The study investigates the role of DHX9 stress granules (SGs) in compartmentalizing UV-induced RNA damage. DHX9 SGs, marked by the dsRNA helicase DHX9, are specifically formed in daughter cells following UV exposure, sequestering damaged intron RNA and activating multiple stress responses. These SGs are enriched in damaged intron RNA, unlike classical SGs composed of mature mRNA. UV-induced RNA crosslinking damage, but not DNA damage, triggers DHX9 SG formation. DHX9 SGs promote cell survival, induce a dsRNA-related immune response, and trigger translation shutdown in daughter cells. The assembly of DHX9 SGs is dependent on mitotic NE disassembly and involves G3BP1/2. DHX9 modulates dsRNA levels in SGs, protecting daughter cells from deleterious dsRNA immune responses. Autophagy receptor p62 is involved in the disassembly of DHX9 SGs, promoting cell survival after RNA damage stress. This study highlights a non-canonical mechanism by which daughter cells protect themselves from parental RNA damage.The study investigates the role of DHX9 stress granules (SGs) in compartmentalizing UV-induced RNA damage. DHX9 SGs, marked by the dsRNA helicase DHX9, are specifically formed in daughter cells following UV exposure, sequestering damaged intron RNA and activating multiple stress responses. These SGs are enriched in damaged intron RNA, unlike classical SGs composed of mature mRNA. UV-induced RNA crosslinking damage, but not DNA damage, triggers DHX9 SG formation. DHX9 SGs promote cell survival, induce a dsRNA-related immune response, and trigger translation shutdown in daughter cells. The assembly of DHX9 SGs is dependent on mitotic NE disassembly and involves G3BP1/2. DHX9 modulates dsRNA levels in SGs, protecting daughter cells from deleterious dsRNA immune responses. Autophagy receptor p62 is involved in the disassembly of DHX9 SGs, promoting cell survival after RNA damage stress. This study highlights a non-canonical mechanism by which daughter cells protect themselves from parental RNA damage.