作者: B. R. Chaffee , F. Shang , M.-L. Chang , T. M. Clement , E. M. Eddy
DOI: 10.1242/DEV.106005
关键词:
摘要: Lens epithelial cells and early lens fiber contain the typical complement of intracellular organelles. However, as mature they must destroy their organelles, including nuclei, in a process that has remained enigmatic for over century, but which is crucial formation organelle-free zone center assures clarity function to transmit light. Nuclear degradation requires nuclease DNase IIβ (DLAD) mechanism by DLAD gains access nuclear DNA remains unknown. In eukaryotic cells, cyclin-dependent kinase 1 (CDK1), combination with either activator cyclins A or B, stimulates mitotic entry, part, phosphorylating lamin proteins leading disassembly lamina subsequent envelope breakdown. Although most post-mitotic lack CDK1 cyclins, maintain these proteins. Here, we show loss from inhibited phosphorylation lamins C, prevented entry into nucleus, resulted abnormal retention nuclei. presence CDK1, single focus phosphonuclear apparatus observed, it not focused CDK1-deficient lenses. deficiency mitosis, did prevent replication, resulting an overall reduction remaining possessing abnormally large nucleus. These observations suggest CDK1-dependent phosphorylations required initiation membrane during mitosis are adapted removal nuclei cell differentiation.