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FANCD2 facilitates replication through common fragile sites

AutorMadireddy, Advaitha; Herrera-Moyano, Emilia ; García-Rubio, María L. ; Aguilera, Andrés ; Schildkraut, Carl L.
Palabras claveFanconi anemia
DNA replication
Common fragile sites
Genomic instability
DNA:RNA hybrids
Fecha de publicación2016
EditorElsevier
Cell Press
CitaciónMolecular Cell 64(2): 388-404 (2016)
ResumenCommon fragile sites (CFSs) are genomic regions that are unstable under conditions of replicative stress. Although the characteristics of CFSs that render them vulnerable to stress are associated mainly with replication, the cellular pathways that protect CFSs during replication remain unclear. Here, we identify and describe a role for FANCD2 as a trans-acting facilitator of CFS replication, in the absence of exogenous replicative stress. In the absence of FANCD2, replication forks stall within the AT-rich fragility core of CFS, leading to dormant origin activation. Furthermore, FANCD2 deficiency is associated with DNA:RNA hybrid formation at CFS-FRA16D, and inhibition of DNA:RNA hybrid formation suppresses replication perturbation. In addition, we also found that FANCD2 reduces the number of potential sites of replication initiation. Our data demonstrate that FANCD2 protein is required to ensure efficient CFS replication and provide mechanistic insight into how FANCD2 regulates CFS stability.
DescripciónMadireddy, Advaitha et al.
Versión del editorhttps://doi.org/10.1016/j.molcel.2016.09.017
URIhttp://hdl.handle.net/10261/165206
Identificadoresdoi: 10.1016/j.molcel.2016.09.017
issn: 1097-2765
e-issn: 1097-4164
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