The Aurora-B-dependent NoCut checkpoint prevents damage of anaphase bridges after DNA replication stress View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2016-05

AUTHORS

Nuno Amaral, Alexandre Vendrell, Charlotta Funaya, Fatima-Zahra Idrissi, Michael Maier, Arun Kumar, Gabriel Neurohr, Neus Colomina, Jordi Torres-Rosell, María-Isabel Geli, Manuel Mendoza

ABSTRACT

Anaphase chromatin bridges can lead to chromosome breakage if not properly resolved before completion of cytokinesis. The NoCut checkpoint, which depends on Aurora B at the spindle midzone, delays abscission in response to chromosome segregation defects in yeast and animal cells. How chromatin bridges are detected, and whether abscission inhibition prevents their damage, remain key unresolved questions. We find that bridges induced by DNA replication stress and by condensation or decatenation defects, but not dicentric chromosomes, delay abscission in a NoCut-dependent manner. Decatenation and condensation defects lead to spindle stabilization during cytokinesis, allowing bridge detection by Aurora B. NoCut does not prevent DNA damage following condensin or topoisomerase II inactivation; however, it protects anaphase bridges and promotes cellular viability after replication stress. Therefore, the molecular origin of chromatin bridges is critical for activation of NoCut, which plays a key role in the maintenance of genome stability after replicative stress. More... »

PAGES

516-526

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/ncb3343

DOI

http://dx.doi.org/10.1038/ncb3343

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1001101061

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/27111841


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