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p53 partners with RNA in the DNA damage response

Nature Genetics volume 48, pages 1298–1299 (2016)Cite this article

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Stabilization of p53 protein is a key step in the cellular response to DNA damage. A new study describes a long noncoding RNA, DINO, transcribed from the CDKN1A promoter region that induces stabilization of p53 protein and promotes efficient activation of p53 target genes in response to DNA damage.

DNA-damaging agents can cause genetic mutations that lead to cell transformation. Mechanisms to protect organisms against this type of damage are therefore essential, with the response orchestrated by p53 being the most prominent of all. Upon exposure to DNA-damaging stimuli, p53 activates a program that, depending on the type and intensity of the damage and the cellular context, leads to cell cycle arrest or elimination of the damaged cells through programmed cell death. The vast majority of the downstream effects of p53 are mediated through its intrinsic activity as a transcription factor1. Upon stress, p53 protein is stabilized and recognizes its target genes through consensus p53 response elements (p53REs). These genes are the effectors of the p53 response. For decades, researchers have focused their attention on proteins that contribute to this pathway. It is known, however, that another class of molecules—noncoding RNAs—are part of the p53 network2. Among the different types of noncoding RNA, probably the most abundant are those longer than 200 nt, named long noncoding RNAs (lncRNAs)3. Despite their defining feature of being noncoding transcripts, many lncRNAs participate in a variety of cellular processes, including the p53 pathway4; p53 activates the transcription of several lncRNAs, some of which are known to fine-tune the p53 response2. On page 1370 of this issue5, Howard Chang and colleagues present a study that further elucidates the role of lncRNAs in this important pathway by identifying DINO (damage-induced noncoding RNA), a lncRNA that is required for optimal activation of the p53 response following DNA damage.

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Figure 1: Model of DINO function.

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Authors and Affiliations

  1. Department of Gene Therapy and Regulation of Gene Expression, Maite Huarte is at the Center for Applied Medical Research (CIMA), University of Navarra and the Institute of Health Research of Navarra (IdiSNA), Pamplona, Spain.,

    Maite Huarte

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  1. Maite Huarte
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Correspondence to Maite Huarte.

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Huarte, M. p53 partners with RNA in the DNA damage response. Nat Genet 48, 1298–1299 (2016). https://doi.org/10.1038/ng.3702

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