SVIL
protein-codingsupervillin, the group of Gelsolin/villins|MicroRNA protein coding host genes
Gene summary
This gene encodes a bipartite protein with distinct amino- and carboxy-terminal domains. The amino-terminus contains nuclear localization signals and the carboxy-terminus contains numerous consecutive sequences with extensive similarity to proteins in the gelsolin family of actin-binding proteins, which cap, nucleate, and/or sever actin filaments. The gene product is tightly associated with both actin filaments and plasma membranes, suggesting a role as a high-affinity link between the actin cytoskeleton and the membrane. The encoded protein appears to aid in both myosin II assembly during cell spreading and disassembly of focal adhesions. Several transcript variants encoding different isoforms of supervillin have been described. [provided by RefSeq, Apr 2016]
MANE transcript
Inheritance
ClinVar variants
Top phenotype
gnomAD constraint
Max pathogenic AF
Genomic locus
External References & Databases
Transcript & Mutation Effects
hg38 • Region Span ~279.6 kbGenCC Phenotypes & Disease Associations
Curated gene-disease validity assertions and inheritance patterns
Inheritance Pattern: AR
Disease ID:MONDO:0033620
Submitter: PanelApp Australia
Inheritance Pattern: AR
Disease ID:MONDO:0033620
Submitter: Ambry Genetics
Inheritance Pattern: AR
Disease ID:MONDO:0033620
Submitter: Labcorp Genetics (formerly Invitae)
Clinical Genomic Database (CGD)
Manifestation: Cardiovascular; Musculoskeletal
Intervention: Cardiovascular
Rationale: The condition can involve cardiovascular sequelae, including ventricular hypertrophy with EKG abnormalities, and elevated cardiac enzymes, and awareness may allow early diagnosis and management
ClinVar Associated Diseases & Phenotypes
Reported disease conditions connected to SVIL variants in ClinVar
ClinVar Variants & Pathogenicity by Type
Statistics based on transcript NM_021738.3. Only rare variants are included.
We include only reliable ClinVar variants with their consequences to MANE Select, MANE Plus Clinical transcripts, or transcripts with TSL equal to 1. Click a count to filter the variants table below.
Slight differences between displayed counts and ClinVar may occur due to a different transcript/consequence chosen by our variant effect predictor, or because we classify Benign/Likely benign as Likely benign and Pathogenic/Likely pathogenic as Likely pathogenic.
| Effect | PathogenicP | Likely pathogenicLP | VUS | Likely benignLB | BenignB | Sum |
|---|---|---|---|---|---|---|
| synonymous | 10 | 43 | 9 | 62 | ||
| missense | 1 | 349 | 28 | 4 | 382 | |
| nonsense | 1 | 2 | 3 | |||
| start loss | 0 | |||||
| frameshift | 1 | 1 | 2 | |||
| splice donor/acceptor (+/-2bp) | 4 | 12 | 16 | |||
| Total | 2 | 7 | 372 | 71 | 13 | 465 |
Highest pathogenic variant AF is 0.000047736543
Transcript Catalog
Annotated transcript isoforms across RefSeq and Ensembl databases
| Transcript ID | Source | Protein ID | Coding Exons | MANE Status |
|---|---|---|---|---|
| RefSeq | NP_068506.2 | 35 | MANE Select | |
| Ensembl | ENSP00000348128.4 | 35 | MANE Select | |
| RefSeq | NP_001310528.1 | 34 | Standard | |
| RefSeq | NP_001310529.1 | 32 | Standard |
Model Organisms & Knockout Phenotypes
Observed phenotypic effects in mouse and zebrafish models
| Gene / Model | Organism | Observed Phenotype |
|---|---|---|
| svila | Danio rerio | Structure: pericardium Quality: edematous abnormal |
Gene Ontology (GO) Annotations & Pathways
Biological processes, molecular functions, cellular components and pathways
Pathways ConsensusPathDB
- AndrogenReceptor
- Coregulation of Androgen receptor activity
Biological Process
- cytoskeleton organization
- skeletal muscle tissue development
- positive regulation of cytokinesis
Molecular Function
- protein binding
- actin filament binding
Cellular Component
- podosome
- nucleus
- cytoplasm
- cytosol
- plasma membrane
gnomAD Constraint
Source:
- Gene type
- protein_coding
- Transcript type
- protein_coding
- Transcript
- ENST00000375398
- Coding exons
- 35
- Length
- 279444
- Individuals with no LoFs
- 125677
- Homozygous LoFs
- 0
- Heterozygous LoFs
- 71
- Defined
- 125748
- p
- 0.000282
| Z-Score | Observed | Expected | Observed/Expected | Mutation Rate | Total Possible | |
|---|---|---|---|---|---|---|
| Missense | 0.885 | 1202 | 1.29e+3 | 0.931 | 0.0000799 | 14427 |
| Missense (PolyPhen) | 344 | 411 | 0.83698 | 4624 | ||
| Synonymous | -0.619 | 554 | 536 | 1.03 | 0.0000380 | 4362 |
| Loss of Function | 7.19 | 29 | 111 | 0.262 | 0.00000639 | 1252 |
Population LoF Frequency
| Population | CAF | p-value | Status |
|---|---|---|---|
| African | 0.00025 | 0.00025 | rare |
| Latino/Admixed American | 0.00017 | 0.00017 | rare |
| Ashkenazi Jewish | 0.00073 | 0.00069 | rare |
| East Asian | 0.00016 | 0.00016 | rare |
| Finnish | 0.000046 | 0.000046 | rare |
| European (Non-Finnish) | 0.00035 | 0.00035 | rare |
| South Asian | 0.00023 | 0.00023 | rare |
| Other | 0.00049 | 0.00049 | rare |
dbNSFP Gene Annotations
Source:
- Function
- FUNCTION: Isoform 1: Forms a high-affinity link between the actin cytoskeleton and the membrane. Is among the first costameric proteins to assemble during myogenesis and it contributes to myogenic membrane structure and differentiation (PubMed:12711699). Appears to be involved in myosin II assembly. May modulate myosin II regulation through MLCK during cell spreading, an initial step in cell migration. May play a role in invadopodial function (PubMed:19109420). {ECO:0000269|PubMed:12711699, ECO:0000269|PubMed:19109420}.;
Recessive Scores
- pRec
- 0.122
Intolerance Scores
- LoFtool
- 0.573
- RVIS EVS
- -1.38
- RVIS percentile EVS
- 4.34
Essentials
- Essential (CRISPR)
- N
- Essential (CRISPR2)
- N
- Essential (gene trap)
- N
- Indispensability pred.
- E
- Indispensability score
- 0.820
Gene Damage Prediction
| All | Recessive | Dominant | |
|---|---|---|---|
| Mendelian | Medium | Medium | Medium |
| Primary Immunodeficiency | Medium | Medium | High |
| Cancer | High | Medium | High |