{"gene":"TG_305050","gene_symbol":"ELC2","run_date":"2026-09-08T15:15:12","timeline":{"discoveries":[{"year":2015,"finding":"ELC2 (essential light chain 2) is a novel component of the MyoA glideosome in Toxoplasma gondii, binding to the MyoA lever arm alongside ELC1 and MLC1; ELC1 and ELC2 are functionally redundant but both are required for invasion, egress, and gliding motility.","method":"Genetic characterization (loss-of-function), identification of glideosome complex component","journal":"mBio","confidence":"Medium","confidence_rationale":"Tier 2 / Moderate — functional characterization via loss-of-function with specific phenotypic readouts (invasion, egress, motility) and molecular simulations, single lab","pmids":["26374117"],"is_preprint":false,"attribution":[{"species":"Toxoplasma gondii","strain":""}]},{"year":2015,"finding":"Ca2+ promotes intermolecular contacts between ELC1/ELC2 and the adjacent MLC1 light chain within the MyoA lever arm, stabilizing this domain; point mutations ablating either Ca2+ interaction or the inter-light-chain interface reduce the quality, displacement, and speed of gliding motility.","method":"Molecular dynamics simulations combined with point mutagenesis and gliding motility assays","journal":"mBio","confidence":"Medium","confidence_rationale":"Tier 2 / Moderate — mutagenesis with functional readouts supported by molecular simulation, single lab, two orthogonal approaches","pmids":["26374117"],"is_preprint":false,"attribution":[{"species":"Toxoplasma gondii","strain":""}]}],"current_model":"ELC2 is a glideosome component that binds the MyoA lever arm alongside ELC1 and MLC1; Ca2+ stabilizes this lever arm by promoting contacts between ELC1/ELC2 and MLC1, and both ELCs are required for efficient MyoA-driven gliding motility, invasion, and egress in Toxoplasma gondii."},"narrative":{"mechanistic_narrative":"ELC2 (essential light chain 2) is a component of the MyoA glideosome in Toxoplasma gondii, binding the MyoA lever arm alongside the light chains ELC1 and MLC1 [PMID:26374117]. ELC1 and ELC2 are functionally redundant, but the presence of at least one is required for efficient MyoA-driven gliding motility, host cell invasion, and egress [PMID:26374117]. Within the lever arm, Ca2+ promotes intermolecular contacts between ELC1/ELC2 and the adjacent MLC1, stabilizing this domain; point mutations that ablate either the Ca2+ interaction or the inter-light-chain interface degrade the quality, displacement, and speed of gliding motility [PMID:26374117]. Beyond this Ca2+-dependent lever-arm stabilization role, no further mechanistic detail for ELC2 has been characterized in the available corpus.","teleology":[{"year":2015,"claim":"Established that the MyoA glideosome contains a previously unrecognized essential light chain, ELC2, and defined its place in the motor complex — answering whether MyoA lever-arm composition extends beyond ELC1 and MLC1.","evidence":"Genetic loss-of-function characterization with invasion, egress, and gliding-motility readouts identifying ELC2 as a glideosome component in Toxoplasma gondii","pmids":["26374117"],"confidence":"Medium","gaps":["The molecular basis of ELC1/ELC2 redundancy (identical vs. distinct contributions) is not resolved","No structural model of ELC2 bound to the MyoA lever arm at atomic resolution","Regulation of ELC2 expression or assembly timing is uncharacterized"],"attribution":[{"species":"Toxoplasma gondii","strain":""}]},{"year":2015,"claim":"Defined how Ca2+ mechanically stabilizes the MyoA lever arm — showing that ELC1/ELC2 contacts with MLC1 are Ca2+-dependent and functionally required for productive motility.","evidence":"Molecular dynamics simulations combined with point mutagenesis of the Ca2+ and inter-light-chain interfaces and gliding motility assays in Toxoplasma gondii","pmids":["26374117"],"confidence":"Medium","gaps":["The physiological Ca2+ signal that triggers lever-arm stabilization in vivo is not defined","Quantitative force/step-size consequences of destabilization at the single-motor level are not measured","Whether ELC1 and ELC2 differ in Ca2+ sensitivity is not addressed"],"attribution":[{"species":"Toxoplasma gondii","strain":""}]},{"year":null,"claim":"It remains unknown whether ELC1 and ELC2 have any non-redundant functions, how ELC2 assembly is regulated, and what its structure in the assembled glideosome is.","evidence":"","pmids":[],"confidence":"Medium","gaps":["No