LMO4 encodes a transcription cofactor that contains two LIM domains and functions in establishing motor neuron identity by disrupting LDB1-LHX3 complexes to negatively regulate interneuron genes in motor neurons. Mutations cause autosomal dominant developmental and epileptic encephalopathy with onset in infancy, characterized by severe intellectual disability, seizures, and motor dysfunction. The gene shows moderate constraint against loss-of-function variants (LOEUF 0.595), consistent with its essential role in neurodevelopment.

Summary from RefSeq, UniProt
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0
Active trials
13
Pubs (1 yr)
12
P/LP submissions
0%
P/LP missense
0.59
LOEUF
Multiple*
Mechanism· predicted
Clinical SummaryLMO4
Population Constraint (gnomAD)
Moderately constrained gene (pLI 0.68) — some intolerance to loss-of-function variants.
📋
ClinVar Variants
12 unique Pathogenic / Likely Pathogenic· 16 VUS of 41 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Moderate LoF intolerance
LoF Constraint
0.59LOEUF
pLI 0.677
Z-score 2.29
OE 0.13 (0.040.59)
Moderately constrained

More LoF-intolerant than ~75% of genes

Missense Constraint
2.10Z-score
OE missense 0.42 (0.330.54)
43 obs / 103.0 exp
Mild constraint

Moderately missense-constrained (top ~2.5%)

Observed / Expected Ratios
LoF OE0.13 (0.040.59)
00.351.4
Missense OE0.42 (0.330.54)
00.61.4
Synonymous OE1.17
01.21.6
LoF obs/exp: 1 / 8.0Missense obs/exp: 43 / 103.0Syn Z: -0.90
DN
0.4983th %ile
GOF
0.6541th %ile
LOF
0.68top 25%

This gene has evidence for multiple mechanisms of pathogenicity (loss-of-function and gain-of-function). 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
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

41 submitted variants in ClinVar

Classification Summary

Pathogenic11
Likely Pathogenic1
VUS16
11
Pathogenic
1
Likely Pathogenic
16
VUS

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
11
0
11
Likely Pathogenic
0
0
1
0
1
VUS
0
13
3
0
16
Likely Benign
0
0
0
0
0
Benign
0
0
0
0
0
Total01315028

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

View in ClinVar →

Protein Context — Lollipop Plot

LMO4 · protein map & ClinVar variants

Showing all ClinVar variants across the protein. Search a specific variant to highlight its position.

Clinical Trials

Active and recruiting trials from ClinicalTrials.gov

No active trials found for this gene.

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Clinical Literature
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