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• W3084116367 abstract "Abstract Ribosomal DNA (rDNA) consists of highly repeated sequences that are prone to incurring damage. Delays or failure of rDNA double-strand break (DSB) repair are deleterious, and can lead to rDNA transcriptional arrest, chromosomal translocations, genomic losses, and cell death. Here, we show that the zinc-finger transcription factor GLI1, a terminal effector of the Hedgehog (Hh) pathway, is required for the repair of rDNA DSBs. We found that GLI1 is activated in triple-negative breast cancer cells in response to ionizing radiation (IR) and localizes to rDNA sequences in response to both global DSBs generated by IR and site-specific DSBs in rDNA. Inhibiting GLI1 interferes with rDNA DSB repair and impacts RNA polymerase I activity and cell viability. Our findings tie Hh signaling to rDNA repair and this heretofore unknown function may be critically important in proliferating cancer cells." @default.
• W3084116367 created "2020-09-14" @default.
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• W3084116367 date "2020-09-07" @default.
• W3084116367 modified "2023-10-17" @default.
• W3084116367 title "Hedgehog signaling enables repair of ribosomal DNA double-strand breaks" @default.
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• W3084116367 doi "https://doi.org/10.1093/nar/gkaa733" @default.
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