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Título: | Physical proximity of chromatin to nuclear pores prevents harmful R loop accumulation contributing to maintain genome stability |
Autor: | García-Benítez, Francisco CSIC; Gaillard, Hélène CSIC ORCID; Aguilera, Andrés CSIC ORCID | Palabras clave: | Genome instability R loop Transcription Nuclear pores Mpl1/2 |
Fecha de publicación: | 2017 | Editor: | National Academy of Sciences (U.S.) | Citación: | Proceedings of the National Academy of Sciences 114(41): 10942-10947 (2017) | Resumen: | During transcription, the mRNA may hybridize with DNA, forming an R loop, which can be physiological or pathological, constituting in this case a source of genomic instability. To understand the mechanism by which eukaryotic cells prevent harmful R loops, we used human activation-induced cytidine deaminase (AID) to identify genes preventing R loops. A screening of 400 Saccharomyces cerevisiae selected strains deleted in nuclear genes revealed that cells lacking the Mlp1/2 nuclear basket proteins show AID-dependent genomic instability and replication defects that were suppressed by RNase H1 overexpression. Importantly, DNA–RNA hybrids accumulated at transcribed genes in mlp1/2 mutants, indicating that Mlp1/2 prevents R loops. Consistent with the Mlp1/2 role in gene gating to nuclear pores, artificial tethering to the nuclear periphery of a transcribed locus suppressed R loops in mlp1Δ cells. The same occurred in THO-deficient hpr1Δ cells. We conclude that proximity of transcribed chromatin to the nuclear pore helps restrain pathological R loops. | URI: | http://hdl.handle.net/10261/165664 | DOI: | 10.1073/pnas.1707845114 | Identificadores: | doi: 10.1073/pnas.1707845114 e-issn: 1091-6490 issn: 0027-8424 |
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