OPA1

Chr 3ARAD

OPA1 mitochondrial dynamin like GTPase

OPA1 encodes a dynamin-related GTPase that mediates fusion of mitochondrial inner membranes, regulates cristae morphology, and maintains respiratory chain function. Mutations cause autosomal dominant optic atrophy type 1 with progressive visual loss, as well as autosomal recessive conditions including Behr syndrome, optic atrophy plus syndrome, and mitochondrial DNA depletion syndromes affecting the heart, brain, and muscle. The gene is highly constrained against loss-of-function variants (pLI 0.99, LOEUF 0.29), reflecting its essential role in mitochondrial function.

OMIMResearchSummary from RefSeq, OMIM, UniProt
LOFmechanismAR/ADLOEUF 0.297 OMIM phenotypes
Clinical SummaryOPA1
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Gene-Disease Validity (ClinGen)
Leigh syndrome · ARModerate

Moderate evidence — consider for supplementary testing

2 total gene-disease associations curated

Population Constraint (gnomAD)
Highly constrained gene — heterozygous loss-of-function variants are very rare in the population (pLI 0.99). One damaged copy is likely sufficient to cause disease.
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Clinical Trials
4 active or recruiting trials — potential therapeutic options may be available
Some data sources returned errors (1)

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Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

LoF intolerant — likely haploinsufficient
LoF Constraint
0.29LOEUF
pLI 0.986
Z-score 6.33
OE 0.18 (0.120.29)
Highly constrained

Highly LoF-intolerant (top ~10% of genes)

Missense Constraint
1.97Z-score
OE missense 0.76 (0.700.83)
411 obs / 540.1 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.18 (0.120.29)
00.351.4
Missense OE0.76 (0.700.83)
00.61.4
Synonymous OE0.94
01.21.6
LoF obs/exp: 13 / 70.3Missense obs/exp: 411 / 540.1Syn Z: 0.57
Curated Mechanism (G2P)Gene2Phenotype (DDG2P) ↗
definitiveOPA1-related optic atrophy plus syndromeLOFAD
strongOPA1-related Behr syndromeLOFAR
definitiveOPA1-related optic atrophyOTHERAD
DN
0.5279th %ile
GOF
0.4481th %ile
LOF
0.64top 25%

This gene has evidence for multiple mechanisms of pathogenicity (loss-of-function and dominant-negative). Both the Badonyi & Marsh prediction and the broader genomic evidence point to loss-of-function as the predominant mechanism. Different variants in this gene may act through different mechanisms — interpret in context of the specific variant.

LOF1 literature citation · LOEUF 0.29
DN1 literature citation

Literature Evidence

DNThe majority of OPA1 mutations encodes truncated forms of the protein and causes DOA through haploinsufficiency, whereas missense OPA1 mutations are predicted to cause disease through deleterious dominant-negative mechanisms.PMID:28378518
LOFOur results emphasize the value of cDNA analysis in the characterization of OPA1 mutations and further strengthen the model of haploinsufficiency as a major pathomechanism in OPA1-associated adOA.PMID:17722006

Predictions from Badonyi M, Marsh JA. PLoS ONE. 2024;19(8):e0307312. Mechanism ranking also informed by gnomAD constraint, ClinVar, and ClinGen data.

ClinVar Variant Classifications

0 submitted variants in ClinVar

Protein Context — Lollipop Plot

OPA1 · protein map & ClinVar variants

Showing all ClinVar variants across the protein. Search a specific variant to highlight its position.

3D Protein StructureAlphaFold
Clinical Literature
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Full-Text Mentions
NLP-detected gene mentions in article bodies · via PubTator3
PubTator3
Top 5 full-text resultsSearch PubTator3 ↗