A unified view of spatio-temporal control of mitotic entry: Polo kinase as the key

Pintard, Lionel; Archambault, Vincent

doi:10.1098/rsob.180114

Cited by 34 publications

(36 citation statements)

References 90 publications

(133 reference statements)

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“…Changes in localisation that are likely dependent on specific thresholds in Cdk1 activity could also provide a potential delay mechanism. This has been observed for a variety of G2/M regulators such as Cdc25s, Wee1, Plk1, cyclin B, and Greatwall (reviewed by Refs [7,15,156]).…”

Section: Timing Of Mitotic Entrymentioning

confidence: 75%

Triggering mitosis

Crncec

Hochegger

2019

FEBS Letters

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Entry into mitosis is triggered by the activation of cyclin‐dependent kinase 1 (Cdk1). This simple reaction rapidly and irreversibly sets the cell up for division. Even though the core step in triggering mitosis is so simple, the regulation of this cellular switch is highly complex, involving a large number of interconnected signalling cascades. We do have a detailed knowledge of most of the components of this network, but only a poor understanding of how they work together to create a precise and robust system that ensures that mitosis is triggered at the right time and in an orderly fashion. In this review, we will give an overview of the literature that describes the Cdk1 activation network and then address questions relating to the systems biology of this switch. How is the timing of the trigger controlled? How is mitosis insulated from interphase? What determines the sequence of events, following the initial trigger of Cdk1 activation? Which elements ensure robustness in the timing and execution of the switch? How has this system been adapted to the high levels of replication stress in cancer cells?

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Section: Timing Of Mitotic Entrymentioning

confidence: 75%

Triggering mitosis

Crncec

Hochegger

2019

FEBS Letters

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“…In addition, the CycB is phosphorylated at the multiple sites by Plk1 in the cytoplasm. This inhibits the nuclear export of the protein, and consequently promotes its nuclear import [52]. The Cdc25 can be also activated by the Plk1 in the cytoplasm before acting in the nucleus [53].…”

Section: Selective Nuclear Export Of Cycb Essential For the Cdk Fullmentioning

confidence: 99%

Nuclear Export of Cyclin B Mediated by the Nup62 Complex Is Required for Meiotic Initiation in Drosophila Males

Okazaki

Yamazoe

Inoué

2020

Cells

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Background: The central channel of the nuclear pore complex plays an important role in the selective transport of proteins between the nucleus and cytoplasm. Previous studies have demonstrated that the depletion of the Nup62 complex, constructing the nuclear pore channel in premeiotic Drosophila cells, resulted in the absence of meiotic cells. We attempted to understand the mechanism underlying the cell cycle arrest before meiosis. Methods: We induced dsRNAs against the nucleoporin mRNAs using the Gal4/UAS system in Drosophila. Results: The cell cycle of the Nup62-depleted cells was arrested before meiosis without CDK1 activation. The ectopic over-expression of CycB, but not constitutively active CDK1, resulted in partial rescue from the arrest. CycB continued to exist in the nuclei of Nup62-depleted cells and cells depleted of exportin encoded by emb. Protein complexes containing CycB, Emb, and Nup62 were observed in premeiotic spermatocytes. CycB, which had temporally entered the nucleus, was associated with Emb, and the complex was transported back to the cytoplasm through the central channel, interacting with the Nup62 complex. Conclusion: We proposed that CycB is exported with Emb through the channel interacting with the Nup62 complex before the onset of meiosis. The nuclear export ensures the modification and formation of sufficient CycB-CDK1 in the cytoplasm.

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“…Many regulators of cyclin-CDK activity are also direct or indirect targets of cyclin-CDK activity, creating positive feedback loops that ensure that cyclin-CDK activity continues to rise once activated (Hégarat et al, 2016;Lindqvist et al, 2009;Pomerening, 2009). One such regulator is the kinase PLK1, which, apart from activating cyclin-CDK, plays a key role in mitotic entry and progression (Combes et al, 2017;Joukov and De Nicolo, 2018;Pintard and Archambault, 2018). Here we discuss how spiraling cyclin-CDK activities are kept in check and coordinated with genome duplication.…”

Section: Introductionmentioning

confidence: 99%

DNA replication and mitotic entry: A brake model for cell cycle progression

Lemmens

Lindqvist

2019

Journal of Cell Biology

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The core function of the cell cycle is to duplicate the genome and divide the duplicated DNA into two daughter cells. These processes need to be carefully coordinated, as cell division before DNA replication is complete leads to genome instability and cell death. Recent observations show that DNA replication, far from being only a consequence of cell cycle progression, plays a key role in coordinating cell cycle activities. DNA replication, through checkpoint kinase signaling, restricts the activity of cyclin-dependent kinases (CDKs) that promote cell division. The S/G2 transition is therefore emerging as a crucial regulatory step to determine the timing of mitosis. Here we discuss recent observations that redefine the coupling between DNA replication and cell division and incorporate these insights into an updated cell cycle model for human cells. We propose a cell cycle model based on a single trigger and sequential releases of three molecular brakes that determine the kinetics of CDK activation.

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A unified view of spatio-temporal control of mitotic entry: Polo kinase as the key

Cited by 34 publications

References 90 publications

Triggering mitosis

Triggering mitosis

Nuclear Export of Cyclin B Mediated by the Nup62 Complex Is Required for Meiotic Initiation in Drosophila Males

DNA replication and mitotic entry: A brake model for cell cycle progression

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