in mice.\",\n      \"method\": \"Co-immunoprecipitation; mouse knockout genetics; electron microscopy of cilia ultrastructure\",\n      \"journal\": \"Nature\",\n      \"confidence\": \"High\",\n      \"confidence_rationale\": \"Tier 2 / Strong — reciprocal Co-IP demonstrating physical interaction, combined with KO phenotypic analysis and ultrastructural evidence, replicated across multiple tissues\",\n      \"pmids\": [\"19305393\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2009,\n      \"finding\": \"In vitro analysis of mammalian Kif7 and Kif27 led to the conclusion that neither protein has a role in Hh signaling (negative result for Hh pathway function in mammals). Kif7 accumulates at the distal tip of primary cilia in a Hh-dependent manner and is required for Gli3 localization to cilia and processing of Gli3 to its repressor form.\",\n      \"method\": \"Kif7 knockout mice; immunofluorescence localization; Gli3 processing assays\",\n      \"journal\": \"Current biology : CB\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 2 / Moderate — KO mouse with defined molecular phenotype (Gli3 processing); KIF27 negative result for Hh signaling is from in vitro analysis cited within this paper\",\n      \"pmids\": [\"19592253\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2009,\n      \"finding\": \"In planarians, RNAi knockdown of Cos2/Kif27/Kif7 orthologs does not result in detectable Hh signaling defects but is essential for ciliogenesis, establishing a mechanistic link between Kif27-family proteins and cilia function independent of Hh signaling.\",\n      \"method\": \"RNA interference in planarians; phenotypic analysis of cilia and Hh pathway readouts\",\n      \"journal\": \"Science (New York, N.Y.)\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 2 / Moderate — RNAi loss-of-function with specific cellular phenotypes (ciliogenesis vs. Hh signaling) assessed separately\",\n      \"pmids\": [\"19933103\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2011,\n      \"finding\": \"Kif27 knockout mice develop autosomal recessive congenital hydrocephalus, and the pathogenic mechanism is attributed to dysfunctional motile cilia, placing KIF27 as an essential component of motile ciliogenesis in vivo.\",\n      \"method\": \"Gene knockout mouse; neuropathological and histological analysis; ciliary function assessment\",\n      \"journal\": \"Veterinary pathology\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 2 / Moderate — KO mouse with defined organismal phenotype attributed to ciliary dysfunction; single report\",\n      \"pmids\": [\"21746835\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2013,\n      \"finding\": \"Fu (Stk36) physically associates with Kif27 at the base of motile cilia and with known central pair components Spag16 and Pcdp1 in oviductal epithelium. Fu-deficient mouse oviducts show defects in central pair construction and cilia orientation, placing Kif27 as part of a complex required for central pair apparatus assembly.\",\n      \"method\": \"Co-immunoprecipitation; immunofluorescence localization; Fu-deficient mouse oviduct analysis\",\n      \"journal\": \"Developmental dynamics : an official publication of the American Association of Anatomists\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 2 / Moderate — Co-IP and localization with functional KO phenotype, single lab replicating earlier findings in a new tissue\",\n      \"pmids\": [\"23907739\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2014,\n      \"finding\": \"Kif27 is detected in the manchette of spermatids, and Fu (Stk36) interacts with Kif27 in the context of spermatogenesis. Conditional inactivation of Fu in male germ cells causes infertility with abnormal sperm head shaping and periaxonemal structure defects, placing Kif27 as part of the Fu-containing complex in spermatid head shaping structures.\",\n      \"method\": \"Co-immunoprecipitation; immunofluorescence localization in manchette; conditional KO mouse\",\n      \"journal\": \"Developmental biology\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 2 / Moderate — Co-IP and localization data with conditional KO phenotype; Kif27 role is inferred from its interaction and co-localization with Fu rather than direct Kif27 KO\",\n      \"pmids\": [\"24525297\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2016,\n      \"finding\": \"Sequence similarities between KIF21A, KIF7, and KIF27 in the regulatory domain suggest a conserved autoinhibitory mechanism (antiparallel coiled-coil regulatory domain inhibiting the motor domain) shared among kinesin-4 family members. The KIF21A regulatory domain interacts with the KIF21B motor domain, and analogous sequences in KIF27 suggest this regulation is conserved.