{"gene":"TG_292950","gene_symbol":"AC10","run_date":"2026-09-08T17:00:03+00:00","timeline":{"discoveries":[{"year":2020,"finding":"AC10 localizes to the alveolin network intercalated between the subpellicular microtubules (SPMTs) at the apical cap, as identified by BioID as a partner of AC9 and confirmed by ultrastructure expansion microscopy (U-ExM).","method":"BioID proximity ligation, ultrastructure expansion microscopy (U-ExM)","journal":"eLife","confidence":"High","confidence_rationale":"Tier 2 / Moderate — BioID and U-ExM are orthogonal methods; single lab but two complementary approaches with high resolution","pmids":["32379047"],"is_preprint":false,"attribution":[{"species":"Toxoplasma gondii","strain":""}]},{"year":2020,"finding":"Conditional depletion of AC10 results in parasites that replicate normally but are defective in microneme secretion, fail to invade host cells, and cannot egress from infected cells, demonstrating an essential role for AC10 in these processes.","method":"Conditional knockdown (auxin-inducible degron or similar), invasion/egress assays, microneme secretion assay","journal":"eLife","confidence":"High","confidence_rationale":"Tier 2 / Moderate — conditional depletion with multiple defined phenotypic readouts (secretion, invasion, egress) in a single rigorous study","pmids":["32379047"],"is_preprint":false,"attribution":[{"species":"Toxoplasma gondii","strain":""}]},{"year":2020,"finding":"Loss of AC10 in mature parasites causes disorganization of the SPMTs leading to loss of the apical polar ring (APR) and conoid, establishing AC10 as structurally required for apical complex integrity.","method":"Conditional knockdown, electron microscopy, ultrastructure expansion microscopy (U-ExM)","journal":"eLife","confidence":"High","confidence_rationale":"Tier 2 / Moderate — electron microscopy and U-ExM are orthogonal structural methods with clear loss-of-function phenotype","pmids":["32379047"],"is_preprint":false,"attribution":[{"species":"Toxoplasma gondii","strain":""}]},{"year":2021,"finding":"Depletion of AC10 phenocopies depletion of ERK7 kinase: both lead to loss of the APR, disorganization of SPMTs, severe impairment of microneme secretion, and accumulation of microneme proteins, placing AC10 and ERK7 in the same functional pathway for apical complex stability.","method":"Conditional depletion, comparative proteomics, U-ExM, NHS-ester staining, microneme secretion assay","journal":"mBio","confidence":"High","confidence_rationale":"Tier 2 / Strong — phenocopy established by multiple orthogonal methods (proteomics, U-ExM, functional assays) and replicated across AC9, AC10, and ERK7 depletions","pmids":["34607461"],"is_preprint":false,"attribution":[{"species":"Toxoplasma gondii","strain":""}]},{"year":2022,"finding":"AC10 is a foundational component of the AC9:AC10:ERK7 trimeric complex in the apical cap, forming multiple independent pairwise interactions with both AC9 and ERK7, enabling multivalent oligomerization of the complex.","method":"Deletion analyses, yeast two-hybrid experiments","journal":"mBio","confidence":"Medium","confidence_rationale":"Tier 2 / Moderate — yeast two-hybrid with deletion mapping provides pairwise interaction evidence; single lab, no in vitro reconstitution","pmids":["35130732"],"is_preprint":false,"attribution":[{"species":"Toxoplasma gondii","strain":""}]},{"year":2022,"finding":"The multivalent AC9:AC10:ERK7 complex assembly into the cytoskeletal IMC serves as a structural scaffold that concentrates ERK7 kinase activity in the apical cap; disruption of interactions among these proteins impairs apical complex maintenance.","method":"Deletion analyses, yeast two-hybrid experiments, functional complementation assays","journal":"mBio","confidence":"Medium","confidence_rationale":"Tier 2 / Moderate — mechanistic model supported by deletion mapping and interaction studies in a single lab; kinase concentration inferred from complex assembly data without direct enzymatic reconstitution","pmids":["35130732"],"is_preprint":false,"attribution":[{"species":"Toxoplasma gondii","strain":""}]}],"current_model":"AC10 is an essential structural component of the apical cap alveolin network in Toxoplasma gondii that localizes intercalated between subpellicular microtubules and forms a foundational multivalent complex with AC9 and the kinase ERK7; loss of AC10 disorganizes the SPMTs, eliminates the apical polar ring and conoid, and blocks microneme secretion, invasion, and egress, while its scaffold function within the AC9:AC10:ERK7 complex concentrates ERK7 kinase activity at the apical cap to maintain apical complex integrity."