ATP5ME

Chr 4

ATP synthase membrane subunit e

Also known as: ATP5I, ATP5K

The ATP5ME gene encodes the e subunit of mitochondrial ATP synthase (Complex V), which synthesizes ATP from ADP using the proton gradient generated by the respiratory chain. Mutations cause autosomal recessive mitochondrial complex V deficiency, leading to early-onset neurodegeneration, developmental delay, seizures, and cardiomyopathy. The gene shows relatively low constraint to loss-of-function mutations, consistent with recessive inheritance patterns.

Summary from RefSeq, UniProt
Research Assistant →
0
Active trials
3
Pubs (1 yr)
152
P/LP submissions
0%
P/LP missense
1.37
LOEUF
Multiple*
Mechanism· predicted
Clinical SummaryATP5ME
Population Constraint (gnomAD)
Low constraint (pLI 0.09) — loss-of-function variants are relatively tolerated in the population.
📋
ClinVar Variants
147 unique Pathogenic / Likely Pathogenic· 40 VUS of 198 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
1.37LOEUF
pLI 0.086
Z-score 1.09
OE 0.45 (0.181.37)
Tolerant

Highly tolerant — LoF variants common in population

Missense Constraint
-0.59Z-score
OE missense 1.26 (1.001.59)
51 obs / 40.5 exp
Tolerant

Tolerant to missense variation

Observed / Expected Ratios
LoF OE0.45 (0.181.37)
00.351.4
Missense OE1.26 (1.001.59)
00.61.4
Synonymous OE1.46
01.21.6
LoF obs/exp: 2 / 4.5Missense obs/exp: 51 / 40.5Syn Z: -1.41
DN
0.80top 10%
GOF
0.77top 25%
LOF
0.2777th %ile

This gene has evidence for multiple mechanisms of pathogenicity (dominant-negative and gain-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.

DNprediction above median
GOFprediction above median

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.

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

ClinVar Variant Classifications

198 submitted variants in ClinVar

Classification Summary

Pathogenic142
Likely Pathogenic5
VUS40
Conflicting1
142
Pathogenic
5
Likely Pathogenic
40
VUS
1
Conflicting

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
142
0
142
Likely Pathogenic
1
0
4
0
5
VUS
0
18
22
0
40
Likely Benign
0
0
0
0
0
Benign
0
0
0
0
0
Conflicting
1
Total1181680188

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

View in ClinVar →

Protein Context — Lollipop Plot

ATP5ME · 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 →
Key Publications
Landmark & review papers · by relevance
PubMed
Top 1 results · since 2015Search PubMed ↗
Recent Gene-Specific Literature
Gene in title · MEDLINE · newest first
Europe PMC