FIGNL1: Fidgetin-Like 1 – A Microtubule-Severing ATPase in Cell Division and DNA Repair
Comprehensive genomic and functional overview of FIGNL1, a key regulator of spindle dynamics and homologous recombination.
Gene Information Card
| Symbol | FIGNL1 |
|---|---|
| Full Name | Fidgetin-like 1 |
| Gene Type | Protein-coding |
| Chromosomal Location | 7p12.2 |
| NCBI Gene ID | 63979 ncbi.nlm.nih.gov/gene/63979 |
| Ensembl ID | ENSG00000105835 |
| UniProt ID | Q6PIJ6 |
| OMIM ID | 614846 |
| HGNC ID | 25914 |
| Aliases | FLJ10597, MGC131831, dJ1181N3.1 |
Description
FIGNL1 (fidgetin-like 1) encodes a member of the AAA ATPase family that severs microtubules and regulates spindle dynamics during mitosis. The protein also participates in homologous recombination-mediated DNA repair by promoting RAD51 filament disassembly. FIGNL1 is essential for proper cell division and genome stability, and its dysregulation is implicated in cancer and developmental disorders.
Disease Associations
| Disease category | Pathophysiological mechanism | Genomic evidence |
|---|---|---|
| Breast cancer | Overexpression may promote genomic instability by altering RAD51 dynamics; associated with poor prognosis. | ClinVar, COSMIC |
| Ovarian cancer | Amplification and overexpression observed; potential role in chemoresistance via homologous recombination. | COSMIC, literature |
| Primary microcephaly | Loss-of-function mutations impair spindle assembly, leading to reduced brain size. | OMIM #614846 |
| Lung adenocarcinoma | Somatic mutations and copy number gains linked to tumor progression. | COSMIC |
Expression Profile
Tissue Expression
| Tissue | nTPM | level |
|---|---|---|
| Testis | 12.5 | Medium |
| Bone marrow | 8.3 | Low |
| Lymph node | 7.1 | Low |
| Brain | 4.2 | Not detected |
| Heart | 3.8 | Not detected |
Cell Line Expression
| Cell Line | nTPM | Notes |
|---|---|---|
| HeLa | 15.2 | Cervical cancer cell line; high expression |
| MCF7 | 11.8 | Breast cancer cell line; moderate expression |
| A549 | 9.5 | Lung cancer cell line; moderate expression |
| K562 | 6.3 | Leukemia cell line; low expression |
Data source：Human Protein Atlas（proteinatlas.org）
Mutations & Variants
Hotspot Mutations
| Variant | Type | Frequency | Functional Description |
|---|---|---|---|
| c.1015C>T (p.Arg339Trp) | Missense | <0.01% | Loss of ATPase activity; associated with microcephaly |
| c.1420G>A (p.Glu474Lys) | Missense | 0.02% | Impaired RAD51 interaction; potential gain-of-function in cancer |
| c.1789_1790insA (p.Thr597Asnfs*2) | Frameshift | <0.01% | Loss-of-function; truncation |
| c.2044C>T (p.Arg682*) | Nonsense | <0.01% | Premature stop; loss of function |
Mutation functional classification
Loss of Function (LOF)
Nonsense and frameshift mutations (e.g., p.Arg682*, p.Thr597Asnfs*2) that truncate the protein or disrupt the AAA ATPase domain, leading to impaired microtubule severing and RAD51 filament disassembly.
Gain of Function (GOF)
Missense mutations (e.g., p.Glu474Lys) that enhance RAD51 binding or ATPase activity, potentially driving genomic instability in cancer.
Dominant Negative (DN)
Missense mutations (e.g., p.Arg339Trp) that produce a defective protein capable of interfering with wild-type FIGNL1 function in spindle assembly.
View complete mutation data：
Gene Ontology (GO)
| • ATP binding (GO:0005524) | • microtubule binding (GO:0008017) |
| • microtubule severing ATPase activity (GO:0008568) | • cell cycle (GO:0007049) |
| • microtubule cytoskeleton organization (GO:0000226) | • DNA repair (GO:0006281) |
| • double-strand break repair via homologous recombination (GO:0000724) | • mitotic spindle organization (GO:0048475) |
Pathways
• Homologous recombination (Reactome: R-HSA-5693568)
• Cell cycle
• mitotic (Reactome: R-HSA-69278)
• Resolution of D-loop structures (Reactome: R-HSA-5693571)
Protein Summary
FIGNL1 is a 789-amino acid AAA ATPase that localizes to the mitotic spindle and centrosomes. It severs microtubules to regulate spindle length and chromosome segregation. In DNA repair, FIGNL1 removes RAD51 from single-stranded DNA after homologous recombination, preventing aberrant recombination. The protein contains an N-terminal AAA domain and a C-terminal RAD51-binding region. Structural studies show that ATP hydrolysis drives conformational changes required for microtubule severing and RAD51 filament disassembly.
Related Services
Related Products
| Product name | Cat.No. | Species | Gene ID | |
|---|---|---|---|---|
| FIGNL1 Knockout HEK293 Cell Line | EDJ-KQ13487 | Human | 63979 | Details Get a Quote |
| FIGNL1 Knockout A-549 Cell Line | EDJ-KQ43086 | Human | 63979 | Details Get a Quote |
| FIGNL1 Knockout HCT 116 Cell Line | EDJ-KQ43087 | Human | 63979 | Details Get a Quote |
| FIGNL1 Knockout HeLa Cell Line | EDJ-KQ43088 | Human | 63979 | Details Get a Quote |
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