scholarly journals Use of DT40 conditional-knockout cell lines to study chromosomal passenger protein function

2010 ◽  
Vol 38 (6) ◽  
pp. 1655-1659 ◽  
Author(s):  
Xavier Fant ◽  
Kumiko Samejima ◽  
Ana Carvalho ◽  
Hiromi Ogawa ◽  
Zhenjie Xu ◽  
...  
Keyword(s):  
Cell Lines ◽  
Protein Function ◽  
Kinase Activity ◽  
Current Knowledge ◽  
Conditional Knockout ◽  
Aurora B ◽  
Aurora B Kinase ◽  
Chromosomal Passenger ◽  
Passenger Protein

The CPC [chromosomal passenger complex; INCENP (inner centromere protein), Aurora B kinase, survivin and borealin] is implicated in many mitotic processes. In the present paper we describe how we generated DT40 conditional-knockout cell lines for incenp1 and survivin1 to better understand the role of these CPC subunits in the control of Aurora B kinase activity. These lines enabled us to reassess current knowledge of survivin function and to show that INCENP acts as a rheostat for Aurora B activity.

scholarly journals Aurora B kinase activity is regulated by SET/TAF1 on Sgo2 at the inner centromere

2019 ◽  
Vol 218 (10) ◽  
pp. 3223-3236 ◽  
Author(s):  
Yuichiro Asai ◽  
Koh Fukuchi ◽  
Yuji Tanno ◽  
Saki Koitabashi-Kiyozuka ◽  
Tatsuyuki Kiyozuka ◽  
...  
Keyword(s):  
Chromosome Segregation ◽  
Chromosomal Instability ◽  
Kinase Activity ◽  
Fine Tuning ◽  
Aurora B ◽  
The Novel ◽  
Aurora B Kinase ◽  
Microtubule Attachment ◽  
Molecular Events

The accurate regulation of phosphorylation at the kinetochore is essential for establishing chromosome bi-orientation. Phosphorylation of kinetochore proteins by the Aurora B kinase destabilizes improper kinetochore–microtubule attachments, whereas the phosphatase PP2A has a counteracting role. Imbalanced phosphoregulation leads to error-prone chromosome segregation and aneuploidy, a hallmark of cancer cells. However, little is known about the molecular events that control the balance of phosphorylation at the kinetochore. Here, we show that localization of SET/TAF1, an oncogene product, to centromeres maintains Aurora B kinase activity by inhibiting PP2A, thereby correcting erroneous kinetochore–microtubule attachment. SET localizes at the inner centromere by interacting directly with shugoshin 2, with SET levels declining at increased distances between kinetochore pairs, leading to establishment of chromosome bi-orientation. Moreover, SET overexpression induces chromosomal instability by disrupting kinetochore–microtubule attachment. Thus, our findings reveal the novel role of SET in fine-tuning the phosphorylation level at the kinetochore by balancing the activities of Aurora B and PP2A.

scholarly journals Phosphorylation at serine 331 is required for Aurora B activation

2011 ◽  
Vol 195 (3) ◽  
pp. 449-466 ◽  
Author(s):  
Eleni Petsalaki ◽  
Tonia Akoumianaki ◽  
Elizabeth J. Black ◽  
David A.F. Gillespie ◽  
George Zachos
Keyword(s):  
Cell Division ◽  
Kinase Activity ◽  
Aurora B ◽  
Aurora B Kinase ◽  
Chromosomal Passenger Complex ◽  
Chromosome Missegregation ◽  
Mitotic Delay ◽  
Chromosomal Passenger ◽  
Spontaneous Chromosome ◽  
Chk1 Kinase

Aurora B kinase activity is required for successful cell division. In this paper, we show that Aurora B is phosphorylated at serine 331 (Ser331) during mitosis and that phosphorylated Aurora B localizes to kinetochores in prometaphase cells. Chk1 kinase is essential for Ser331 phosphorylation during unperturbed prometaphase or during spindle disruption by taxol but not nocodazole. Phosphorylation at Ser331 is required for optimal phosphorylation of INCENP at TSS residues, for Survivin association with the chromosomal passenger complex, and for complete Aurora B activation, but it is dispensable for Aurora B localization to centromeres, for autophosphorylation at threonine 232, and for association with INCENP. Overexpression of Aurora BS331A, in which Ser331 is mutated to alanine, results in spontaneous chromosome missegregation, cell multinucleation, unstable binding of BubR1 to kinetochores, and impaired mitotic delay in the presence of taxol. We propose that Chk1 phosphorylates Aurora B at Ser331 to fully induce Aurora B kinase activity. These results indicate that phosphorylation at Ser331 is an essential mechanism for Aurora B activation.

scholarly journals Disassembly of actin and keratin networks by Aurora B kinase at the midplane of cleaving Xenopus laevis eggs

2019 ◽  
Author(s):  
Christine M. Field ◽  
James F. Pelletier ◽  
Timothy J. Mitchison
Keyword(s):  
Xenopus Laevis ◽  
Kinase Activity ◽  
Flow Patterns ◽  
Aurora B ◽  
Aurora B Kinase ◽  
Chromosomal Passenger Complex ◽  
Chromosomal Passenger ◽  
Dividing Cells ◽  
Local Softening

AbstractWe investigated how bulk cytoplasm prepares for cytokinesis in Xenopus laevis eggs, which are large, rapidly dividing cells. The egg midplane is demarcated by Chromosomal Passenger Complex (CPC) localized on microtubule bundles between asters. Using an extract system and intact eggs we found that local kinase activity of the AURKB subunit of the CPC caused disassembly of F-actin and keratin between asters, and local softening of the cytoplasm as assayed by flow patterns. Beads coated with active CPC mimicked aster boundaries and caused AURKB-dependent disassembly of F-actin and keratin that propagated ~40 μm without microtubules, and much farther with microtubules present, due to CPC auto-activation. We propose that active CPC at aster boundaries locally reduces cytoplasmic stiffness by disassembling actin and keratin networks. This may help sister centrosomes move apart after mitosis, prepare a soft path for furrow ingression and/or release G-actin to build the furrow cortex.

