Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.7.11.22 (cdc2)
 8,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Rat liver Golgi stacks fragmented when incubated with mitotic but not interphase cytosol in a process dependent on time, temperature, energy (added in the form of ATP) and cdc2 kinase. The cross-sectional length of Golgi stacks fell in the presence of mitotic cytosol by approximately 50% over 30 min without a corresponding decrease in the number of cisternae in the stack. The loss of membrane from stacked and single cisternae occurred with a half-time of approximately 20 min, and was matched by the appearance of both small (50-100 nm in diameter) and large (100-200 nm in diameter) vesicular profiles. Small vesicular profiles constituted more than 50% of the total membrane after 60 min of incubation and they were shown to be vesicles or very short tubules by serial sectioning. In the presence of GTP gamma S all of the small vesicles were COP-coated and both the extent and the rate at which they formed were sufficient to account for the production of small vesicles during mitotic incubation. The involvement of the COP-mediated budding mechanism was confirmed by immunodepletion of one of the subunits of COP coats (the coatomer) from mitotic cytosol. Vesicles were no longer formed but highly fenestrated networks appeared, an effect reversed by the readdition of purified coatomer. Together these experiments provide strong support for our hypothesis that the observed vesiculation of the Golgi apparatus during mitosis in animal cells is caused by continued budding of COP-coated transport vesicles but an inhibition of their fusion with their target membranes.
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PMID:COP-coated vesicles are involved in the mitotic fragmentation of Golgi stacks in a cell-free system. 816 45

The mitotic disassembly and reassembly of the mammalian Golgi apparatus is an ideal system to study the molecular mechanisms involved in biogenesis and maintenance of membranous organelles. As cells enter M-phase, Golgi stacks are converted into Golgi clusters of small membrane fragments, which are dispersed throughout the cytoplasmic space during metaphase. Disassembly is dependent on the action of cdc2-kinase and at least two distinct pathways contribute to the fragmentation: one involves the budding of COP I-coated vesicles from Golgi cisternae, the other is a less well characterised COP I-independent pathway. During telophase, the Golgi fragments reassemble and fuse into a fully functional Golgi stack, using at least two distinct ATPase-mediated fusion pathways.
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PMID:Molecular mechanisms in the disassembly and reassembly of the mammalian Golgi apparatus during M-phase. 868 8

The Golgi apparatus in mammalian cells disassembles into several thousand vesicles as cells enter M-phase. Disassembly is dependent on the action of cdc2-kinase and at least two pathways contribute to the fragmentation: One involves the budding of COP-coated vesicles from Golgi cisternae with concomitant inhibition of fusion with their target membranes, the other is a less well characterised COP-independent pathway. During telophase, the Golgi fragments reassemble and fuse into a fully functional Golgi stack, using at least two distinct fusion pathways. The morphological changes of the Golgi apparatus during M-phase offer an ideal system to study how cellular organelles are generated and how their structure is maintained during interphase.
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PMID:The mammalian Golgi apparatus during M-phase. 955 1