Breaks in the 45S rDNA Lead to Recombination-Mediated Loss of Repeats | Zendy

Daniël O. Warmerdam | Zendy; Jeroen van den Berg | Zendy; René H. Medema | Zendy

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Breaks in the 45S rDNA Lead to Recombination-Mediated Loss of Repeats

Author(s) -

Daniël O. Warmerdam,

Jeroen van den Berg,

René H. Medema

Publication year - 2016

Publication title -

cell reports

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 6.264

H-Index - 154

eISSN - 2639-1856

pISSN - 2211-1247

DOI - 10.1016/j.celrep.2016.02.048

Subject(s) - homologous recombination , biology , recombination , dna repair , genetics , dna , non allelic homologous recombination , genome , genome instability , ribosomal dna , dna damage , genetic recombination , gene , phylogenetics

rDNA repeats constitute the most heavily transcribed region in the human genome. Tumors frequently display elevated levels of recombination in rDNA, indicating that the repeats are a liability to the genomic integrity of a cell. However, little is known about how cells deal with DNA double-stranded breaks in rDNA. Using selective endonucleases, we show that human cells are highly sensitive to breaks in 45S but not the 5S rDNA repeats. We find that homologous recombination inhibits repair of breaks in 45S rDNA, and this results in repeat loss. We identify the structural maintenance of chromosomes protein 5 (SMC5) as contributing to recombination-mediated repair of rDNA breaks. Together, our data demonstrate that SMC5-mediated recombination can lead to error-prone repair of 45S rDNA repeats, resulting in their loss and thereby reducing cellular viability.

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