ArticleProceedings of the National Academy of Sciences of the United States of America2024
FAM110A promotes mitotic spindle formation by linking microtubules with actin cytoskeleton.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Article
- Knocking down FAM110A suppresses colon adenocarcinoma progression by inhibiting the Nrf2/HO-1 axis to induce ferroptosis.World journal of surgical oncology · 2026Article
- HMMR/RHAMM recruits SACK1D/FAM83D-CK1α complex at the mitotic spindle to control spindle alignment.iScience · 2026Article
- Spindle-localized F-actin regulates polar MTOC organization and the fidelity of meiotic spindle formation.Nature communications · 2025Article
- FAM110A promotes mitotic spindle formation by linking microtubules with actin cytoskeleton.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
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Authors and funding
7 authors.
Funding
Abstract
Precise segregation of chromosomes during mitosis requires assembly of a bipolar mitotic spindle followed by correct attachment of microtubules to the kinetochores. This highly spatiotemporally organized process is controlled by various mitotic kinases and molecular motors. We have recently shown that Casein Kinase 1 (CK1) promotes timely progression through mitosis by phosphorylating FAM110A leading to its enrichment at spindle poles. However, the mechanism by which FAM110A exerts its function in mitosis is unknown. Using structure prediction and a set of deletion mutants, we mapped here the interaction of the N- and C-terminal domains of FAM110A with actin and tubulin, respectively. Next, we found that the FAM110A-Δ40-61 mutant deficient in actin binding failed to rescue defects in chromosomal alignment caused by depletion of endogenous FAM110A. Depletion of FAM110A impaired assembly of F-actin in the proximity of spindle poles and was rescued by expression of the wild-type FAM110A, but not the FAM110A-Δ40-61 mutant. Purified FAM110A promoted binding of F-actin to microtubules as well as bundling of actin filaments in vitro. Finally, we found that the inhibition of CK1 impaired spindle actin formation and delayed progression through mitosis. We propose that CK1 and FAM110A promote timely progression through mitosis by mediating the interaction between spindle microtubules and filamentous actin to ensure proper mitotic spindle formation.
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