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GartnerAnton

Gartner, Anton
DNA Damage Response and Genetic Toxicology
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LEM-3 is a midbody-tethered DNA nuclease that resolves chromatin bridges during late mitosis

Author(s)
Hong, YeSonneville, RemiWang, BinScheidt, ViktorMeier, BettinaWoglar, AlexanderDemetriou, SarahLabib, KarimJantsch, VerenaGartner, Anton
Issued Date
2018-02
DOI
10.1038/s41467-018-03135-w
URI
https://scholarworks.unist.ac.kr/handle/201301/27473
Fulltext
https://www.nature.com/articles/s41467-018-03135-w
Citation
NATURE COMMUNICATIONS, v.9, pp.728
Abstract
Faithful chromosome segregation and genome maintenance requires the removal of all DNA bridges that physically link chromosomes before cells divide. Using C. elegans embryos we show that the LEM-3/Ankle1 nuclease defines a previously undescribed genome integrity mechanism by processing DNA bridges right before cells divide. LEM-3 acts at the midbody, the structure where abscission occurs at the end of cytokinesis. LEM-3 localization depends on factors needed for midbody assembly, and LEM-3 accumulation is increased and prolonged when chromatin bridges are trapped at the cleavage plane. LEM-3 locally processes chromatin bridges that arise from incomplete DNA replication, unresolved recombination intermediates, or the perturbance of chromosome structure. Proper LEM-3 midbody localization and function is regulated by AIR-2/Aurora B kinase. Strikingly, LEM-3 acts cooperatively with the BRC-1/BRCA1 homologous recombination factor to promote genome integrity. These findings provide a molecular basis for the suspected role of the LEM-3 orthologue Ankle1 in human breast cancer.
Publisher
NATURE PUBLISHING GROUP
ISSN
2041-1723
Keyword
C. ELEGANS EMBRYOSCAENORHABDITIS-ELEGANSANAPHASE BRIDGESOVARIAN-CANCERCYTOKINESISRESOLUTIONREPAIRCELLSSUSCEPTIBILITYCOMPLETION

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