GNAO1

Chr 16AD

G protein subunit alpha o1

Also known as: DEE17, EIEE17, G-ALPHA-o, GNAO, HG1G, NEDIM

The protein encodes the alpha subunit of the Go heterotrimeric G-protein complex, which mediates signal transduction at the cell membrane. Mutations cause early-onset epileptic encephalopathy and neurodevelopmental disorders with involuntary movements through an autosomal dominant inheritance pattern. The gene is highly constrained against loss-of-function variants, and mutations can cause disease through multiple mechanisms depending on the specific variant type.

GeneReviewsOMIMResearchSummary from RefSeq, OMIM, UniProt
LOFmechanismADLOEUF 0.262 OMIM phenotypes
Clinical SummaryGNAO1
🧬
Gene-Disease Validity (ClinGen)
movement disorder · ADDefinitive

Definitive — sufficient evidence for diagnostic panels

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.
💊
Clinical Trials
2 active or recruiting trials — potential therapeutic options may be available
📖
GeneReview available — GNAO1
Authoritative clinical overview · Recommended first read
Open GeneReview ↗

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Dual constrained — LoF & missense intolerant
LoF Constraint
0.26LOEUF
pLI 0.990
Z-score 3.73
OE 0.06 (0.020.26)
Highly constrained

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

Missense Constraint
3.19Z-score
OE missense 0.41 (0.340.48)
93 obs / 228.9 exp
Constrained

Highly missense-constrained (top ~0.1%)

Observed / Expected Ratios
LoF OE0.06 (0.020.26)
00.351.4
Missense OE0.41 (0.340.48)
00.61.4
Synonymous OE0.90
01.21.6
LoF obs/exp: 1 / 18.1Missense obs/exp: 93 / 228.9Syn Z: 0.77
Curated Mechanism (G2P)Gene2Phenotype (DDG2P) ↗
definitiveGNAO1-related epileptic encephalopathyLOFAD
DN
0.4884th %ile
GOF
0.6639th %ile
LOF
0.53top 25%

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

GOFprediction above median · 1 literature citation
LOFLOEUF 0.26
DN1 literature citation

Note: In-silico variant effect predictors (SIFT, PolyPhen, REVEL, CADD) may underestimate pathogenicity of missense variants in genes with GOF or DN mechanisms. Consider functional evidence and clinical context.

Literature Evidence

DNExperiments in mice confirmed dominant negative effects of GNAO1 G42R, which impaired numerous motor behaviors.PMID:34508586
GOFMovement disorder in GNAO1 encephalopathy associated with gain-of-function mutationsPMID:28747448

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

GNAO1 · protein map & ClinVar variants

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

3D Protein StructureAlphaFold
Clinical Literature
Open Research Assistant →
Key Publications
Landmark & review papers · by relevance
PubMed
Top 5 results · since 2015Search PubMed ↗