But why? How does a simple U-code target transposons? It’s a brilliant exploit of retrotransposon evolution: their genomes are intrinsically A-rich. When transcribed in antisense (as in clusters), they become exceptionally U-rich, placing them squarely in Yb’s crosshairs. 🎯 (11/19)

Check this out: we designed "U-ramp" reporters with entirely synthetic 3’ UTRs by varying in their uridine content (20% to 45%). The result was striking: U-density behaves like a threshold—below ~30% U, barely any piRNAs; above it, output shoots up in a Yb-dependent manner. (7/19)

I want to amplify this statement so much. Cool work can be cool without overdoing the claims.

The central dogma is too often badly taught.

Regulation of genes by non-coding regions is such an important part of molecular biology from its inception.