2019
DOI: 10.18632/oncotarget.27034
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Dicer prevents genome instability in response to replication stress

Abstract: Dicer, an endoribonuclease best-known for its role in microRNA biogenesis and RNA interference pathway, has been shown to play a role in the DNA damage response and repair of double-stranded DNA breaks (DSBs) in mammalian cells. However, it remains unknown whether Dicer is also important to preserve genome integrity upon replication stress. To address this question, we focused our study on common fragile sites (CFSs), which are susceptible to breakage after replication stress. We show that inhibition of the Di… Show more

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Cited by 14 publications
(9 citation statements)
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“…Homologous recombination (HR) factors such as RAD51, BRCA1 and BRCA2 and members of the FA pathway, disabled in the chromosome instability and cancer predisposition syndrome Fanconi anemia, are central regulators of replication stress tolerance through their functions in replication fork protection, which are distinct from their canonical roles in the HR-mediated repair of collapsed forks [63]. Following replication stress, the recruitment of the FA protein FANCD2 and of TOPBP1 to stalled forks is promoted by the microRNA pathway enzymes Dicer and Drosha, which foster the activation of the ATR-dependent S phase checkpoint and limit cells with under-replicated DNA from proceeding into mitosis [64].…”
Section: Mechanisms Protecting Against Replication Stress and Under-rmentioning
confidence: 99%
“…Homologous recombination (HR) factors such as RAD51, BRCA1 and BRCA2 and members of the FA pathway, disabled in the chromosome instability and cancer predisposition syndrome Fanconi anemia, are central regulators of replication stress tolerance through their functions in replication fork protection, which are distinct from their canonical roles in the HR-mediated repair of collapsed forks [63]. Following replication stress, the recruitment of the FA protein FANCD2 and of TOPBP1 to stalled forks is promoted by the microRNA pathway enzymes Dicer and Drosha, which foster the activation of the ATR-dependent S phase checkpoint and limit cells with under-replicated DNA from proceeding into mitosis [64].…”
Section: Mechanisms Protecting Against Replication Stress and Under-rmentioning
confidence: 99%
“…For RNAi, cells were plated in 6-well dishes one day before transfection [ 17 ] and the siRNA transfection was performed as previously described [ 16 ]. Briefly, cells were transfected with a specific siRNA targeting CENP-E (siCENP-E: 5′-AAC GAAGAGUUACUUGGUGCCtt-3′) at a final concentration of 40 nM, which does not affect cell viability, as previously described [ 9 ].…”
Section: Methodsmentioning
confidence: 99%
“…Some of the key proteins involved in these pathways are summarized in Table 1. Interestingly, deficiency in some of these proteins such as FANCD2, ATR, RNase H1, and Dicer, have been linked to CFSs fragility (Casper et al, 2002;Madireddy et al, 2016;Di Marco et al, 2017;Fragkos et al, 2019), indicating cells employ these pathways to counteract transcription induced obstacles or RS to maintain CFS stability. Of note, most of these pathways seem to largely operate in S phase of the cell cycle.…”
Section: Pathways In Dealing With Transcription Associated Rs At Cfssmentioning
confidence: 99%