DCTN1

Chr 2ADAR

dynactin subunit 1

Also known as: DAP-150, DP-150, HMND14, P135

The encoded protein is the largest subunit of dynactin, which binds to microtubules and cytoplasmic dynein to facilitate intracellular transport including ER-to-Golgi transport, organelle movement, and axonogenesis. Mutations cause autosomal dominant distal hereditary motor neuronopathy type 14 and Perry syndrome, as well as autosomal recessive forms, through disruption of dynein-mediated axonal transport. The protein contains a conserved CAP-Gly domain that directly binds microtubules and interacts with dynein intermediate chains.

GeneReviewsOMIMResearchSummary from RefSeq, OMIM, UniProt
MultiplemechanismAD/ARLOEUF 0.363 OMIM phenotypes
Clinical SummaryDCTN1
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Gene-Disease Validity (ClinGen)
amyotrophic lateral sclerosis · ADModerate

Moderate evidence — consider for supplementary testing

Population Constraint (gnomAD)
Constrained for loss-of-function variants (OE-LoF 0.24) despite low pLI — interpret in context.
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ClinVar Variants
9 unique Pathogenic / Likely Pathogenic· 293 VUS of 600 total submissions
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Clinical Trials
1 active or recruiting trial — potential therapeutic options may be available
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GeneReview available — DCTN1
Authoritative clinical overview · Recommended first read
Open GeneReview ↗

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Moderate LoF intolerance
LoF Constraint
0.36LOEUF
pLI 0.084
Z-score 5.88
OE 0.24 (0.170.36)
Moderately constrained

More LoF-intolerant than ~75% of genes

Missense Constraint
0.89Z-score
OE missense 0.91 (0.850.97)
642 obs / 708.9 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.24 (0.170.36)
00.351.4
Missense OE0.91 (0.850.97)
00.61.4
Synonymous OE1.06
01.21.6
LoF obs/exp: 17 / 70.1Missense obs/exp: 642 / 708.9Syn Z: -0.79
DN
0.6162th %ile
GOF
0.5562th %ile
LOF
0.4529th %ile

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

DN1 literature citation
LOF22% of P/LP variants are LoF · LOEUF 0.36

Literature Evidence

DNA Novel Cosegregating DCTN1 Splice Site Variant in a Family with Bipolar Disorder May Hold the Key to Understanding the Etiology. This variant is analogous to the dominant-negative GLUED Gl1 mutation in Drosophila, which is responsible for a neurodegenerative phenotype.PMID:32325768

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

600 submitted variants in ClinVar

Classification Summary

Pathogenic5
Likely Pathogenic4
VUS293
Likely Benign256
Benign9
Conflicting3
5
Pathogenic
4
Likely Pathogenic
293
VUS
256
Likely Benign
9
Benign
3
Conflicting

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
1
0
4
0
5
Likely Pathogenic
1
2
1
0
4
VUS
15
246
27
5
293
Likely Benign
0
8
147
101
256
Benign
0
0
7
2
9
Conflicting
3
Total17256186108570

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

View in ClinVar →

Protein Context — Lollipop Plot

DCTN1 · 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 →
Full-Text Mentions
NLP-detected gene mentions in article bodies · via PubTator3
PubTator3
Top 5 full-text resultsSearch PubTator3 ↗