Ribosomal RNAs (rRNAs) account for 80-90% of all transcripts in eukaryotic cells. To meet this demand, the ribosomal DNA (rDNA) gene that codes for rRNA is tandemly repeated hundreds of times, comprising rDNA loci on eukaryotic chromosomes. This repetitiveness imposes a challenge to maintaining sufficient copy number due to spontaneous intra-chromatid recombination between repetitive units causing copy number loss. The progressive shrinking of rDNA loci from generation to generation could lead to extinction of the lineage, yet the mechanism(s) to counteract spontaneous copy number loss remained unclear. Here, we show that the rDNA-specific retrotransposon R2 is essential for rDNA copy number (CN) maintenance in the Drosophila male germline, despite the perceived disruptive nature of transposable elements. Depletion of R2 led to defective rDNA CN maintenance in multiple contexts, causing a decline in fecundity over generations and eventual extinction of the lineage. Our data suggests that DNA double strand breaks generated by R2 is the initiating event of rDNA CN expansion, stimulating the repair processes proposed to underlie rDNA CN expansion. This study reveals that retrotransposons can provide a benefit to their hosts, contrary to their reputation as genomic parasitic, which may contribute to their widespread success throughout taxa.
Selective replication of ribosomal DNA repeats after loss of the abnormal oocyte phenotype in Drosophila melanogaster.
