Abstract
A new study shows that the expression of two classes of repetitive elements in the mouse genome is controlled through two complementary mechanisms: DNA methylation and p53-mediated transcription suppression.¹ When both lines of defense fail, expression of the repeats yields large quantities of double-stranded RNA, triggering interferon response that leads to caspase-dependent cell death. These notable findings highlight two fundamental trends: tight coupling of defense and cell death mechanisms that appears to be universal in cellular life and the exploitation of the expression of "junk" DNA as a signal triggering "altruistic" cell suicide.