TOP3A

Chr 17AR

DNA topoisomerase III alpha

Also known as: MGRISCE2, PEOB5, TOP3, ZGRF7

The protein functions as a DNA topoisomerase that relieves supercoiling tension during DNA replication and transcription by transiently cleaving and rejoining single DNA strands, and is essential for mitochondrial DNA decatenation and segregation. Biallelic mutations cause autosomal recessive disorders including microcephaly with growth restriction and increased sister chromatid exchange, as well as progressive external ophthalmoplegia with mitochondrial DNA deletions. This gene is highly constrained against loss-of-function mutations (pLI near 1.0), indicating intolerance to protein truncation.

GeneReviewsOMIMResearchSummary from RefSeq, OMIM, UniProt
LOFmechanismARLOEUF 0.682 OMIM phenotypes
Clinical SummaryTOP3A
Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.
📋
ClinVar Variants
15 unique Pathogenic / Likely Pathogenic· 92 VUS of 200 total submissions
📖
GeneReview available — TOP3A
Authoritative clinical overview · Recommended first read
Open GeneReview ↗

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
0.68LOEUF
pLI 0.000
Z-score 3.42
OE 0.49 (0.360.68)
Tolerant

Typical tolerance to LoF variation

Missense Constraint
1.31Z-score
OE missense 0.85 (0.790.91)
493 obs / 582.0 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.49 (0.360.68)
00.351.4
Missense OE0.85 (0.790.91)
00.61.4
Synonymous OE1.09
01.21.6
LoF obs/exp: 26 / 52.8Missense obs/exp: 493 / 582.0Syn Z: -1.08
Curated Mechanism (G2P)Gene2Phenotype (DDG2P) ↗
definitiveTOP3A-related Bloom syndrome like disorderLOFAR

Predictions shown for reference only — model trained on dominant genes, not applicable to AR conditions.

DN
0.7035th %ile
GOF
0.5465th %ile
LOF
0.2969th %ile

The Badonyi & Marsh prediction model was trained exclusively on dominant disease genes. Predictions are not reliable for genes with autosomal recessive inheritance and are shown at reduced opacity for reference only.

Predictions from Badonyi M, Marsh JA. PLoS ONE. 2024;19(8):e0307312.

ClinVar Variant Classifications

200 submitted variants in ClinVar

Classification Summary

Pathogenic12
Likely Pathogenic3
VUS92
Likely Benign61
Benign6
Conflicting5
12
Pathogenic
3
Likely Pathogenic
92
VUS
61
Likely Benign
6
Benign
5
Conflicting

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
10
0
2
0
12
Likely Pathogenic
2
1
0
0
3
VUS
2
89
1
0
92
Likely Benign
0
2
21
38
61
Benign
0
0
3
3
6
Conflicting
5
Total14922741179

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

View in ClinVar →

Protein Context — Lollipop Plot

TOP3A · protein map & ClinVar variants

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

3D Protein StructureAlphaFold

Clinical Trials

Active and recruiting trials from ClinicalTrials.gov

No active trials found for this gene.

Search ClinicalTrials.gov →
Clinical Literature
Open Research Assistant →
Full-Text Mentions
NLP-detected gene mentions in article bodies · via PubTator3
PubTator3
Top 5 full-text resultsSearch PubTator3 ↗
Recent Gene-Specific Literature
Gene in title · MEDLINE · newest first
Europe PMC