A role for Drosophila Polo protein in chromosome resolution and segregation during mitosis

Godinho, Susana A.; Tavares, Álvaro A.

doi:10.4161/cc.7.16.6439

Cited by 13 publications

(10 citation statements)

References 22 publications

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“…The founding member of the family, Plk1, and its orthologs polo and Cdc5 are master regulators of cell division. By phosphorylating different substrates, Plk1 controls a number of processes throughout the cell cycle, including centrosome maturation, 6 mitotic entry, [7][8][9][10] chromosome segregation 9,11,12 and cytokinesis [13][14][15][16][17][18][19] ( Fig. 3).…”

mentioning

confidence: 99%

From Plk1 to Plk5

2011

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Mammalian polo-like kinases (Plks) are characterized by the presence of an N-terminal protein kinase domain and a C-terminal polo-box domain (PBD) involved in substrate binding and regulation of kinase activity. Plk1-4 have traditionally been linked to cell cycle progression, genotoxic stress and, more recently, neuron biology. Recently, a fifth mammalian Plk family member, Plk5, has been characterized in murine and human cells. Plk5 is expressed mainly in differentiated tissues such as the cerebellum. Despite apparent loss of catalytic activity and a stop codon in the middle of the human gene, Plk5 proteins retain important functions in neuron biology. Notably, its expression is silenced by epigenetic alterations in brain tumors, such as glioblastomas, and its re-expression prevents cell proliferation of these tumor cells. In this review, we will focus on the non-cell cycle roles of Plks, the biology of the new member of the family and the possible kinase- and PBD-independent functions of polo-like kinases.

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confidence: 99%

From Plk1 to Plk5

2011

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“…When separase was depleted from cells, it was observed that sister chromatid resolution was delayed, similar to the outcome when Plk1 or Aurora B were depleted or inhibited. 70,73 Thus, separase and these kinase activities collaborate to allow sister resolution. Correspondingly, similar experiments showed that exogenous expression of NC-Rad21, a mutant version of Rad21 that cannot be cleaved by separase, also delays sister chromatid resolution.…”

Section: The Two-step Model Of Cohesin Removal From Vertebrate Chromomentioning

confidence: 99%

Chromosome cohesion and the spindle checkpoint

Díaz-Martínez

Clarke

2009

Cell Cycle

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Accurate chromosome segregation constitutes the basis of inheritance. Mistakes in chromosome segregation during mitosis lead to aneuploidy, a common feature of tumors. The accuracy of chromosome segregation is governed by a complex network of processes which ensure that each daughter cell receives the correct number of chromosomes. Herein we review recent developments in the understanding of chromosome segregation, focusing on the cohesion that holds the sister chromatids together and the spindle checkpoint which regulates anaphase onset.

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“…Polo‐like kinase 1 is a master regulator of cell division, controlling several important processes throughout the cell cycle, such as centrosome maturation , Golgi breakdown , spindle assembly , chromosome segregation and cytokinesis . All these processes are regulated by Plk1 upon phosphorylation of many different substrates .…”

Section: Introductionmentioning

confidence: 99%

“…Subsequently, Plk1 was revealed as a kinase very well conserved through evolution, from yeast (Cdc5 in Saccharomyces Cerevisae) to insects (Polo in D. melanogaster), amphibians (Plx1 in Xenopus laevis) and mammals (Plk1 in Homo sapiens) [4][5][6][7][8][9]. In the following years, the Polo-like kinase family expanded, and four members were added (Plk1, Plk3, Plk4 and very recently Plk5) [10][11][12] Polo-like kinase 1 is a master regulator of cell division, controlling several important processes throughout the cell cycle, such as centrosome maturation [13], Golgi breakdown [14][15][16][17], spindle assembly [18][19][20][21], chromosome segregation [20,22,23] and cytokinesis [24][25][26][27][28][29][30]. All these processes are regulated by Plk1 upon phosphorylation of many different substrates [31].…”

Section: Introductionmentioning

confidence: 99%

Genetic depletion of Polo-like kinase 1 leads to embryonic lethality due to mitotic aberrancies

et al. 2015

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Polo‐like kinase 1 (PLK1) is a serine/threonine kinase that plays multiple and essential roles during the cell division cycle. Its inhibition in cultured cells leads to severe mitotic aberrancies and cell death. Whereas previous reports suggested that Plk1 depletion in mice leads to a non‐mitotic arrest in early embryos, we show here that the bi‐allelic Plk1 depletion in mice certainly results in embryonic lethality due to extensive mitotic aberrations at the morula stage, including multi‐ and mono‐polar spindles, impaired chromosome segregation and cytokinesis failure. In addition, the conditional depletion of Plk1 during mid‐gestation leads also to severe mitotic aberrancies. Our data also confirms that Plk1 is completely dispensable for mitotic entry in vivo. On the other hand, Plk1 haploinsufficient mice are viable, and Plk1‐heterozygous fibroblasts do not harbor any cell cycle alterations. Plk1 is overexpressed in many human tumors, suggesting a therapeutic benefit of inhibiting Plk1, and specific small‐molecule inhibitors for this kinase are now being evaluated in clinical trials. Therefore, the different Plk1 mouse models here presented are a valuable tool to reexamine the relevance of the mitotic kinase Plk1 during mammalian development and animal physiology.

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A role for Drosophila Polo protein in chromosome resolution and segregation during mitosis

Cited by 13 publications

References 22 publications

From Plk1 to Plk5

From Plk1 to Plk5

Chromosome cohesion and the spindle checkpoint

Genetic depletion of Polo-like kinase 1 leads to embryonic lethality due to mitotic aberrancies

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