Aurora-C kinase is a novel chromosomal passenger protein that can complement Aurora-B kinase function in mitotic cells

2004 ◽  
Vol 59 (4) ◽  
pp. 249-263 ◽  
Author(s):  
Kaori Sasai ◽  
Hiroshi Katayama ◽  
David L. Stenoien ◽  
Satoshi Fujii ◽  
Reiko Honda ◽  
...  
Keyword(s):  
Aurora B ◽  
Aurora B Kinase ◽  
Chromosomal Passenger ◽  
Passenger Protein ◽  
Mitotic Cells

scholarly journals Aurora B–mediated localized delays in nuclear envelope formation facilitate inclusion of late-segregating chromosome fragments

2015 ◽  
Vol 26 (12) ◽  
pp. 2227-2241 ◽  
Author(s):  
Travis Karg ◽  
Brandt Warecki ◽  
William Sullivan
Keyword(s):  
Nuclear Envelope ◽  
Chromosome Segregation ◽  
Daughter Nucleus ◽  
Kinase Activity ◽  
Aurora B ◽  
Genomic Integrity ◽  
Aurora B Kinase ◽  
Chromosome Fragments ◽  
Nuclear Envelope Formation

To determine how chromosome segregation is coordinated with nuclear envelope formation (NEF), we examined the dynamics of NEF in the presence of lagging acentric chromosomes in Drosophila neuroblasts. Acentric chromosomes often exhibit delayed but ultimately successful segregation and incorporation into daughter nuclei. However, it is unknown whether these late-segregating acentric fragments influence NEF to ensure their inclusion in daughter nuclei. Through live analysis, we show that acentric chromosomes induce highly localized delays in the reassembly of the nuclear envelope. These delays result in a gap in the nuclear envelope that facilitates the inclusion of lagging acentrics into telophase daughter nuclei. Localized delays of nuclear envelope reassembly require Aurora B kinase activity. In cells with reduced Aurora B activity, there is a decrease in the frequency of local nuclear envelope reassembly delays, resulting in an increase in the frequency of acentric-bearing, lamin-coated micronuclei. These studies reveal a novel role of Aurora B in maintaining genomic integrity by promoting the formation of a passageway in the nuclear envelope through which late-segregating acentric chromosomes enter the telophase daughter nucleus.

scholarly journals Endopolyploidy in irradiated p53-deficient tumour cell lines: Persistence of cell division activity in giant cells expressing Aurora-B kinase

2008 ◽  
Vol 32 (9) ◽  
pp. 1044-1056 ◽  
Author(s):  
Jekaterina Erenpreisa ◽  
Andrei Ivanov ◽  
Sally P. Wheatley ◽  
Elizabeth A. Kosmacek ◽  
Fiorenza Ianzini ◽  
...  
Keyword(s):  
Cell Division ◽  
Cell Lines ◽  
Tumour Cell ◽  
Giant Cells ◽  
Aurora B ◽  
Aurora B Kinase ◽  
Tumour Cell Lines

Lung epithelial NOX/DUOX and respiratory virus infections

2014 ◽  
Vol 128 (6) ◽  
pp. 337-347 ◽  
Author(s):  
Nathalie Grandvaux ◽  
Mélissa Mariani ◽  
Karin Fink
Keyword(s):  
Respiratory Virus ◽  
Inflammatory Responses ◽  
Current Knowledge ◽  
Conditional Knockout ◽  
In Vivo Studies ◽  
Virus Infections ◽  
Lung Epithelial ◽  
Respiratory Virus Infections

Determining the role of NADPH oxidases in the context of virus infection is an emerging area of research and our knowledge is still sparse. The expression of various isoforms of NOX/DUOX (NADPH oxidase/dual oxidase) in the epithelial cells (ECs) lining the respiratory tract renders them primary sites from which to orchestrate the host defence against respiratory viruses. Accumulating evidence reveals distinct facets of the involvement of NOX/DUOX in host antiviral and pro-inflammatory responses and in the control of the epithelial barrier integrity, with individual isoforms mediating co-operative, but surprisingly also opposing, functions. Although in vivo studies in mice are in line with some of these observations, a complete understanding of the specific functions of epithelial NOX/DUOX awaits lung epithelial-specific conditional knockout mice. The goal of the present review is to summarize our current knowledge of the role of individual NOX/DUOX isoforms expressed in the lung epithelium in the context of respiratory virus infections so as to highlight potential opportunities for therapeutic intervention.

scholarly journals VX-680 Inhibits Aurora A and Aurora B Kinase Activity in Human Cells

Cell Cycle ◽  
2007 ◽  
Vol 6 (22) ◽  
pp. 2846-2854 ◽  
Author(s):  
Rebecca K. Tyler ◽  
Natalia Shpiro ◽  
Rodolfo Marquez ◽  
Patrick A. Eyers
Keyword(s):  
Kinase Activity ◽  
Human Cells ◽  
Aurora B ◽  
Aurora A ◽  
Aurora B Kinase
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