Depletion of Chk2 affects transposons' abundance

Transposons are prevalent cross nearly all species due to their capacity to mobilize and integrate into the host genome. However, their products in the cytoplasm may begin to affect the host before integration occurs. Here, we identified that activation of transposons results in significantly smaller mid-stage oocytes and prolonged mid-oogenesis of Drosophila. Notably, one specific LTR-retrotransposon, 3S18, primarily contributes to this phenotype. We found that 3S18 mRNA and its integrase form micrometer-scaled ribonucleoprotein aggregates at cell-cell bridges during these stages. Interestingly, disruption of the host checkpoint pathway not only suppressed the formation of these RNP aggregates, but also substantially reduced 3S18 mRNA level. Our results suggest that 3S18 aggregates do not merely reflect a response to checkpoint activation, but also serve a protective function for the retrotransposon products. Live-imaging reveals that accumulation of 3S18 RNP aggregates obstructs the transport of host materials, resulting in the prolonged mid-oogenesis phenotype. Finally, we showed that forcefully extending oogenesis significantly enhances the propagation for 3S18. These results highlight unique characteristics of retrotransposon 3S18, which forms self-protective aggregates and prolongs the host mid-oogenesis, and may shed light on studies of other parasitic elements including viruses.