distinction of ELC1 vs. ELC2 specific roles","No atomic-resolution structure of the ELC2-containing lever arm","No characterization of ELC2 outside the gliding-motility context"],"attribution":[{"species":"Toxoplasma gondii","strain":""}]}],"mechanism_profile":{"molecular_activity":[],"localization":[],"pathway":[],"complexes":["MyoA glideosome (MyoA lever arm with ELC1, ELC2, MLC1)"],"partners":["MYOA","ELC1","MLC1"],"other_free_text":["ELC1 and ELC2 are functionally redundant essential light chains; at least one is required for invasion, egress, and gliding motility [#0].","Ca2+ promotes ELC1/ELC2–MLC1 intermolecular contacts that stabilize the MyoA lever arm; disrupting either the Ca2+ interaction or the inter-light-chain interface reduces gliding quality, displacement, and speed [#1]."]},"strain_conflicts":[]},"prefetch_data":{},"corpus_meta":[{"pmid":"26374117","id":"PMC_26374117","title":"Two Essential Light Chains Regulate the MyoA Lever Arm To Promote Toxoplasma Gliding Motility.","date":"2015","source":"mBio","url":"https://pubmed.ncbi.nlm.nih.gov/26374117","citation_count":40,"is_preprint":false}],"cost":{"stage1":{"model":"claude-sonnet-4-6","input_tokens":3106,"output_tokens":579,"usd":0.009002,"stage1_stop_reason":"end_turn"},"stage2":{"model":"claude-opus-4-8","input_tokens":5274,"output_tokens":1794,"usd":0.03561,"stage2_stop_reason":"end_turn"},"total_usd":0.044612,"stage1_batch_id":"msgbatch_01S6GjoYQm8LTPUsdhASdqag","stage2_batch_id":"msgbatch_01VX63RTMdBJqsG6gQMqoCjz","note":"batch pricing = 50% of standard"},"stage1_raw":"```json\n{\n  \"discoveries\": [\n    {\n      \"year\": 2015,\n      \"finding\": \"ELC2 (essential light chain 2) is a novel component of the MyoA glideosome in Toxoplasma gondii, binding to the MyoA lever arm alongside ELC1 and MLC1; ELC1 and ELC2 are functionally redundant but both are required for invasion, egress, and gliding motility.\",\n      \"method\": \"Genetic characterization (loss-of-function), identification of glideosome complex component\",\n      \"journal\": \"mBio\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 2 / Moderate — functional characterization via loss-of-function with specific phenotypic readouts (invasion, egress, motility) and molecular simulations, single lab\",\n      \"pmids\": [\"26374117\"],\n      \"is_preprint\": false,\n      \"attribution\": [{\"species\": \"Toxoplasma gondii\", \"strain\": \"\"}]\n    },\n    {\n      \"year\": 2015,\n      \"finding\": \"Ca2+ promotes intermolecular contacts between ELC1/ELC2 and the adjacent MLC1 light chain within the MyoA lever arm, stabilizing this domain; point mutations ablating either Ca2+ interaction or the inter-light-chain interface reduce the quality, displacement, and speed of gliding motility.\",\n      \"method\": \"Molecular dynamics simulations combined with point mutagenesis and gliding motility assays\",\n      \"journal\": \"mBio\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 2 / Moderate — mutagenesis with functional readouts supported by molecular simulation, single lab, two orthogonal approaches\",\n      \"pmids\": [\"26374117\"],\n      \"is_preprint\": false,\n      \"attribution\": [{\"species\": \"Toxoplasma gondii\", \"strain\": \"\"}]\n    }\n  ],\n  \"current_model\": \"ELC2 is a glideosome component that binds the MyoA lever arm alongside ELC1 and MLC1; Ca2+ stabilizes this lever arm by promoting contacts between ELC1/ELC2 and MLC1, and both ELCs are required for efficient MyoA-driven gliding motility, invasion, and egress in Toxoplasma gondii.\"\n}\n```","stage2_raw":"```json\n{\n  \"mechanistic_narrative\": \"ELC2 (essential light chain 2) is a component of the MyoA glideosome in Toxoplasma gondii, binding the MyoA lever arm alongside the light chains ELC1 and MLC1 [#0]. ELC1 and ELC2 are functionally redundant, but the presence of at least one is required for efficient MyoA-driven gliding motility, host cell invasion, and egress [#0]. Within the lever arm, Ca2+ promotes intermolecular contacts between ELC1/ELC2 and the adjacent MLC1, stabilizing this domain; point mutations that ablate either the Ca2+ interaction or the inter-light-chain interface degrade the quality, displacement, and speed of gliding motility [#1]. Beyond this Ca2+-dependent lever-arm stabilization role, no further mechanistic detail for ELC2 has been characterized in the available corpus.