Abstract
Transposons are parasitic nucleic acids present in most genomes. The ability of transposons to mobilize makes them a source of genetic diversity and a threat to genome integrity. Interestingly, mutations in the C. elegans gene mut-2/rde-3 increases the rate of transposition in the germline, but not in the soma, suggesting that the C. elegans germline and soma employ different strategies to regulate Tc1 transposition. Here, we develop fluorescence reporters for studying DNA transposon regulation in living C. elegans in a tissue-specific manner and we use candidate gene testing and genetic screening approaches to identify factors that regulate Tc1 mobility in the germline and/or the soma of the animal. We find that both cytoplasmic and nuclear components of the RNA interference (RNAi) pathway silence Tc1 in the germline, but not in the soma. We identify a novel pathway involving the C. elegans ortholog of HNRNPC, and a gene we term suppressor of transposon mobilization (stm)-1, which regulates Tc1 primarily in the soma, likely by binding Tc1 RNA and preventing its splicing. Our findings reveal tissue-specific strategies for regulating parasitic nucleic acids and pave the way for future studies exploring how and why different tissues adopt different transposon silencing systems.