TBR1

Chr 2AD

T-box brain transcription factor 1

Also known as: AUTS5, IDDAS, TBR-1, TES-56

TBR1 encodes a T-box transcription factor that regulates neuronal migration and axonal projection in the cerebral cortex, hippocampus, amygdala, and olfactory bulb. Loss-of-function mutations cause autosomal dominant intellectual developmental disorder with autism and speech delay. The gene is highly intolerant to loss-of-function variants, indicating haploinsufficiency as the mechanism of pathogenicity.

OMIMResearchSummary from RefSeq, OMIM, UniProt, Mechanism
LOFmechanismADLOEUF 0.191 OMIM phenotype
Clinical SummaryTBR1
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Gene-Disease Validity (ClinGen)
complex neurodevelopmental disorder · ADDefinitive

Definitive — sufficient evidence for diagnostic panels

Population Constraint (gnomAD)
Highly constrained gene — heterozygous loss-of-function variants are very rare in the population (pLI 1.00). One damaged copy is likely sufficient to cause disease.
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Clinical Trials
2 active or recruiting trials — potential therapeutic options may be available

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Dual constrained — LoF & missense intolerant
LoF Constraint
0.19LOEUF
pLI 0.999
Z-score 4.39
OE 0.04 (0.010.19)
Highly constrained

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

Missense Constraint
3.64Z-score
OE missense 0.47 (0.410.53)
172 obs / 368.4 exp
Constrained

Highly missense-constrained (top ~0.1%)

Observed / Expected Ratios
LoF OE0.04 (0.010.19)
00.351.4
Missense OE0.47 (0.410.53)
00.61.4
Synonymous OE0.93
01.21.6
LoF obs/exp: 1 / 24.5Missense obs/exp: 172 / 368.4Syn Z: 0.69
Curated Mechanism (G2P)Gene2Phenotype (DDG2P) ↗
definitiveTBR1-related autismLOFAD
DN
0.3196th %ile
GOF
0.2696th %ile
LOF
0.87top 5%

This gene has evidence for multiple mechanisms of pathogenicity (loss-of-function and dominant-negative). 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 · 1 literature citation · LOEUF 0.19
DN1 literature citation

Literature Evidence

DNThe mutant protein retained the ability to homodimerize with wildtype TBR1 and to interact with CASK (300173), suggesting a dominant-negative effect, but was unable to interact with FOXP2 (605317).PMID:25232744
LOFThe identification of TBR1 as candidate for ID encourages further molecular studies to identify novel mutations to understand the pathogenic effects of its haploinsufficiency.PMID:24458984

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

TBR1 · 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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