A role for Drosophila SMC4 in the resolution of sister chromatids in mitosis

Steffensen, S.; Coelho, Paula A.; Cobbe, Neville; Vass, Sharron; Costa, María Teresa; Hassan, Bassem A.; Prokopenko, Sergei N.; Bellen, Hugo J.; Heck, Margarete M. S.; Sunkel, Cláudio E.

doi:10.1016/s0960-9822(01)00096-3

Cited by 179 publications

(231 citation statements)

References 41 publications

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“…It can be speculated that impaired association of condensation factors on hyperacetylated chromatin may alter the dissociation of cohesins during early mitotic stages, resulting in persistent cohesion along chromatid arms. The separin-dependent release of centromeric cohesins at anaphase onset would promote the formation of chromatin bridges between sister chromatids due to poor sister chromatid arm resolution, as already reported for condensin mutants (Bhat et al, 1996;Ouspenski et al, 2000, Steffensen et al, 2001 or after inhibition of sister chromatid decatenation by topoisomerase II inhibitors (Cimini et al, 1997). On the other hand, a lack of sister chromatid separation at the centromere level is clearly indicated by the observation of chromatin bridges spanning the centromeric region.…”

Section: Histone Hyperacetylation Prevents Sister Chromatid Resolutiosupporting

confidence: 65%

Histone Hyperacetylation in Mitosis Prevents Sister Chromatid Separation and Produces Chromosome Segregation Defects

Cimini

Mattiuzzo

Torosantucci

et al. 2003

MBoC

169

160

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Posttranslational modifications of core histones contribute to driving changes in chromatin conformation and compaction. Herein, we investigated the role of histone deacetylation on the mitotic process by inhibiting histone deacetylases shortly before mitosis in human primary fibroblasts. Cells entering mitosis with hyperacetylated histones displayed altered chromatin conformation associated with decreased reactivity to the anti-Ser 10 phospho H3 antibody, increased recruitment of protein phosphatase 1-δ on mitotic chromosomes, and depletion of heterochromatin protein 1 from the centromeric heterochromatin. Inhibition of histone deacetylation before mitosis produced defective chromosome condensation and impaired mitotic progression in living cells, suggesting that improper chromosome condensation may induce mitotic checkpoint activation. In situ hybridization analysis on anaphase cells demonstrated the presence of chromatin bridges, which were caused by persisting cohesion along sister chromatid arms after centromere separation. Thus, the presence of hyperacetylated chromatin during mitosis impairs proper chromosome condensation during the pre-anaphase stages, resulting in poor sister chromatid resolution. Lagging chromosomes consisting of single or paired sisters were also induced by the presence of hyperacetylated histones, indicating that the less constrained centromeric organization associated with heterochromatin protein 1 depletion may promote the attachment of kinetochores to microtubules coming from both poles

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Section: Histone Hyperacetylation Prevents Sister Chromatid Resolutiosupporting

confidence: 65%

Histone Hyperacetylation in Mitosis Prevents Sister Chromatid Separation and Produces Chromosome Segregation Defects

Cimini

Mattiuzzo

Torosantucci

et al. 2003

MBoC

169

160

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“…Inhibition of condensin blocks the ability of mitotic Xenopus extracts to reorganize sperm chromatin into linear rod-shaped chromosomes (5,6), suggesting an essential role in chromosome compaction and resolution. However, inhibiting condensin in Drosophila (7,8), Caenorhabditis elegans (9), and vertebrate cells (10,11) delays, but does not prevent, compaction. The compacted chromosomes that form after condensin inhibition are sensitive to hypotonic fixation conditions and exhibit defects during alignment and segregation that suggest compromised structural integrity (1).…”

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confidence: 99%

Molecular analysis of mitotic chromosome condensation using a quantitative time-resolved fluorescence microscopy assay

Maddox

Portier

Desai

et al. 2006

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

111

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Chromosomes condense during mitotic entry to facilitate their segregation. Condensation is typically assayed in fixed preparations, limiting analysis of contributing factors. Here, we describe a quantitative method to monitor condensation kinetics in living cells expressing GFP fused to a core histone. We demonstrate the utility of this method by using it to analyze the molecular requirements for the condensation of holocentric chromosomes during the first division of the Caenorhabditis elegans embryo. In control embryos, the fluorescence intensity distribution for nuclear GFP:histone changes during two distinct time intervals separated by a plateau phase. During the first interval, primary condensation converts diffuse chromatin into discrete linear chromosomes. After the plateau, secondary condensation compacts the curvilinear chromosomes to form shorter bar-shaped structures. We quantitatively compared the consequences on this characteristic profile of depleting the condensin complex, the mitosis-specific histone H3 kinase Aurora B, the centromeric histone CENP-A, and CENP-C, a conserved protein required for kinetochore assembly. Both condensin and CENP-A play critical but distinct roles in primary condensation. In contrast, depletion of CENP-C slows but does not prevent primary condensation. Finally, Aurora B inhibition has no effect on primary condensation, but slightly delays secondary condensation. These results provide insights into the process of condensation, help resolve apparent contradictions from prior studies, and indicate that CENP-A chromatin has an intrinsic role in the condensation of holocentric chromosomes that is independent of its requirement for kinetochore assembly. Aurora B ͉ CENP-A ͉ condensin ͉ kinetochore ͉ C. elegans

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“…2B). 13 We found that, even in overcondensed wt metaphase chromosomes, sister chromatids appeared resolved in most cells (79%) However, sister chromatids were only resolved in 46% of prometaphase/metaphase mutant neuroblasts (Fig. 2B).…”

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confidence: 80%

“…The chromosome missegregation phenotype of Polo-depleted cells resemble the ones described for lack of SMC4 (structural maintenance chromosome 4) and Topoisomerase II, proteins required for chromosome resolution. [11][12][13] Interestingly, Plk1-dependent phosphorylation of Topoisomerase II is essential for its function in chromosome segregation during mitosis. 14 We therefore examined prometaphase/ metaphase chromosome resolution in Polo-depleted cells.…”

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confidence: 99%

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

Godinho

Tavares²

2008

Cell Cycle

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A role for Drosophila SMC4 in the resolution of sister chromatids in mitosis

Abstract: Our results demonstrate that SMC4 is critically important for the resolution of sister chromatids during mitosis prior to anaphase onset.

Cited by 179 publications

References 41 publications

Histone Hyperacetylation in Mitosis Prevents Sister Chromatid Separation and Produces Chromosome Segregation Defects

Histone Hyperacetylation in Mitosis Prevents Sister Chromatid Separation and Produces Chromosome Segregation Defects

Molecular analysis of mitotic chromosome condensation using a quantitative time-resolved fluorescence microscopy assay

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

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