Utilize este identificador para referenciar este registo: http://hdl.handle.net/10400.7/367
Título: Centromere-Independent Accumulation of Cohesin at Ectopic Heterochromatin Sites Induces Chromosome Stretching during Anaphase
Autor: Oliveira, Raquel A.
Kotadia, Shaila
Tavares, Alexandra
Mirkovic, Mihailo
Bowlin, Katherine
Eichinger, Christian S.
Nasmyth, Kim
Sullivan, William
Data: 7-Out-2014
Editora: PLOS
Citação: Oliveira RA, Kotadia S, Tavares A, Mirkovic M, Bowlin K, et al. (2014) Centromere-Independent Accumulation of Cohesin at Ectopic Heterochromatin Sites Induces Chromosome Stretching during Anaphase. PLoS Biol 12(10): e1001962. doi:10.1371/journal.pbio.1001962
Resumo: Pericentric heterochromatin, while often considered as "junk" DNA, plays important functions in chromosome biology. It contributes to sister chromatid cohesion, a process mediated by the cohesin complex that ensures proper genome segregation during nuclear division. Long stretches of heterochromatin are almost exclusively placed at centromere-proximal regions but it remains unclear if there is functional (or mechanistic) importance in linking the sites of sister chromatid cohesion to the chromosomal regions that mediate spindle attachment (the centromere). Using engineered chromosomes in Drosophila melanogaster, we demonstrate that cohesin enrichment is dictated by the presence of heterochromatin rather than centromere proximity. This preferential accumulation is caused by an enrichment of the cohesin-loading factor (Nipped-B/NIPBL/Scc2) at dense heterochromatic regions. As a result, chromosome translocations containing ectopic pericentric heterochromatin embedded in euchromatin display additional cohesin-dependent constrictions. These ectopic cohesion sites, placed away from the centromere, disjoin abnormally during anaphase and chromosomes exhibit a significant increase in length during anaphase (termed chromatin stretching). These results provide evidence that long stretches of heterochromatin distant from the centromere, as often found in many cancers, are sufficient to induce abnormal accumulation of cohesin at these sites and thereby compromise the fidelity of chromosome segregation.
Peer review: yes
URI: http://hdl.handle.net/10400.7/367
DOI: 10.1371/journal.pbio.1001962
Versão do Editor: http://www.plosbiology.org/article/Authors/info:doi/10.1371/journal.pbio.1001962
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