AI Article Synopsis
- The DNA-repair capacity in somatic cells is naturally lower than in germ cells, and the role of the DREAM repressor complex in regulating this capacity was previously unknown.
- Mutations in the DREAM complex enhance DNA repair mechanisms in somatic tissues of Caenorhabditis elegans, leading to increased resistance to various types of DNA damage during development and aging.
- Inhibition of the DREAM complex in human cells also boosts DNA repair gene expression, reduces DNA damage, and helps protect against photoreceptor loss in aging mice, positioning DREAM as a key regulator of DNA repair limitations in somatic cells.
Article Abstract
The DNA-repair capacity in somatic cells is limited compared with that in germ cells. It has remained unknown whether not only lesion-type-specific, but overall repair capacities could be improved. Here we show that the DREAM repressor complex curbs the DNA-repair capacities in somatic tissues of Caenorhabditis elegans. Mutations in the DREAM complex induce germline-like expression patterns of multiple mechanisms of DNA repair in the soma. Consequently, DREAM mutants confer resistance to a wide range of DNA-damage types during development and aging. Similarly, inhibition of the DREAM complex in human cells boosts DNA-repair gene expression and resistance to distinct DNA-damage types. DREAM inhibition leads to decreased DNA damage and prevents photoreceptor loss in progeroid Ercc1 mice. We show that the DREAM complex transcriptionally represses essentially all DNA-repair systems and thus operates as a highly conserved master regulator of the somatic limitation of DNA-repair capacities.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10113156 | PMC |
| http://dx.doi.org/10.1038/s41594-023-00942-8 | DOI Listing |
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