DEPDC5

Chr 22ARAD

DEP domain containing 5, GATOR1 subcomplex subunit

The protein functions as a component of the GATOR1 complex that inhibits the mTORC1 pathway by acting as a GTPase activating protein for Rag GTPases in response to amino acid depletion, thereby regulating cell growth and metabolism. Mutations cause autosomal dominant familial focal epilepsy with variable foci and developmental and epileptic encephalopathy through loss of function mechanisms that lead to mTORC1 hyperactivation. The pathogenic mechanism involves haploinsufficiency, where reduced GATOR1 complex function results in dysregulated mTOR signaling in neurons.

OMIMResearchSummary from RefSeq, OMIM, UniProt
LOFmechanismAR/ADLOEUF 0.332 OMIM phenotypes
VCEP Guidelines: Brain MalformationsReleased
View SpecificationsClinGen Panel
Clinical SummaryDEPDC5
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Gene-Disease Validity (ClinGen)
focal epilepsy · ADDefinitive

Definitive — sufficient evidence for diagnostic panels

Population Constraint (gnomAD)
Constrained for loss-of-function variants (OE-LoF 0.24) despite low pLI — interpret in context.
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Clinical Trials
1 active or recruiting trial — potential therapeutic options may be available

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

LoF intolerant — likely haploinsufficient
LoF Constraint
0.33LOEUF
pLI 0.116
Z-score 7.15
OE 0.24 (0.170.33)
Highly constrained

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

Missense Constraint
2.65Z-score
OE missense 0.76 (0.710.81)
713 obs / 941.9 exp
Mild constraint

Moderately missense-constrained (top ~2.5%)

Observed / Expected Ratios
LoF OE0.24 (0.170.33)
00.351.4
Missense OE0.76 (0.710.81)
00.61.4
Synonymous OE0.94
01.21.6
LoF obs/exp: 24 / 102.0Missense obs/exp: 713 / 941.9Syn Z: 0.84
Curated Mechanism (G2P)Gene2Phenotype (DDG2P) ↗
definitiveDEPDC5-related familial focal epilepsy with variable fociLOFAD
DN
0.5181th %ile
GOF
0.5367th %ile
LOF
0.50top 25%

The Badonyi & Marsh model scores gain-of-function highest, but genomic evidence most strongly supports loss-of-function (haploinsufficiency) as the primary mechanism.

LOF1 literature citation · LOEUF 0.33

Literature Evidence

LOFThese data indicate that human cells heterozygous for DEPDC5 loss-of-function mutations are haploinsufficient for control of mTORC1 signaling.PMID:32574724

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

DEPDC5 · 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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