The cellular geography of Aurora kinases

Carmena, Mar; Earnshaw, William C.

doi:10.1038/nrm1245

Cited by 1,069 publications

(1,114 citation statements)

References 122 publications

(142 reference statements)

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“…The discovery of a role for the motor protein left-right Dynein in this process is also extremely suggestive (Armakolas and Klar, 2007). Because the centrosome interacts with cortical membrane cues to achieve biased DNA segregation (Carmena and Earnshaw, 2003;Tajbakhsh and Gonzalez, 2009), this model is compatible with a variety of proposals about how the centrosomes orient cytokinesis with respect to the other two axes to achieve consistent segregation bias along the LR axis.…”

Section: Introductionsupporting

confidence: 55%

Far from solved: A perspective on what we know about early mechanisms of left–right asymmetry

Vandenberg

Levin

2010

Developmental Dynamics

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Consistent laterality is a crucial aspect of embryonic development, physiology, and behavior. While strides have been made in understanding unilaterally expressed genes and the asymmetries of organogenesis, early mechanisms are still poorly understood. One popular model centers on the structure and function of motile cilia and subsequent chiral extracellular fluid flow during gastrulation. Alternative models focus on intracellular roles of the cytoskeleton in driving asymmetries of physiological signals or asymmetric chromatid segregation, at much earlier stages. All three models trace the origin of asymmetry back to the chirality of cytoskeletal organizing centers, but significant controversy exists about how this intracellular chirality is amplified onto cell fields. Analysis of specific predictions of each model and crucial recent data on new mutants suggest that ciliary function may not be a broadly conserved, initiating event in left-right patterning. Many questions about embryonic left-right asymmetry remain open, offering fascinating avenues for further research in cell, developmental, and evolutionary biology. Developmental Dynamics 239:3131-3146,

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Section: Introductionsupporting

confidence: 55%

Far from solved: A perspective on what we know about early mechanisms of left–right asymmetry

Vandenberg

Levin

2010

Developmental Dynamics

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“…As for candidate genes on chromosome 20, which could explain its amplification, it is interesting to note that the Aurora kinase A gene has been located to chromosome 20q13.2. Aurora kinase A has been found previously to be overexpressed in tumours and in cancer cell lines (Giet et al, 1999;Zou et al, 1999;Carmena and Earnshaw, 2003) and is involved in the separation of centrosomes as well as spindle assembly (Carmena and Earnshaw, 2003). Hence, amplification of chromosome 20 may reflect abnormalities of this protein kinase, whose altered function may have a role in the further development of aneuploidy, and hence genetic instability in carcinogenesis.…”

Section: Discussionmentioning

confidence: 99%

Fluorescence in situ hybridisation analysis of chromosomal aberrations in gastric tissue: the potential involvement of Helicobacter pylori

et al. 2005

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In this series of experiments, a novel protocol was developed whereby gastric cells were collected using endoscopic cytology brush techniques, and prepared, such that interphase fluorescence in situ hybridization (FISH) could be performed. In total, 80 distinct histological samples from 37 patients were studied using four chromosome probes (over 32 000 cells analysed). Studies have previously identified abnormalities of these four chromosomes in upper GI tumours. Using premalignant tissues, we aimed to determine how early in Correa's pathway to gastric cancer these chromosome abnormalities occurred. Aneuploidy of chromosomes 4, 8, 20 and 17(p53) was detected in histologically normal gastric mucosa, as well as in gastritis, intestinal metaplasia, dysplasia and cancer samples. The levels of aneuploidy increased as disease severity increased. Amplification of chromosome 4 and chromosome 20, and deletion of chromosome 17(p53) were the more common findings. Hence, a role for these abnormalities may exist in the initiation of, and the progression to, gastric cancer. Helicobactor pylori infection was determined in premalignant tissue using histological analysis and PCR technology. Detection rates were comparable. PCR was used to subtype H. pylori for CagA status. The amplification of chromosome 4 in gastric tissue was significantly more prevalent in H. pylori-positive patients (n ¼ 7) compared to H. pylori-negative patients (n ¼ 11), possibly reflecting a role for chromosome 4 amplification in H. pylori-induced gastric cancer. The more virulent CagA strain of H. pylori was associated with increased disease pathology and chromosomal abnormalities, although numbers were small (CagA þ n ¼ 3, CagAÀ n ¼ 4). Finally, in vitro work demonstrated that the aneuploidy induced in a human cell line after exposure to the reactive oxygen species (ROS) hydrogen peroxide was similar to that already shown in the gastric cancer pathway, and may further strengthen the hypothesis that H. pylori causes gastric cancer progression via an ROS-mediated mechanism.

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“…INCENP, a microtubule-binding protein is responsible for binding Aurora B (Honda et al, 2003). Survivin has an essential role in chromosome alignment (Lens et al, 2003) and is important during mitosis for proper localization of INCENP and Aurora B (reviewed by Carmena and Earnshaw, 2003). Aurora B, which phosphorylates histone H3 on serine 10, is important for chromosome condensation, and monitors chromosome biorientation during congression by sensing tension across the centromere established once sister kinetochores are attached to the opposite spindle poles (reviewed by Meraldi et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

Chromosomes with delayed replication timing lead to checkpoint activation, delayed recruitment of Aurora B and chromosome instability

et al. 2006

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Certain chromosome rearrangements display a significant delay in chromosome replication timing (DRT) that is associated with a subsequent delay in mitotic chromosome condensation (DMC). DRT/DMC chromosomes are common in tumor cells in vitro and in vivo and occur frequently in cells exposed to ionizing radiation. A hallmark for these chromosomes is the delayed phosphorylation of serine 10 of histone H3 during mitosis. The chromosome passenger complex, consisting of multiple proteins including Aurora B kinase and INCENP is thought to be responsible for H3 phosphorylation, chromosome condensation and the subsequent segregation of chromosomes. In this report, we show that chromosomes with DRT/DMC contain phosphorylated Chk1, consistent with activation of the S-M phase checkpoint. Furthermore, we show that INCENP is recruited to the DRT/DMC chromosomes during all phases of mitosis. In contrast, Aurora B kinase is absent on DRT/DMC chromosomes when these chromosomes lack serine 10 phosphorylation of H3. We also show that mitotic arrest deficient 2 (Mad2), a member of the spindle assembly checkpoint, is present on DRT/DMC chromosomes at a time when the normally condensed chromosomes show no Mad2 staining, indicating that DRT/DMC activates the spindle assembly checkpoint. Finally, cells with DRT/ DMC chromosomes have centrosome amplification, abnormal spindle assembly, endoreduplication and significant chromosome instability.

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The cellular geography of Aurora kinases

Cited by 1,069 publications

References 122 publications

Far from solved: A perspective on what we know about early mechanisms of left–right asymmetry

Far from solved: A perspective on what we know about early mechanisms of left–right asymmetry

Fluorescence in situ hybridisation analysis of chromosomal aberrations in gastric tissue: the potential involvement of Helicobacter pylori

Chromosomes with delayed replication timing lead to checkpoint activation, delayed recruitment of Aurora B and chromosome instability

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