COL3A1

Chr 2ADAR

collagen type III alpha 1 chain

Also known as: EDS4A, EDSVASC, PMGEDSV

The encoded protein forms pro-alpha1 chains of type III collagen, which is found in extensible connective tissues including skin, blood vessels, and lung, and serves as a major ligand regulating cortical development and neuronal migration in the developing brain. Mutations cause Ehlers-Danlos syndrome vascular type and polymicrogyria with or without vascular-type EDS, following autosomal dominant or autosomal recessive inheritance patterns. This gene is highly constrained against loss-of-function variants, reflecting the critical importance of proper collagen function for vascular integrity and brain development.

GeneReviewsOMIMResearchSummary from RefSeq, OMIM, UniProt
DNmechanismAD/ARLOEUF 0.102 OMIM phenotypes
Clinical SummaryCOL3A1
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Gene-Disease Validity (ClinGen)
Ehlers-Danlos syndrome, vascular type · ADDefinitive

Definitive — sufficient evidence for diagnostic panels

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.
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Clinical Trials
5 active or recruiting trials — potential therapeutic options may be available
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GeneReview available — COL3A1
Authoritative clinical overview · Recommended first read
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Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Dual constrained — LoF & missense intolerant
LoF Constraint
0.10LOEUF
pLI 1.000
Z-score 8.59
OE 0.04 (0.020.10)
Highly constrained

Among the most LoF-intolerant genes (~top 3%)

Missense Constraint
4.09Z-score
OE missense 0.61 (0.560.65)
516 obs / 851.7 exp
Constrained

Highly missense-constrained (top ~0.1%)

Observed / Expected Ratios
LoF OE0.04 (0.020.10)
00.351.4
Missense OE0.61 (0.560.65)
00.61.4
Synonymous OE1.07
01.21.6
LoF obs/exp: 4 / 93.7Missense obs/exp: 516 / 851.7Syn Z: -0.96
Curated Mechanism (G2P)Gene2Phenotype (DDG2P) ↗
definitiveCOL3A1-related Ehlers-Danlos syndromeDNAD
DN
0.5181th %ile
GOF
0.3292th %ile
LOF
0.69top 10%

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.

LOFprediction above median · 1 literature citation · LOEUF 0.10
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

DNTranscriptome analysis of skin fibroblasts with dominant negative COL3A1 mutations provides molecular insights into the etiopathology of vascular Ehlers-Danlos syndrome.PMID:29346445
LOFThe expected COL3A1 haploinsufficiency in her healthy ascendants did not lead to the manifestations of vascular EDS.PMID:19455184

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

COL3A1 · 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 ↗