\",\n      \"method\": \"Crystal structure of KIF21A regulatory domain; domain-interaction assay; sequence conservation analysis with KIF27\",\n      \"journal\": \"Scientific reports\",\n      \"confidence\": \"Low\",\n      \"confidence_rationale\": \"Tier 3 / Weak — structural data is for KIF21A; KIF27 involvement is inferred from sequence similarity without direct experimental validation in KIF27\",\n      \"pmids\": [\"27485312\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2018,\n      \"finding\": \"KIF27 is a slow and processive kinesin whose mechanochemical behavior arises from a slow ATPase rate and high affinity for both ATP and microtubules. KIF27 can influence microtubule dynamics. Unlike KIF7 (immotile due to inability to release ADP upon microtubule binding), KIF27 moves slowly and processively but cannot cooperate for fast processive transport in teams. Neither KIF7 nor KIF27 functions as a transporter; instead they are proposed to act as microtubule-based tethers of signaling complexes.\",\n      \"method\": \"In vitro single-molecule motility assays; microtubule dynamics assays; ATPase kinetics; mutagenesis-guided mechanistic analysis\",\n      \"journal\": \"The Journal of cell biology\",\n      \"confidence\": \"High\",\n      \"confidence_rationale\": \"Tier 1 / Strong — reconstituted in vitro with multiple orthogonal biochemical and biophysical assays (motility, ATPase, microtubule dynamics) providing direct mechanistic characterization\",\n      \"pmids\": [\"29351996\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2025,\n      \"finding\": \"KIF27 localizes to the transition zone (TZ) of motile cilia and forms a cytoskeletal scaffold that promotes TZ integrity. Loss of KIF27 causes specific defects in axonemal structure and disrupts cilia beating, leading to a primary ciliary dyskinesia (PCD)-like phenotype. The motile properties of KIF27 are dispensable for its function in cilia assembly; instead, KIF27 acts as a microtubule scaffold to regulate TZ architecture and enable correct ciliary incorporation of motility-generating proteins. KIF27 interactors at the TZ were identified by proteomics.\",\n      \"method\": \"Mouse genetics (KO); high-resolution imaging; in situ cryo-electron tomography; single-molecule motility assays; proteomics\",\n      \"journal\": \"Proceedings of the National Academy of Sciences of the United States of America\",\n      \"confidence\": \"High\",\n      \"confidence_rationale\": \"Tier 1 / Strong — multiple orthogonal methods including cryo-ET structural analysis, KO mouse genetics with defined phenotype, single-molecule motility assays, and proteomics in a single rigorous study\",\n      \"pmids\": [\"41400996\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2025,\n      \"finding\": \"KIF27 promotes the integrity of the transition zone (TZ), a diffusion barrier at the cilium base. Loss of KIF27 results in defects in axonemal structure and cilia beating recapitulating primary ciliary dyskinesia. KIF27's motile properties are dispensable for this function; it acts as a microtubule scaffold to regulate TZ architecture and enable ciliary incorporation of motility-generating proteins. (Preprint version of PMID:41400996, confirms same findings prior to peer review.)\",\n      \"method\": \"Mouse genetics; single-molecule motility assays; proteomics; high-resolution imaging; in situ cryo-tomography\",\n      \"journal\": \"bioRxiv\",\n      \"confidence\": \"High\",\n      \"confidence_rationale\": \"Tier 1 / Strong — same study as PMID:41400996 with multiple orthogonal experimental methods; preprint predating the published version\",\n      \"pmids\": [],\n      \"is_preprint\": true\n    }\n  ],\n  \"current_model\": \"KIF27 is a kinesin-4 family motor protein that functions primarily as a microtubule-associated scaffold at the ciliary transition zone to promote motile cilia assembly and structural integrity, acting through physical interactions with Fu (Stk36) and central pair apparatus components rather than through its motile properties, and does not play a significant role in mammalian Hedgehog signal transduction despite being a structural ortholog of the Drosophila Hh pathway component Costal-2.