ArticleThe EMBO journal2025
Molecular mechanism of condensin I activation by KIF4A.
Article in The EMBO journal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed.
- Condensin complexes: from chromatin organization to disease.Nucleus (Austin, Tex.) · 2026Review
- Non-structural maintenance of chromosome condensin I complex subunit H knockdown suppresses malignant progression of esophageal squamous cell carcinoma via the Wnt/β-catenin signaling pathway.Journal of gastrointestinal oncology · 2026Article
- Comprehensive bioinformatics analysis of NCAPH expression and its clinical importance in endometrial cancer.Oncology letters · 2026Article
- Dual phosphoregulatory mechanisms of condensin I revealed by biochemical reconstitution.PNAS nexus · 2026Article
- Article
- A phospho-switch to trigger mitotic chromosome condensation.Biology direct · 2026Article
- Spatial Chromatin Organization Across the Cell Cycle: Insights from Auxin-Inducible Protein Depletion.Cells · 2025Review
- KIF4A in disease pathogenesis and therapeutics: from molecular mechanisms to clinical translation.Biology direct · 2025Review
- The effects of DMSO on DNA conformations and mechanics.Biophysical journal · 2025Article
- Mitotic genome folding.The Journal of cell biology · 2025Review
- Quantitative imaging of loop extruders rebuilding interphase genome architecture after mitosis.The Journal of cell biology · 2025Article
- Review
- Quantitative imaging of loop extruders rebuilding interphase genome architecture after mitosis.bioRxiv : the preprint server for biology · 2024Article
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Authors and funding
4 authors.
Funding
Abstract
During mitosis, the condensin I and II complexes compact chromatin into chromosomes. Loss of the chromokinesin, KIF4A, results in reduced condensin I association with chromosomes, but the molecular mechanism behind this phenotype is unknown. In this study, we reveal that KIF4A binds directly to the human condensin I HAWK subunit, NCAPG, via a conserved disordered short linear motif (SLiM) located in its C-terminal tail. KIF4A competes for NCAPG binding to an overlapping site with SLiMs at the N-terminus of NCAPH and the C-terminus of NCAPD2, which mediate two auto-inhibitory interactions within condensin I. Consistently, the KIF4A SLiM peptide alone is sufficient to stimulate ATPase and DNA loop extrusion activities of condensin I. We identify similar SLiMs in the known yeast condensin interactors, Sgo1 and Lrs4, which bind yeast condensin subunit, Ycg1, the equivalent HAWK to NCAPG. Our findings, together with previous work on condensin II and cohesin, demonstrate that SLiM binding to the NCAPG-equivalent HAWK subunit is a conserved mechanism of regulation in SMC complexes.
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