TIMMDC1

Chr 3AR

translocase of inner mitochondrial membrane domain containing 1

Also known as: C3orf1, MC1DN31

TIMMDC1 encodes a chaperone protein that assembles mitochondrial complex I (NADH:ubiquinone oxidoreductase), specifically participating in construction of the membrane arm of this respiratory chain complex. Mutations cause mitochondrial complex I deficiency, nuclear type 31, inherited in an autosomal recessive pattern. This gene shows minimal constraint against loss-of-function variants (very low pLI score), which is consistent with its recessive inheritance pattern where heterozygous carriers are typically unaffected.

OMIMResearchSummary from RefSeq, OMIM, UniProt
MultiplemechanismARLOEUF 1.271 OMIM phenotype
Clinical SummaryTIMMDC1
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Gene-Disease Validity (ClinGen)
Leigh syndrome · ARLimited

Limited evidence — not for standalone diagnostic reporting

2 total gene-disease associations curated

Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.
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ClinVar Variants
23 unique Pathogenic / Likely Pathogenic· 87 VUS of 173 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
1.27LOEUF
pLI 0.000
Z-score 0.73
OE 0.81 (0.541.27)
Tolerant

Highly tolerant — LoF variants common in population

Missense Constraint
0.00Z-score
OE missense 1.00 (0.881.14)
156 obs / 156.2 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.81 (0.541.27)
00.351.4
Missense OE1.00 (0.881.14)
00.61.4
Synonymous OE1.17
01.21.6
LoF obs/exp: 14 / 17.3Missense obs/exp: 156 / 156.2Syn Z: -1.01
DN
0.6938th %ile
GOF
0.6737th %ile
LOF
0.3357th %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

173 submitted variants in ClinVar

Classification Summary

Pathogenic16
Likely Pathogenic7
VUS87
Likely Benign30
Benign12
Conflicting3
16
Pathogenic
7
Likely Pathogenic
87
VUS
30
Likely Benign
12
Benign
3
Conflicting

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
1
0
15
0
16
Likely Pathogenic
6
1
0
0
7
VUS
5
72
9
1
87
Likely Benign
0
3
13
14
30
Benign
0
3
7
2
12
Conflicting
3
Total12794417155

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

View in ClinVar →

Protein Context — Lollipop Plot

TIMMDC1 · 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
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