\"\n}\n```","stage2_raw":"{\n  \"mechanistic_narrative\": \"KIF27 is a kinesin-4 family motor protein that functions as a microtubule-based scaffold for the assembly and structural integrity of motile cilia rather than as a transporter [#9, #10]. Although originally identified by phylogenetics as the human ortholog of Drosophila Costal-2 (Cos2), sharing its kinesin motor, Ci-binding, and Smo-binding domain architecture and being paralogous to KIF7 [#0], mammalian KIF27 does not contribute to Hedgehog signal transduction; loss-of-function across mouse, planarian, and in vitro systems consistently fails to perturb Hh pathway readouts while disrupting ciliogenesis [#3, #4]. Biochemically, KIF27 is a slow, processive motor with a low ATPase rate and high affinity for ATP and microtubules, can influence microtubule dynamics, and does not cooperate for fast team-based transport, consistent with a role as a microtubule-based tether of signaling complexes rather than a cargo-moving motor [#9]. KIF27 physically associates with the kinase Fu (Stk36) at the base of motile cilia, linking it to central pair apparatus components including Spag16 and Pcdp1, and Fu/KIF27 complexes are required for central pair construction and cilia orientation in oviductal epithelium [#2, #6]. KIF27 localizes to the ciliary transition zone, where it forms a cytoskeletal scaffold that maintains transition zone architecture and enables correct ciliary incorporation of motility-generating proteins; its motile properties are dispensable for this function [#10]. Consistent with this structural role, Kif27-knockout mice develop autosomal recessive congenital hydrocephalus from dysfunctional motile cilia, and KIF27 loss produces axonemal defects and disrupted ciliary beating recapitulating a primary ciliary dyskinesia-like phenotype [#5, #10].\",\n  \"teleology\": [\n    {\n      \"year\": 2004,\n      \"claim\": \"Established KIF27's identity and domain architecture by defining it as the human Costal-2 ortholog, framing the hypothesis that it might function in Hedgehog signaling like its Drosophila counterpart.\",\n      \"evidence\": \"Bioinformatics and phylogenetic analysis with domain architecture comparison\",\n      \"pmids\": [\"15547729\"],\n      \"confidence\": \"Low\",\n      \"gaps\": [\"Computational prediction only with no experimental validation of interactions or function\", \"Hh-pathway role inferred from Drosophila ortholog, not tested in mammals\", \"No localization or biochemical data\"]\n    },\n    {\n      \"year\": 2005,\n      \"claim\": \"Tested whether the Fu\\u2013Kif27/Kif7 module conserves a Hh signaling role in mammals, and found it does not, redirecting attention away from canonical Hh function.\",\n      \"evidence\": \"Stk36 (Fu)-deficient knockout mouse with phenotypic analysis\",\n      \"pmids\": [\"16055716\"],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\"Negative result for Hh does not define the alternative function\", \"Does not directly assay KIF27 loss\", \"No mechanistic readout for cilia at this stage\"]\n    },\n    {\n      \"year\": 2009,\n      \"claim\": \"Connected KIF27 to ciliogenesis by demonstrating a physical interaction with Fu and linking the complex to the central pair apparatus of motile cilia rather than Hh signaling.\",\n      \"evidence\": \"Co-immunoprecipitation, mouse knockout genetics, and electron microscopy of cilia ultrastructure (Fu); parallel Kif7 KO and planarian RNAi establishing cilia-not-Hh roles\",\n      \"pmids\": [\"19305393\", \"19592253\", \"19933103\"],\n      \"confidence\": \"High\",\n      \"gaps\": [\"KIF27's direct contribution separated from Fu and from KIF7 not fully resolved\", \"Mechanism of central pair assembly by the complex undefined\", \"No structural detail of the interaction\"]\n    },\n    {\n      \"year\": 2011,\n      \"claim\": \"Demonstrated that KIF27 is required in vivo for motile cilia function by showing its loss causes congenital hydrocephalus, establishing an organismal phenotype.