MYO7A

Chr 11ADAR

myosin VIIA

Also known as: DFNA11, DFNB2, MYOVIIA, MYU7A, NSRD2, USH1B

This unconventional myosin functions as an actin-based motor protein with ATPase activity that plays critical roles in retinal photoreceptor disk renewal, melanosome distribution in retinal pigment epithelium, and cochlear hair cell bundle organization and mechanotransduction. Mutations cause Usher syndrome type 1B, characterized by congenital severe-to-profound sensorineural hearing loss, vestibular dysfunction, and progressive retinal degeneration leading to blindness, with autosomal recessive inheritance. The gene shows extremely low tolerance to loss-of-function variants (pLI approaching 1), indicating that even heterozygous loss-of-function is likely deleterious.

OMIMResearchSummary from RefSeq, UniProt
LOFmechanismAD/ARLOEUF 0.853 OMIM phenotypes
Clinical SummaryMYO7A
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Gene-Disease Validity (ClinGen)
Usher syndrome type 1 · ARDefinitive

Definitive — sufficient evidence for diagnostic panels

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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Clinical Trials
2 active or recruiting trials — potential therapeutic options may be available

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
0.85LOEUF
pLI 0.000
Z-score 2.89
OE 0.70 (0.580.85)
Tolerant

Typical tolerance to LoF variation

Missense Constraint
1.07Z-score
OE missense 0.92 (0.880.96)
1242 obs / 1353.0 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.70 (0.580.85)
00.351.4
Missense OE0.92 (0.880.96)
00.61.4
Synonymous OE1.04
01.21.6
LoF obs/exp: 77 / 109.7Missense obs/exp: 1242 / 1353.0Syn Z: -0.75
Curated Mechanism (G2P)Gene2Phenotype (DDG2P) ↗
definitiveMYO7A-related deafnessLOFAR
definitiveMYO7A-related Usher syndromeOTHERAR

Predictions shown for reference only — model trained on dominant genes, not applicable to AR conditions.

DN
0.7034th %ile
GOF
0.6736th %ile
LOF
0.3066th %ile

The Badonyi & Marsh prediction model was trained exclusively on dominant disease genes. Predictions are not reliable for genes with autosomal recessive inheritance and are shown at reduced opacity for reference only.

Literature Evidence

DNIt has been shown that the coiled-coil region is responsible for the dimerization of MY07A8• Thus it is possible that the DFNAll mutant allele encodes a product that interacts with normal wildtype protein, resulting in a dominant negative effect. Indeed, unlike USHlB and nonsyndromic recessive DFNPMID:9354784

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

ClinVar Variant Classifications

0 submitted variants in ClinVar

Protein Context — Lollipop Plot

MYO7A · protein map & ClinVar variants

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

3D Protein StructureAlphaFold
Clinical Literature
Open Research Assistant →
Key Publications
Landmark & review papers · by relevance
PubMed
Top 5 results · since 2015Search PubMed ↗