},"narrative":{"mechanistic_narrative":"AC10 is an essential structural component of the apical cap alveolin network in Toxoplasma gondii, required for the integrity of the apical complex and for the invasion-related secretory machinery [PMID:32379047]. It localizes to the alveolin network intercalated between the subpellicular microtubules (SPMTs) at the apical cap, where it was identified as a partner of AC9 [PMID:32379047]. AC10 is a foundational component of a trimeric AC9:AC10:ERK7 complex, forming multiple independent pairwise interactions with both AC9 and the kinase ERK7 that enable multivalent oligomerization; this scaffold concentrates ERK7 kinase activity in the apical cap to maintain apical complex integrity [PMID:35130732]. Consistent with this scaffolding role, AC10 depletion phenocopies ERK7 depletion [PMID:34607461]. Conditional loss of AC10 disorganizes the SPMTs, eliminating the apical polar ring and conoid, and blocks microneme secretion, host-cell invasion, and egress while leaving replication intact [PMID:32379047].","teleology":[{"year":2020,"claim":"Establishing where AC10 acts and what it partners with was the entry point: BioID and expansion microscopy placed AC10 in the apical cap alveolin network between the subpellicular microtubules as an AC9 partner, defining it as a cytoskeletal apical-cap protein.","evidence":"BioID proximity ligation with AC9 and ultrastructure expansion microscopy in T. gondii","pmids":["32379047"],"confidence":"High","gaps":["Molecular basis of the AC10–AC9 interaction not mapped at this stage","No functional consequence of localization established yet"],"attribution":[{"species":"Toxoplasma gondii","strain":""}]},{"year":2020,"claim":"Whether AC10 is functionally essential was answered by conditional depletion, which separated a structural/secretory role from replication and showed AC10 is required for microneme secretion, invasion, and egress.","evidence":"Conditional knockdown with microneme secretion, invasion, and egress assays in T. gondii","pmids":["32379047"],"confidence":"High","gaps":["Does not distinguish direct structural role from downstream secretory signalling","Molecular step blocked in microneme secretion not defined"],"attribution":[{"species":"Toxoplasma gondii","strain":""}]},{"year":2020,"claim":"The structural basis of the invasion defect was resolved by ultrastructure: loss of AC10 disorganizes the SPMTs and eliminates the apical polar ring and conoid, establishing AC10 as required for apical complex architecture.","evidence":"Conditional knockdown with electron microscopy and U-ExM in T. gondii","pmids":["32379047"],"confidence":"High","gaps":["Mechanism linking AC10 loss to SPMT disorganization unresolved","Whether AC10 stabilizes microtubules directly or via partners unknown"],"attribution":[{"species":"Toxoplasma gondii","strain":""}]},{"year":2021,"claim":"Placing AC10 in a defined pathway rather than a standalone role, comparative depletion showed AC10 loss phenocopies ERK7 kinase loss across structural and secretory readouts, linking a scaffold protein to a kinase.","evidence":"Conditional depletion with comparative proteomics, U-ExM, NHS-ester staining, and microneme secretion assays in T. gondii","pmids":["34607461"],"confidence":"High","gaps":["Phenocopy does not by itself establish physical interaction","Direction of regulation between AC10 and ERK7 not defined here"],"attribution":[{"species":"Toxoplasma gondii","strain":""}]},{"year":2022,"claim":"The physical logic of the pathway was defined: deletion mapping and yeast two-hybrid showed AC10 makes multiple independent pairwise contacts with both AC9 and ERK7, establishing it as the foundational, multivalent hub of a trimeric AC9:AC10:ERK7 complex.","evidence":"Deletion analyses and yeast two-hybrid interaction mapping in T. gondii","pmids":["35130732"],"confidence":"Medium","gaps":["No in vitro reconstitution or structure of the complex","Stoichiometry