APC/C CDH1 targets CDC20 for proteolysis, resulting in a cellular switch from APC/C CDC20 to APC/C CDH1 activity. For example, the dephosphorylation of CDH1 allows the APC/C to bind CDH1. Ĭdc14-mediated dephosphorylation activates downstream regulatory processes unique to telophase. Complete release and maintained activation of cdc14 is achieved by the separate Mitotic Exit Network (MEN) pathway to a sufficient degree (to trigger the spindle disassembly and nuclear envelope assembly) only after late anaphase. The Cdc-14 Early Anaphase Release pathway, which stabilizes the spindle, also releases cdc14 from the nucleolus but restricts it to the nucleus. Cdc14 is activated by its release into the nucleus, from sequestration in the nucleolus, and subsequent export into the cytoplasm. However, the existence of differential phases to cdc14 activity between anaphase and telophase is suggestive of additional, unexplored late- mitotic checkpoints. Historically, it has been thought that anaphase and telophase are events that occur passively after satisfaction of the spindle-assembly checkpoint (SAC) that defines the metaphase-anaphase transition. ![]() Blocking cdc14 activation in these cells results in the same phenotypic arrest as does blocking M-cyclin degradation. The requirement for phosphatase activation can be seen in budding yeast, which do not have redundant phosphatases for mitotic exit and rely on the phosphatase cdc14. This has been shown in frog ( Xenopus) eggs, fruit flies ( Drosophilla melanogaster), budding ( Saccharomyces cerevisiae) and fission ( Schizosaccharomyces pombe) yeast, and in multiple human cell lines. Experimental addition of non-degradable M-cyclin to cells induces cell cycle arrest in a post-anaphase/pre-telophase-like state with condensed chromosomes segregated to cell poles, an intact mitotic spindle, and no reformation of the nuclear envelope. The active, CDC20-bound APC (APC/C CDC20) targets mitotic cyclins for degradation starting in anaphase. Cyclins are targeted for proteolytic degradation by the anaphase promoting complex (APC), also known as the cyclosome, a ubiquitin-ligase. Establishing a degree of dephosphorylation permissive to telophase events requires both the inactivation of Cdks and the activation of phosphatases.Ĭdk inactivation is primarily the result of the destruction of its associated cyclin. The dephosphorylation of these same substrates drives spindle disassembly, chromosome decondensation and the reformation of daughter nuclei in telophase. The phosphorylation of the protein targets of M-Cdks (Mitotic Cyclin-dependent Kinases) drives spindle assembly, chromosome condensation and nuclear envelope breakdown in early mitosis. Telophase is primarily driven by the dephosphorylation of mitotic cyclin-dependent kinase (Cdk) substrates. Telophase accounts for approximately 2% of the cell cycle's duration.Ĭytokinesis typically begins before late telophase and, when complete, segregates the two daughter nuclei between a pair of separate daughter cells. ![]() The mitotic spindle is disassembled and remaining spindle microtubules are depolymerized. As chromosomes reach the cell poles, a nuclear envelope is re-assembled around each set of chromatids, the nucleoli reappear, and chromosomes begin to decondense back into the expanded chromatin that is present during interphase. During telophase, the effects of prophase and prometaphase (the nucleolus and nuclear membrane disintegrating) are reversed. Telophase (from Ancient Greek τέλος ( télos) 'end, result, completion', and φάσις (phásis) 'appearance') is the final stage in both meiosis and mitosis in a eukaryotic cell. Fluorescence micrograph of a human cell in telophase showing chromosomes (DNA) in blue, microtubules in green and kinetochores in pink
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