The Plk3-Cdc25 circuit

Myer, David; Bahassi, El Mustapha; Stambrook, Peter J.

doi:10.1038/sj.onc.1208278

Cited by 54 publications

(45 citation statements)

References 94 publications

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“…Observed in centrosomes and nucleoli during interphase [60,63], PLK3 is found at spindle poles and midbody during cytokinesis [59,60]. PLK3 activity increases rapidly after DNA damage in an ATMdependent manner, and is involved in G2 arrest by phosphorylating and inhibiting CDC25C phosphatase [64][65][66][67]. Its exact functions during mitosis remain unclear, but overexpression of PLK3's polo box domain, but not the kinase domain, causes cytokinesis defects, aneuploidy and cell death [58][59][60].…”

Section: Discussionmentioning

confidence: 99%

Bcl-xL phosphorylation at Ser49 by polo kinase 3 during cell cycle progression and checkpoints

Wang

Beauchemin

Bertrand

2011

Cellular Signalling

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Functional analysis of a Bcl-xL phosphorylation mutant series has revealed that cells expressing Bcl-xL(Ser49Ala) mutant are less stable at G2 checkpoint after DNA damage and enter cytokinesis more slowly after microtubule poisoning, than cells expressing wild-type Bcl-xL. These effects of Bcl-xL(Ser49Ala) mutant seem to be separable from Bcl-xL function in apoptosis. Bcl-xL(Ser49) phosphorylation is cell cycle-dependent. In synchronized cells, phosphoBcl-xL(Ser49) appears during the S phase and G2, whereas it disappears rapidly in early mitosis during prometaphase, metaphase and early anaphase, and re-appears during telophase and cytokinesis. During DNA damage-induced G2 arrest, an important pool of phospho-Bcl-xL(Ser49) accumulates in centrosomes which act as essential decision centers for progression from G2 to mitosis. During telophase/cytokinesis, phospho-Bcl-xL (Ser49) is found with dynein motor protein. In a series of in vitro kinase assays, specific small interfering RNA and pharmacological inhibition experiments, polo kinase 3 (PLK3) was implicated in Bcl-xL(Ser49) phosphorylation. These data indicate that, during G2 checkpoint, phospho-Bcl-xL(Ser49) is another downstream target of PLK3, acting to stabilize G2 arrest. Bcl-xL phosphorylation at Ser49 also correlates with essential PLK3 activity and function, enabling cytokinesis and mitotic exit.

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Section: Discussionmentioning

confidence: 99%

Bcl-xL phosphorylation at Ser49 by polo kinase 3 during cell cycle progression and checkpoints

Wang

Beauchemin

Bertrand

2011

Cellular Signalling

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“…Chk1 or Chk2 phosphorylate several downstream substrates necessary for activating the DNA-damage checkpoints and subsequently halting the cell cycle. In addition to the canonical ATM/ATR-Chk2-p53 and ATM/ATR-Chk1 pathways, a role for polo-like kinase 3 (Plk3) in Cdc25 phosphatase regulation during DNA damage is emerging (Myer et al, 2005). Plk3 has a functional role in a pathway linking ATM, Plk3, Chk2, Cdc25C and Cdc2 in the cellular response to DNA damage and the G2/M checkpoint (Bahassi el et al, 2006).…”

Section: Ddr Signal Transductionmentioning

confidence: 99%

“…Plk3 has a functional role in a pathway linking ATM, Plk3, Chk2, Cdc25C and Cdc2 in the cellular response to DNA damage and the G2/M checkpoint (Bahassi el et al, 2006). Furthermore, a rapid response pathway involving ATM, Plk3, Chk2 and Cdc25A regulates the G1/S transition (Hong and Stambrook, 2004;Myer et al, 2005). More recently, the p38MAPK/MAPKAP-K2 (MK2) complex …”

Section: Ddr Signal Transductionmentioning

confidence: 99%

Harnessing the complexity of DNA-damage response pathways to improve cancer treatment outcomes

et al. 2010

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“…Cdc27 is part of the anaphase promoting complex (APC), which controls late M phase progression. Plk3 phosphorylates and activates Cdc25, thus stabilizing cell cycle progression (29). Upregulation of these genes in yng retinas may retain cells in the cell cycle and/or prevent normal cell cycle withdrawal.…”

Section: Functional Validations Of Brg1-regulated Retinal Differentiamentioning

confidence: 99%

Factorial microarray analysis of zebrafish retinal development

Leung

Ma²,

Link³

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

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In a zebrafish recessive mutant young (yng), retinal cells are specified to distinct cell classes, but they fail to morphologically differentiate. A null mutation in a brahma-related gene 1 (brg1) is responsible for this phenotype. To identify retina-specific Brg1-regulated genes that control cellular differentiation, we conducted a factorial microarray analysis. Gene expression profiles were compared from wild-type and yng retinas and stage-matched whole embryos at 36 and 52 hours postfertilization (hpf). From our analysis, three categories of genes were identified: (i) Brg1-regulated retinal differentiation genes (731 probesets), (ii) retinaspecific genes independent of Brg1 regulation (3,038 probesets), and (iii) Brg1-regulated genes outside the retina (107 probesets). Biological significance was confirmed by further analysis of components of the Cdk5 signaling pathway and Irx transcription factor family, representing genes identified in category 1. This study highlights the utility of factorial microarray analysis to efficiently identify relevant regulatory pathways influenced by both specific gene products and normal developmental events.Brg1-regulated genes ͉ neuronal differentiation ͉ cellular differentiation ͉ signal transduction pathways ͉ transcription factors

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The Plk3-Cdc25 circuit

Cited by 54 publications

References 94 publications

Bcl-xL phosphorylation at Ser49 by polo kinase 3 during cell cycle progression and checkpoints

Bcl-xL phosphorylation at Ser49 by polo kinase 3 during cell cycle progression and checkpoints

Harnessing the complexity of DNA-damage response pathways to improve cancer treatment outcomes

Factorial microarray analysis of zebrafish retinal development

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