\",\n      \"evidence\": \"Kif27 knockout mouse with neuropathological/histological analysis and ciliary function assessment\",\n      \"pmids\": [\"21746835\"],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\"Single report\", \"Molecular basis of the ciliary defect not resolved\", \"Does not distinguish scaffolding from motor activity\"]\n    },\n    {\n      \"year\": 2013,\n      \"claim\": \"Defined the molecular context of KIF27 at the cilium base by placing it in a Fu complex with central pair components Spag16 and Pcdp1 required for central pair construction and cilia orientation.\",\n      \"evidence\": \"Co-immunoprecipitation, immunofluorescence localization, and Fu-deficient oviduct analysis\",\n      \"pmids\": [\"23907739\"],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\"Whether KIF27 directly binds Spag16/Pcdp1 versus via Fu unclear\", \"Single-lab extension to a new tissue\", \"Stoichiometry and assembly order of the complex unknown\"]\n    },\n    {\n      \"year\": 2014,\n      \"claim\": \"Extended the Fu\\u2013KIF27 association to spermatogenesis, localizing KIF27 to the spermatid manchette and implicating the complex in sperm head shaping.\",\n      \"evidence\": \"Co-immunoprecipitation, immunofluorescence in the manchette, and conditional Fu KO mouse\",\n      \"pmids\": [\"24525297\"],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\"KIF27 role inferred from interaction/co-localization, not direct Kif27 KO in germ cells\", \"Functional necessity of KIF27 in manchette untested\", \"Mechanism linking complex to head shaping undefined\"]\n    },\n    {\n      \"year\": 2018,\n      \"claim\": \"Resolved KIF27's mechanochemistry, showing it is a slow processive motor unable to transport in teams, supporting a tethering role rather than cargo transport.\",\n      \"evidence\": \"In vitro single-molecule motility, microtubule dynamics, and ATPase kinetics with mutagenesis\",\n      \"pmids\": [\"29351996\"],\n      \"confidence\": \"High\",\n      \"gaps\": [\"Tethering model not yet demonstrated in cilia in vivo\", \"Identity of tethered signaling complexes not established here\", \"Relationship of motility to ciliary function untested\"]\n    },\n    {\n      \"year\": 2025,\n      \"claim\": \"Established KIF27 as a transition-zone microtubule scaffold whose motility is dispensable, defining the mechanism by which it maintains TZ architecture and enables incorporation of motility proteins.\",\n      \"evidence\": \"Kif27 KO mouse genetics, high-resolution imaging, in situ cryo-electron tomography, single-molecule motility assays, and proteomics\",\n      \"pmids\": [\"41400996\"],\n      \"confidence\": \"High\",\n      \"gaps\": [\"Specific TZ interactors and how they are recruited not fully detailed in this summary\", \"How scaffolding regulates motility-protein incorporation mechanistically unresolved\", \"Human disease genetics for KIF27-associated PCD not established in the corpus\"]\n    },\n    {\n      \"year\": null,\n      \"claim\": \"How KIF27 scaffolding activity is molecularly coupled to transition-zone assembly and to the gating/incorporation of axonemal motility components remains to be defined, as does any direct link to human ciliopathy.\",\n      \"evidence\": \"\",\n      \"pmids\": [],\n      \"confidence\": \"High\",\n      \"gaps\": [\"No structural model of the KIF27 scaffold at the TZ\", \"TZ interactor network only partially characterized\", \"No timeline evidence for KIF27 mutations in human disease\"]\n    }\n  ],\n  \"mechanism_profile\": {\n    \"molecular_activity\": [\n      {\"term_id\": \"GO:0140657\", \"supporting_discovery_ids\": [9]},\n      {\"term_id\": \"GO:0008092\", \"supporting_discovery_ids\": [9, 10]},\n      {\"term_id\": \"GO:0005198\", \"supporting_discovery_ids\": [10]}\n    ],\n    \"localization\": [\n      {\"term_id\": \"GO:0005929\", \"supporting_discovery_ids\": [2, 6, 10]},\n      {\"term_id\": \"GO:0005856\", \"supporting_discovery_ids\": [10]}\n    ],\n    \"pathway\": [\n      {\"term_id\": \"R-HSA-1852241\", \"supporting_discovery_ids\": [5, 10]}\n    ],\n    \"complexes\": [\"central pair apparatus\", \"transition zone\"],\n    \"partners\": [\"STK36\", \"SPAG16\", \"PCDP1\"],\n    \"other_free_text\": []\n  }\n}","audit_flag":null,"evaluation":{"faith_supported":6,"faith_total":6,"faith_pct":100.0}}