Based on previous studies in fruit flies, Andrea Schorn and Rob Martienssen of Cold Spring Harbor Laboratory thought the answer to what protects vulnerable mouse embryo genomes might lie in small RNAs. To find them, they made some tweaks to the usual techniques. As they explain in their paper, “many small RNA sequencing studies omit RNA fragments shorter than 19 [nucleotides] or discard sequencing reads that map to multiple loci in the genome, thus often discarding reads matching young, potentially active transposons…”
By including smaller fragments in their RNA library and analysis, the authors turned up “very abundant” 18- and 22-nucleotide fragments of tRNAs. Results of further experiments suggested the 18-nucleotide fragments occupy the retrotransposons’ primer binding sites, blocking full tRNA molecules from binding there and initiating replication, while the 22-nucleotide fragments post-transcriptionally silence a protein needed for retrotransposition.
See “Tethering transposons”
“It’s plausible that this is a very ancient mechanism that cells have found to not only inhibit retrotransposons but help in protection against viruses as well,” Martienssen says in a statement.