Abstract
Ribosomes are encoded by many copies of ribosomal DNA (rDNA) packed into the nucleolus. High rates of transcription combined with highly repetitive sequences render rDNA loci particularly vulnerable to genomic instability, a proposed underlying cause of cellular senescence. The molecular mechanisms that maintain rDNA stability have remained unclear. A new paper elucidates a sirtuin-dependent mechanism that protects rDNA loci from genomic instability and prevents cellular senescence via heterochromatin silencing mediated by the chromatin remodeler SNF2H. This finding extends our understanding of chromatin dynamics within rDNA regions and offers new mechanistic insights into aging-related pathologies associated with genomic instability.
Highlights
Ribosomes are encoded by many copies of ribosomal DNA packed into the nucleolus
Various types of environmental and cellular stress pathways converge to cause genomic instability by altering DNA damage responses or deregulating chromatin dynamics, resulting in checkpoint responses that lead to cellular senescence
Maintaining chromatin structure is crucial for preventing genomic instability, and ribosomal DNA (rDNA) loci are subject to the influence of chromatin dynamics on both sequence rearrangements and transcription capacity
Summary
Ribosomes are encoded by many copies of ribosomal DNA (rDNA) packed into the nucleolus. Maintaining the integrity of rDNA sequence repeats packed within heterochromatic loci is critical for preventing cellular senescence and aging-related pathologies. Maintaining chromatin structure is crucial for preventing genomic instability, and rDNA loci are subject to the influence of chromatin dynamics on both sequence rearrangements and transcription capacity.
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