Gene Ontology annotation through association of InterPro records with GO terms
Manual transfer of experimentally-verified manual GO annotation data to orthologs by curator judgment of sequence similarity
Annotation inferences using phylogenetic trees
Gene Ontology annotation based on UniProtKB/Swiss-Prot Subcellular Location vocabulary mapping, accompanied by conservative changes to GO terms applied by UniProt
Automatic assignment of GO terms using logical inference, based on inter-ontology links
Combined Automated Annotation using Multiple IEA Methods
Opa1 is required for proper mitochondrial metabolism in early development.
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Opa1 depletion in zebrafish disrupts mitochondrial morphology and development.
"Opa1 catalyzes fusion of inner mitochondrial membranes and formation of the cristae"
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Zebrafish opa1 is a single-copy, ubiquitously expressed gene whose protein is 78% identical to the most abundant human OPA1 isoform (OPA1-4), supporting orthology-based functional interpretation of Q5U3A7.
"as a single-copy gene and is 78% identical and 87% similar to the most abundant human OPA1 isoform (OPA1-4) at the protein level"
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Morpholino-mediated opa1 knockdown produced multi-system developmental phenotypes including small eyes and small pectoral fin buds plus cardiac/circulatory defects, consistent with a core role for Opa1 in mitochondrial function during development.
"small eyes and small pectoral fin buds"
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Opa1 morphants showed significantly decreased total basal respiration with increased respiratory control ratio, indicating Opa1 is required for proper developmental bioenergetic output.
"Total basal respiration was significantly decreased in Opa1 morphants when compared to MMC morphants at 24 and 72 hpf"
Tom70 serves as a molecular switch to determine pathological cardiac hypertrophy.
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Tom70-dependent import of optic atrophy-1 links mitochondrial import to cardiomyocyte stress responses.
"The defective mitochondrial import of Tom70-targeted optic atrophy-1 triggered intracellular oxidative stress"
UniProtKB entry Q5U3A7 for Danio rerio opa1
Falcon deep research report on Danio rerio opa1 (Q5U3A7)
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Synthesis of zebrafish-specific and cross-species evidence concludes that Q5U3A7 is a mitochondrial inner-membrane dynamin-like GTPase whose primary function is GTP-dependent membrane remodeling at the inner membrane and cristae, mediating inner-membrane fusion after mitofusin-dependent outer-membrane fusion.
"OPA1 is a **TRAFAC class dynamin-like GTPase** that localizes to mitochondria and is essential for **IMM fusion**, acting after outer mitochondrial membrane (OMM) fusion mediated by mitofusins (MFN1/MFN2)."
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OPA1 is not a small-molecule metabolic enzyme; its catalytic activity is GTP hydrolysis coupled to conformational changes that power membrane remodeling, tethering, and fusion.
"its catalytic activity is **GTP hydrolysis (GTP → GDP + Pi)**, coupled to conformational changes that power membrane remodeling, tethering, and fusion."
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OPA1 is a key regulator of crista morphogenesis and maintenance, acting in coordination with the MICOS complex (e.g., MIC60) to control crista junction width, stability, and lumen shape; OPA1 deficiency causes fragmented mitochondria and abnormal cristae.
"OPA1 is a key regulator of **crista morphogenesis and maintenance**, and OPA1 deficiency causes fragmented mitochondria and abnormal cristae."
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The long membrane-anchored form (L-OPA1) and the short soluble intermembrane-space form (S-OPA1) arise through regulated proteolysis by OMA1 (S1) and YME1L (S2), and the protease-controlled L/S balance is a primary regulatory lever responding to cellular stress.
"OPA1 exists as **long (L-OPA1)** and **short (S-OPA1)** isoforms; **OMA1** cleaves at S1 and **YME1L** at S2."
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OPA1 is localized to the inner mitochondrial membrane, where the long form is membrane-anchored and the short form is soluble in the intermembrane space.
"OPA1 is localized to the **inner mitochondrial membrane (IMM)**, where the long form is membrane-anchored and the short form is soluble in the intermembrane space."
An LKB1-mitochondria axis controls T(H)17 effector function.
OpenScientist EAT-3 microtubule/peroxisome capacity adjudication (comparative OPA1-family evidence)
opa1 full-gene evidence and PAINT re-review notes
OPA1 disease alleles causing dominant optic atrophy have defects in cardiolipin-stimulated GTP hydrolysis and membrane tubulation.
Molecular basis of selective mitochondrial fusion by heterotypic action between OPA1 and cardiolipin.
Cryo-EM structures of S-OPA1 reveal its interactions with membrane and changes upon nucleotide binding.
Structural mechanism of mitochondrial membrane remodelling by human OPA1.