ATN1

Chr 12AD

atrophin 1

Also known as: B37, CHEDDA, D12S755E, DRPLA, HRS, NOD

This gene encodes atrophin-1, a transcriptional corepressor that recruits other proteins to repress gene transcription and promotes vascular smooth muscle cell migration. Mutations cause dentatorubral-pallidoluysian atrophy (DRPLA), a neurodegenerative disorder with cerebellar ataxia, myoclonic epilepsy, choreoathetosis, and dementia, as well as a congenital form with hypotonia, epilepsy, developmental delay, and digital anomalies. The inheritance pattern is autosomal dominant.

GeneReviewsOMIMResearchSummary from RefSeq, OMIM, UniProt
MultiplemechanismADLOEUF 0.192 OMIM phenotypes
Clinical SummaryATN1
Population Constraint (gnomAD)
Highly constrained gene — heterozygous loss-of-function variants are very rare in the population (pLI 1.00). One damaged copy is likely sufficient to cause disease.
📋
ClinVar Variants
60 unique Pathogenic / Likely Pathogenic· 253 VUS of 443 total submissions
💊
Clinical Trials
4 active or recruiting trials — potential therapeutic options may be available
📖
GeneReview available — ATN1
Authoritative clinical overview · Recommended first read
Open GeneReview ↗

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

LoF intolerant — likely haploinsufficient
LoF Constraint
0.19LOEUF
pLI 1.000
Z-score 5.42
OE 0.07 (0.030.19)
Highly constrained

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

Missense Constraint
1.76Z-score
OE missense 0.81 (0.760.87)
567 obs / 698.0 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.07 (0.030.19)
00.351.4
Missense OE0.81 (0.760.87)
00.61.4
Synonymous OE0.91
01.21.6
LoF obs/exp: 3 / 40.0Missense obs/exp: 567 / 698.0Syn Z: 1.25
Curated Mechanism (G2P)Gene2Phenotype (DDG2P) ↗
strongATN1-related congenital hypotonia, epilepsy, developmental delay, digit abnormalitiesOTHERAD
DN
0.2599th %ile
GOF
0.1699th %ile
LOF
0.90top 5%

This gene has evidence for multiple mechanisms of pathogenicity (loss-of-function and gain-of-function). 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.

LOFprediction above median · LOEUF 0.19
GOF1 literature citation

Literature Evidence

GOFPolyglutamine expansions in the transcriptional co-repressor Atrophin-1, encoded by ATN1, cause the neurodegenerative condition dentatorubral-pallidoluysian atrophy (DRPLA) via a proposed novel toxic gain of function.PMID:30827498

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

443 submitted variants in ClinVar

Classification Summary

Pathogenic50
Likely Pathogenic10
VUS253
Likely Benign77
Benign19
Conflicting17
50
Pathogenic
10
Likely Pathogenic
253
VUS
77
Likely Benign
19
Benign
17
Conflicting

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
4
46
0
50
Likely Pathogenic
0
7
3
0
10
VUS
16
222
14
1
253
Likely Benign
0
39
4
34
77
Benign
1
7
5
6
19
Conflicting
17
Total172797241426

LoF = frameshift, stop gained/lost, canonical splice · Counts from ClinVar esearch · Updated hourly

View in ClinVar →

Protein Context — Lollipop Plot

ATN1 · 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 →