of the oligomerized complex not determined"],"attribution":[{"species":"Toxoplasma gondii","strain":""}]},{"year":2022,"claim":"The purpose of the scaffold was framed mechanistically: assembly of the multivalent complex into the IMC concentrates ERK7 kinase activity in the apical cap, and disrupting the interactions impairs apical complex maintenance.","evidence":"Deletion analyses, yeast two-hybrid, and functional complementation assays in T. gondii","pmids":["35130732"],"confidence":"Medium","gaps":["Local ERK7 kinase activity concentration inferred from assembly, not measured by direct enzymatic reconstitution","ERK7 substrates at the apical cap not identified"],"attribution":[{"species":"Toxoplasma gondii","strain":""}]},{"year":null,"claim":"How AC10-mediated ERK7 concentration is translated into SPMT organization and apical polar ring/conoid assembly at the molecular level remains open.","evidence":"","pmids":[],"confidence":"Medium","gaps":["No identified ERK7 substrates linking the complex to microtubule/APR/conoid integrity","No structural model of the assembled AC9:AC10:ERK7 complex","Mechanism coupling apical structure to microneme secretion undefined"],"attribution":[{"species":"Toxoplasma gondii","strain":""}]}],"mechanism_profile":{"molecular_activity":[],"localization":[],"pathway":[],"complexes":["AC9:AC10:ERK7 trimeric apical cap complex"],"partners":["AC9","ERK7"],"other_free_text":["AC10 localizes intercalated between subpellicular microtubules at the apical cap [#0].","Conditional depletion of AC10 leaves replication intact but abolishes microneme secretion, invasion, and egress [#1].","AC10 loss disorganizes SPMTs and eliminates the apical polar ring and conoid [#2].","AC10 depletion phenocopies ERK7 kinase depletion across structural and secretory phenotypes [#3].","AC10 makes multiple independent pairwise contacts with AC9 and ERK7, enabling multivalent oligomerization [#4].","The assembled complex is proposed to concentrate ERK7 kinase activity in the apical cap [#5]."]},"strain_conflicts":[]},"prefetch_data":{},"corpus_meta":[{"pmid":"32379047","id":"PMC_32379047","title":"Essential function of the alveolin network in the subpellicular microtubules and conoid assembly in Toxoplasma gondii.","date":"2020","source":"eLife","url":"https://pubmed.ncbi.nlm.nih.gov/32379047","citation_count":82,"is_preprint":false},{"pmid":"34607461","id":"PMC_34607461","title":"Revisiting the Role of Toxoplasma gondii ERK7 in the Maintenance and Stability of the Apical Complex.","date":"2021","source":"mBio","url":"https://pubmed.ncbi.nlm.nih.gov/34607461","citation_count":28,"is_preprint":false},{"pmid":"35130732","id":"PMC_35130732","title":"Multivalent Interactions Drive the Toxoplasma AC9:AC10:ERK7 Complex To Concentrate ERK7 in the Apical Cap.","date":"2022","source":"mBio","url":"https://pubmed.ncbi.nlm.nih.gov/35130732","citation_count":21,"is_preprint":false}],"cost":{"stage1":{"model":"claude-sonnet-4-6","input_tokens":4272,"output_tokens":1483,"usd":0.017531,"stage1_stop_reason":"end_turn"},"stage2":{"model":"claude-opus-4-8","input_tokens":6599,"output_tokens":2942,"usd":0.053273,"stage2_stop_reason":"end_turn"},"total_usd":0.0,"stage1_batch_id":"msgbatch_01WgHz6kceqm573AGLyz57at","stage2_batch_id":"msgbatch_01LK4wDYj5zYquahv7gi9893","note":"batch pricing = 50% of standard","skipped":true},"stage1_raw":"```json\n{\n  \"discoveries\": [\n    {\n      \"year\": 2020,\n      \"finding\": \"AC10 localizes to the alveolin network intercalated between the subpellicular microtubules (SPMTs) at the apical cap, as identified by BioID as a partner of AC9 and confirmed by ultrastructure expansion microscopy (U-ExM).\",\n      \"method\": \"BioID proximity ligation, ultrastructure expansion microscopy (U-ExM)\",\n      \"journal\": \"eLife\",\n      \"confidence\": \"High\",\n      \"confidence_rationale\": \"Tier 2 / Moderate — BioID and U-ExM are orthogonal methods; single lab but two complementary approaches with high resolution\",\n      \"pmids\": [\"32379047\"],\n      \"is_preprint\": false,\n      \"attribution\": [{\"species\": \"Toxoplasma gondii\", \"strain\": \"\"}]\n    },\n    {\n      \"year\": 2020,\n      \"finding\": \"Conditional depletion of AC10 results in parasites that replicate normally but are defective in microneme secretion, fail to invade host cells, and cannot egress from infected cells, demonstrating an essential role for AC10 in these processes.