ArticleMolecular biology of the cell2015
Kif2a depletion generates chromosome segregation and pole coalescence defects in animal caps and inhibits gastrulation of the Xenopus embryo.
Article in Molecular biology of the cell, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- Hsa_circ_0088036 promotes tumorigenesis and chemotherapy resistance in hepatocellular carcinoma via the miR-140-3p/KIF2A axis.Histology and histopathology · 2025Article
- Connecting neurodevelopment to neurodegeneration: a spotlight on the role of kinesin superfamily protein 2A (KIF2A).Neural regeneration research · 2024Review
- Article
- Wnt signaling recruits KIF2A to the spindle to ensure chromosome congression and alignment during mitosis.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Arf GAPs and molecular motors.Small GTPases · 2019Review
- Article
- Regulation of neural stem cell proliferation and differentiation by Kinesin family member 2a.PloS one · 2017Article
- Kif2a regulates spindle organization and cell cycle progression in meiotic oocytes.Scientific reports · 2016Article
- ASB7 regulates spindle dynamics and genome integrity by targeting DDA3 for proteasomal degradation.The Journal of cell biology · 2016Article
- The RanGTP Pathway: From Nucleo-Cytoplasmic Transport to Spindle Assembly and Beyond.Frontiers in cell and developmental biology · 2015Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Kif2a is a member of the kinesin-13 microtubule depolymerases, which tightly regulate microtubule dynamics for many cellular processes. We characterized Kif2a depletion in Xenopus animal caps and embryos. Kif2a depletion generates defects in blastopore closure. These defects are rescued by removing the animal cap, suggesting that Kif2a-depleted animal caps are not compliant enough to allow gastrulation movements. Gastrulation defects are not rescued by a Kif2a mutated in an Aurora kinase phosphorylation site, suggesting that the phenotypes are caused by problems in mitosis. During animal cap mitoses, Kif2a localizes to the spindle poles and centromeres. Depletion of Kif2a generated multipolar spindles in stage 12 embryos. Kif2a-depleted animal caps have anaphase lagging chromosomes in stage 9 and 10 embryos and subsequent cytokinesis failure. Later divisions have greater than two centrosomes, generating extra spindle poles. Kif2a-depleted embryos are also defective at coalescing extra spindle poles into a bipolar spindle. The gastrulation and mitotic phenotypes can be rescued by either human Kif2a or Kif2b, which suggests that the two homologues redundantly regulate mitosis in mammals. These studies demonstrate that defects in mitosis can inhibit large-scale developmental movements in vertebrate tissues.
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Registered trials
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