\",\n  \"teleology\": [\n    {\n      \"year\": 2015,\n      \"claim\": \"Established that the MyoA glideosome contains a previously unrecognized essential light chain, ELC2, and defined its place in the motor complex — answering whether MyoA lever-arm composition extends beyond ELC1 and MLC1.\",\n      \"evidence\": \"Genetic loss-of-function characterization with invasion, egress, and gliding-motility readouts identifying ELC2 as a glideosome component in Toxoplasma gondii\",\n      \"pmids\": [\"26374117\"],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\n        \"The molecular basis of ELC1/ELC2 redundancy (identical vs. distinct contributions) is not resolved\",\n        \"No structural model of ELC2 bound to the MyoA lever arm at atomic resolution\",\n        \"Regulation of ELC2 expression or assembly timing is uncharacterized\"\n      ],\n      \"attribution\": [{\"species\": \"Toxoplasma gondii\", \"strain\": \"\"}]\n    },\n    {\n      \"year\": 2015,\n      \"claim\": \"Defined how Ca2+ mechanically stabilizes the MyoA lever arm — showing that ELC1/ELC2 contacts with MLC1 are Ca2+-dependent and functionally required for productive motility.\",\n      \"evidence\": \"Molecular dynamics simulations combined with point mutagenesis of the Ca2+ and inter-light-chain interfaces and gliding motility assays in Toxoplasma gondii\",\n      \"pmids\": [\"26374117\"],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\n        \"The physiological Ca2+ signal that triggers lever-arm stabilization in vivo is not defined\",\n        \"Quantitative force/step-size consequences of destabilization at the single-motor level are not measured\",\n        \"Whether ELC1 and ELC2 differ in Ca2+ sensitivity is not addressed\"\n      ],\n      \"attribution\": [{\"species\": \"Toxoplasma gondii\", \"strain\": \"\"}]\n    },\n    {\n      \"year\": null,\n      \"claim\": \"It remains unknown whether ELC1 and ELC2 have any non-redundant functions, how ELC2 assembly is regulated, and what its structure in the assembled glideosome is.\",\n      \"evidence\": \"\",\n      \"pmids\": [],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\n        \"No distinction of ELC1 vs. ELC2 specific roles\",\n        \"No atomic-resolution structure of the ELC2-containing lever arm\",\n        \"No characterization of ELC2 outside the gliding-motility context\"\n      ],\n      \"attribution\": [{\"species\": \"Toxoplasma gondii\", \"strain\": \"\"}]\n    }\n  ],\n  \"mechanism_profile\": {\n    \"molecular_activity\": [\n      {\"term_id\": \"GO:0005509\", \"supporting_discovery_ids\": [1], \"attribution\": [{\"species\": \"Toxoplasma gondii\", \"strain\": \"\"}]},\n      {\"term_id\": \"GO:0017022\", \"supporting_discovery_ids\": [0], \"attribution\": [{\"species\": \"Toxoplasma gondii\", \"strain\": \"\"}]}\n    ],\n    \"localization\": [\n      {\"term_id\": \"GO:0031034\", \"supporting_discovery_ids\": [0], \"attribution\": [{\"species\": \"Toxoplasma gondii\", \"strain\": \"\"}]}\n    ],\n    \"pathway\": [\n      {\"term_id\": \"GO:0071977\", \"supporting_discovery_ids\": [0, 1], \"attribution\": [{\"species\": \"Toxoplasma gondii\", \"strain\": \"\"}]}\n    ],\n    \"complexes\": [\"MyoA glideosome (MyoA lever arm with ELC1, ELC2, MLC1)\"],\n    \"partners\": [\"MyoA\", \"ELC1\", \"MLC1\"],\n    \"other_free_text\": [\n      \"ELC1 and ELC2 are functionally redundant essential light chains; at least one is required for invasion, egress, and gliding motility [#0].\",\n      \"Ca2+ promotes ELC1/ELC2–MLC1 intermolecular contacts that stabilize the MyoA lever arm; disrupting either the Ca2+ interaction or the inter-light-chain interface reduces gliding quality, displacement, and speed [#1].\"\n    ]\n  },\n  \"strain_conflicts\": []\n}\n```","audit_flag":null,"strains":[{"strain":"ME49","gene_id":"TGME49_305050","name":"ELC2","product":"essential light chain ELC2","uniprot_acc":"A0A125YT26","chromosome":"TGME49_chrIX","start_pos":5203406},{"strain":"GT1","gene_id":"TGGT1_305050","name":null,"product":"putative calmodulin","uniprot_acc":null,"chromosome":"TGGT1_chrIX","start_pos":4983149},{"strain":"RH88","gene_id":"TGRH88_016820","name":null,"product":"putative calmodulin","uniprot_acc":null,"chromosome":"CM023090","start_pos":5325501},{"strain":"VEG","gene_id":"TGVEG_305050","name":null,"product":"putative calmodulin","uniprot_acc":"B9PZ33","chromosome":"TGVEG_chrIX","start_pos":5241261}]}