\",\n      \"method\": \"Conditional knockdown (auxin-inducible degron or similar), invasion/egress assays, microneme secretion assay\",\n      \"journal\": \"eLife\",\n      \"confidence\": \"High\",\n      \"confidence_rationale\": \"Tier 2 / Moderate — conditional depletion with multiple defined phenotypic readouts (secretion, invasion, egress) in a single rigorous study\",\n      \"pmids\": [\"32379047\"],\n      \"is_preprint\": false,\n      \"attribution\": [{\"species\": \"Toxoplasma gondii\", \"strain\": \"\"}]\n    },\n    {\n      \"year\": 2020,\n      \"finding\": \"Loss of AC10 in mature parasites causes disorganization of the SPMTs leading to loss of the apical polar ring (APR) and conoid, establishing AC10 as structurally required for apical complex integrity.\",\n      \"method\": \"Conditional knockdown, electron microscopy, ultrastructure expansion microscopy (U-ExM)\",\n      \"journal\": \"eLife\",\n      \"confidence\": \"High\",\n      \"confidence_rationale\": \"Tier 2 / Moderate — electron microscopy and U-ExM are orthogonal structural methods with clear loss-of-function phenotype\",\n      \"pmids\": [\"32379047\"],\n      \"is_preprint\": false,\n      \"attribution\": [{\"species\": \"Toxoplasma gondii\", \"strain\": \"\"}]\n    },\n    {\n      \"year\": 2021,\n      \"finding\": \"Depletion of AC10 phenocopies depletion of ERK7 kinase: both lead to loss of the APR, disorganization of SPMTs, severe impairment of microneme secretion, and accumulation of microneme proteins, placing AC10 and ERK7 in the same functional pathway for apical complex stability.\",\n      \"method\": \"Conditional depletion, comparative proteomics, U-ExM, NHS-ester staining, microneme secretion assay\",\n      \"journal\": \"mBio\",\n      \"confidence\": \"High\",\n      \"confidence_rationale\": \"Tier 2 / Strong — phenocopy established by multiple orthogonal methods (proteomics, U-ExM, functional assays) and replicated across AC9, AC10, and ERK7 depletions\",\n      \"pmids\": [\"34607461\"],\n      \"is_preprint\": false,\n      \"attribution\": [{\"species\": \"Toxoplasma gondii\", \"strain\": \"\"}]\n    },\n    {\n      \"year\": 2022,\n      \"finding\": \"AC10 is a foundational component of the AC9:AC10:ERK7 trimeric complex in the apical cap, forming multiple independent pairwise interactions with both AC9 and ERK7, enabling multivalent oligomerization of the complex.\",\n      \"method\": \"Deletion analyses, yeast two-hybrid experiments\",\n      \"journal\": \"mBio\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 2 / Moderate — yeast two-hybrid with deletion mapping provides pairwise interaction evidence; single lab, no in vitro reconstitution\",\n      \"pmids\": [\"35130732\"],\n      \"is_preprint\": false,\n      \"attribution\": [{\"species\": \"Toxoplasma gondii\", \"strain\": \"\"}]\n    },\n    {\n      \"year\": 2022,\n      \"finding\": \"The multivalent AC9:AC10:ERK7 complex assembly into the cytoskeletal IMC serves as a structural scaffold that concentrates ERK7 kinase activity in the apical cap; disruption of interactions among these proteins impairs apical complex maintenance.\",\n      \"method\": \"Deletion analyses, yeast two-hybrid experiments, functional complementation assays\",\n      \"journal\": \"mBio\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 2 / Moderate — mechanistic model supported by deletion mapping and interaction studies in a single lab; kinase concentration inferred from complex assembly data without direct enzymatic reconstitution\",\n      \"pmids\": [\"35130732\"],\n      \"is_preprint\": false,\n      \"attribution\": [{\"species\": \"Toxoplasma gondii\", \"strain\": \"\"}]\n    }\n  ],\n  \"current_model\": \"AC10 is an essential structural component of the apical cap alveolin network in Toxoplasma gondii that localizes intercalated between subpellicular microtubules and forms a foundational multivalent complex with AC9 and the kinase ERK7; loss of AC10 disorganizes the SPMTs, eliminates the apical polar ring and conoid, and blocks microneme secretion, invasion, and egress, while its scaffold function within the AC9:AC10:ERK7 complex concentrates ERK7 kinase activity at the apical cap to maintain apical complex integrity.