Fig. 1

Schematic overview of key findings. UV irradiation induces crosslinks between pre-mRNA and nuclear proteins, leading to splicing and 3’-end formation defects, with enhanced intron retention. Decay of these aberrant, lesioned RNAs, e.g., by exonucleases (light blue, “E”), fails. dsRNA-targeted helicase DHX9 (green, “D”) recognizes such damage. Upon mitosis (or leakiness of the nuclear envelope), DHX9-SGs form in G1 phase daughter cells. SG formation is promoted by the canonical SG-nucleating protein G3BP1 (red, “G”). It is likely that RNA and proteins form a 3D network, as known from other types of published SGs. Cells can only resume cell cycle if SGs are cleared by autophagy, dependent on the presence of DHX9