Bovine Liver Chromatin Fraction Contains Actin Polymerization Activity Inducing Micronuclei Formation when Injectcd into Prometaphase Cultured Cells

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  • Matsuoka Yosuke
    Department of Cell Biology and Neuroscience, Graduate School of Medicine, Osaka University
  • Matsuoka Yuriko
    Department of Cell Biology and Neuroscience, Graduate School of Medicine, Osaka University
  • Shibata Satoshi
    Department of Cell Biology and Neuroscience, Graduate School of Medicine, Osaka University
  • Yoneda Yoshihiro
    Department of Cell Biology and Neuroscience, Graduate School of Medicine, Osaka University

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  • Bovine Liver Chromatin Fraction Contains Actin Polymerization Activity Inducing Micronuclei Formation when Injected into Prometaphase Cultured Cells.

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We previously reported that exogenous histone H1, when injected into mitotic cells, disrupts the synchronous progression of mitotic events by delaying chromosome decondensation. This strategy was utilized to determine whether any other interphase proteins are also able to disrupt normal mitotic processes, when introduced into the mitotic phase. We found that a chromatin subfraction from bovine liver nuclei induced postmitotic micronuclei formation in a dose-dependent manner when injected into the prometaphase of rat kangaroo kidney epithelial (PtK2) cells. Close observation showed that, in the case of injected mitotic cells, the mitotic spindles were disrupted, chromosomes became scattered throughout the cytoplasm, and actin filaments were organized ectopically. In addition, when the fraction was injected into interphase cells, extra actin filaments were formed and microtubule organization was affected. In order to determine whether the micronuclei formation resulted from the ectopic formation of actin filaments, we examined the effect of the actin polymerization inhibitor, cytochalasin D. The results showed that the drug inhibited micronuclei formation. From these findings, we concluded that this chromatin subfraction contains actin polymerization activity, thus causing the disruption of mitotic spindles.<br>

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