\"\n}\n```","stage2_raw":"{\n  \"mechanistic_narrative\": \"AC10 is an essential structural component of the apical cap alveolin network in Toxoplasma gondii, required for the integrity of the apical complex and for the invasion-related secretory machinery [#0, #2]. It localizes to the alveolin network intercalated between the subpellicular microtubules (SPMTs) at the apical cap, where it was identified as a partner of AC9 [#0]. AC10 is a foundational component of a trimeric AC9:AC10:ERK7 complex, forming multiple independent pairwise interactions with both AC9 and the kinase ERK7 that enable multivalent oligomerization; this scaffold concentrates ERK7 kinase activity in the apical cap to maintain apical complex integrity [#4, #5]. Consistent with this scaffolding role, AC10 depletion phenocopies ERK7 depletion [#3]. Conditional loss of AC10 disorganizes the SPMTs, eliminating the apical polar ring and conoid, and blocks microneme secretion, host-cell invasion, and egress while leaving replication intact [#1, #2].\",\n  \"teleology\": [\n    {\n      \"year\": 2020,\n      \"claim\": \"Establishing where AC10 acts and what it partners with was the entry point: BioID and expansion microscopy placed AC10 in the apical cap alveolin network between the subpellicular microtubules as an AC9 partner, defining it as a cytoskeletal apical-cap protein.\",\n      \"evidence\": \"BioID proximity ligation with AC9 and ultrastructure expansion microscopy in T. gondii\",\n      \"pmids\": [\"32379047\"],\n      \"confidence\": \"High\",\n      \"gaps\": [\"Molecular basis of the AC10\\u2013AC9 interaction not mapped at this stage\", \"No functional consequence of localization established yet\"],\n      \"attribution\": [{\"species\": \"Toxoplasma gondii\", \"strain\": \"\"}]\n    },\n    {\n      \"year\": 2020,\n      \"claim\": \"Whether AC10 is functionally essential was answered by conditional depletion, which separated a structural/secretory role from replication and showed AC10 is required for microneme secretion, invasion, and egress.\",\n      \"evidence\": \"Conditional knockdown with microneme secretion, invasion, and egress assays in T. gondii\",\n      \"pmids\": [\"32379047\"],\n      \"confidence\": \"High\",\n      \"gaps\": [\"Does not distinguish direct structural role from downstream secretory signalling\", \"Molecular step blocked in microneme secretion not defined\"],\n      \"attribution\": [{\"species\": \"Toxoplasma gondii\", \"strain\": \"\"}]\n    },\n    {\n      \"year\": 2020,\n      \"claim\": \"The structural basis of the invasion defect was resolved by ultrastructure: loss of AC10 disorganizes the SPMTs and eliminates the apical polar ring and conoid, establishing AC10 as required for apical complex architecture.\",\n      \"evidence\": \"Conditional knockdown with electron microscopy and U-ExM in T. gondii\",\n      \"pmids\": [\"32379047\"],\n      \"confidence\": \"High\",\n      \"gaps\": [\"Mechanism linking AC10 loss to SPMT disorganization unresolved\", \"Whether AC10 stabilizes microtubules directly or via partners unknown\"],\n      \"attribution\": [{\"species\": \"Toxoplasma gondii\", \"strain\": \"\"}]\n    },\n    {\n      \"year\": 2021,\n      \"claim\": \"Placing AC10 in a defined pathway rather than a standalone role, comparative depletion showed AC10 loss phenocopies ERK7 kinase loss across structural and secretory readouts, linking a scaffold protein to a kinase.\",\n      \"evidence\": \"Conditional depletion with comparative proteomics, U-ExM, NHS-ester staining, and microneme secretion assays in T. gondii\",\n      \"pmids\": [\"34607461\"],\n      \"confidence\": \"High\",\n      \"gaps\": [\"Phenocopy does not by itself establish physical interaction\", \"Direction of regulation between AC10 and ERK7 not defined here\"],\n      \"attribution\": [{\"species\": \"Toxoplasma gondii\", \"strain\": \"\"}]\n    },\n    {\n      \"year\": 2022,\n      \"claim\": \"The physical logic of the pathway was defined: deletion mapping and yeast two-hybrid showed AC10 makes multiple independent pairwise contacts with both AC9 and ERK7, establishing it as the foundational, multivalent hub of a trimeric AC9:AC10:ERK7 complex.