Description:
<jats:title>Summary</jats:title><jats:p>Telomeres and ribosomal <jats:styled-content style="fixed-case">RNA</jats:styled-content> genes (<jats:styled-content style="fixed-case">rDNA</jats:styled-content>) are essential for cell survival and particularly sensitive to factors affecting genome stability. Here, we examine the role of <jats:styled-content style="fixed-case">RAD</jats:styled-content>51 and its antagonist, <jats:styled-content style="fixed-case">RTEL</jats:styled-content>1, in the moss <jats:italic>Physcomitrella patens</jats:italic>. In corresponding mutants, we analyse their sensitivity to <jats:styled-content style="fixed-case">DNA</jats:styled-content> damage, the maintenance of telomeres and <jats:styled-content style="fixed-case">rDNA</jats:styled-content>, and repair of double‐stranded breaks (<jats:styled-content style="fixed-case">DSB</jats:styled-content>s) induced by genotoxins with various modes of action. While the loss of <jats:styled-content style="fixed-case">RTEL</jats:styled-content>1 results in rapid telomere shortening, concurrent loss of both <jats:styled-content style="fixed-case">RAD</jats:styled-content>51 genes has no effect on telomere lengths. We further demonstrate here the linked arrangement of 5S and 45S <jats:styled-content style="fixed-case">rRNA</jats:styled-content> genes in <jats:italic>P. patens</jats:italic>. The spacer between 5S and 18S <jats:styled-content style="fixed-case">rRNA</jats:styled-content> genes, especially the region downstream from the transcription start site, shows conspicuous clustering of sites with a high propensity to form quadruplex (G4) structures. Copy numbers of 5S and 18S <jats:styled-content style="fixed-case">rDNA</jats:styled-content> are reduced moderately in the <jats:italic>pprtel1</jats:italic> mutant, and significantly in the double <jats:italic>pprad51‐1‐2</jats:italic> mutant, with no progression during subsequent cultivation. While reductions in 45S <jats:styled-content style="fixed-case">rDNA</jats:styled-content> copy numbers observed in <jats:italic>pprtel1</jats:italic> and <jats:italic>pprad51‐1‐2</jats:italic> plants apply also to 5S <jats:styled-content style="fixed-case">rDNA</jats:styled-content>, changes in transcript levels are different for 45S and 5S <jats:styled-content style="fixed-case">rRNA</jats:styled-content>, indicating their independent transcription by <jats:styled-content style="fixed-case">RNA</jats:styled-content> polymerase I and <jats:styled-content style="fixed-case">III</jats:styled-content>, respectively. The loss of <jats:italic><jats:styled-content style="fixed-case">SOL</jats:styled-content></jats:italic> (Sog One‐Like), a transcription factor regulating numerous genes involved in <jats:styled-content style="fixed-case">DSB</jats:styled-content> repair, increases the rate of <jats:styled-content style="fixed-case">DSB</jats:styled-content> repair in dividing as well as differentiated tissue, and through deactivation of G2/M cell‐cycle checkpoint allows the cell‐cycle progression manifested as a phenotype resistant to bleomycin.</jats:p>