\",\n      \"evidence\": \"Deletion analyses and yeast two-hybrid interaction mapping in T. gondii\",\n      \"pmids\": [\"35130732\"],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\"No in vitro reconstitution or structure of the complex\", \"Stoichiometry of the oligomerized complex not determined\"],\n      \"attribution\": [{\"species\": \"Toxoplasma gondii\", \"strain\": \"\"}]\n    },\n    {\n      \"year\": 2022,\n      \"claim\": \"The purpose of the scaffold was framed mechanistically: assembly of the multivalent complex into the IMC concentrates ERK7 kinase activity in the apical cap, and disrupting the interactions impairs apical complex maintenance.\",\n      \"evidence\": \"Deletion analyses, yeast two-hybrid, and functional complementation assays in T. gondii\",\n      \"pmids\": [\"35130732\"],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\"Local ERK7 kinase activity concentration inferred from assembly, not measured by direct enzymatic reconstitution\", \"ERK7 substrates at the apical cap not identified\"],\n      \"attribution\": [{\"species\": \"Toxoplasma gondii\", \"strain\": \"\"}]\n    },\n    {\n      \"year\": null,\n      \"claim\": \"How AC10-mediated ERK7 concentration is translated into SPMT organization and apical polar ring/conoid assembly at the molecular level remains open.\",\n      \"evidence\": \"\",\n      \"pmids\": [],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\"No identified ERK7 substrates linking the complex to microtubule/APR/conoid integrity\", \"No structural model of the assembled AC9:AC10:ERK7 complex\", \"Mechanism coupling apical structure to microneme secretion undefined\"],\n      \"attribution\": [{\"species\": \"Toxoplasma gondii\", \"strain\": \"\"}]\n    }\n  ],\n  \"mechanism_profile\": {\n    \"molecular_activity\": [\n      {\"term_id\": \"GO:0005200\", \"supporting_discovery_ids\": [0, 2], \"attribution\": [{\"species\": \"Toxoplasma gondii\", \"strain\": \"\"}]},\n      {\"term_id\": \"GO:0030674\", \"supporting_discovery_ids\": [4, 5], \"attribution\": [{\"species\": \"Toxoplasma gondii\", \"strain\": \"\"}]}\n    ],\n    \"localization\": [\n      {\"term_id\": \"GO:0033354\", \"supporting_discovery_ids\": [0], \"attribution\": [{\"species\": \"Toxoplasma gondii\", \"strain\": \"\"}]},\n      {\"term_id\": \"GO:0020007\", \"supporting_discovery_ids\": [0], \"attribution\": [{\"species\": \"Toxoplasma gondii\", \"strain\": \"\"}]}\n    ],\n    \"pathway\": [\n      {\"term_id\": \"GO:0007155\", \"supporting_discovery_ids\": [1], \"attribution\": [{\"species\": \"Toxoplasma gondii\", \"strain\": \"\"}]},\n      {\"term_id\": \"GO:0046903\", \"supporting_discovery_ids\": [1, 3], \"attribution\": [{\"species\": \"Toxoplasma gondii\", \"strain\": \"\"}]}\n    ],\n    \"complexes\": [\"AC9:AC10:ERK7 trimeric apical cap complex\"],\n    \"partners\": [\"AC9\", \"ERK7\"],\n    \"other_free_text\": [\n      \"AC10 localizes intercalated between subpellicular microtubules at the apical cap [#0].\",\n      \"Conditional depletion of AC10 leaves replication intact but abolishes microneme secretion, invasion, and egress [#1].\",\n      \"AC10 loss disorganizes SPMTs and eliminates the apical polar ring and conoid [#2].\",\n      \"AC10 depletion phenocopies ERK7 kinase depletion across structural and secretory phenotypes [#3].\",\n      \"AC10 makes multiple independent pairwise contacts with AC9 and ERK7, enabling multivalent oligomerization [#4].\",\n      \"The assembled complex is proposed to concentrate ERK7 kinase activity in the apical cap [#5].\"\n    ]\n  },\n  \"strain_conflicts\": []\n}","audit_flag":null,"strains":[{"strain":"ME49","gene_id":"TGME49_292950","name":"AC10","product":"apical cap protein AC10","uniprot_acc":"A0A125YMU5","chromosome":"TGME49_chrIa","start_pos":36664},{"strain":"GT1","gene_id":"TGGT1_292950","name":null,"product":"hypothetical protein","uniprot_acc":null,"chromosome":"TGGT1_chrIa","start_pos":22336},{"strain":"RH88","gene_id":"TGRH88_018360","name":null,"product":"unspecified product","uniprot_acc":null,"chromosome":"CM023081","start_pos":42536},{"strain":"VEG","gene_id":"TGVEG_292950","name":null,"product":"hypothetical protein","uniprot_acc":"V5B071","chromosome":"TGVEG_chrIa","start_pos":45623}]}