Elaborate security TRAINing to fight against expression of genomic junk.
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.
National Center for Biotechnology Information, National Library of Medicine, National Institutes of Health, Bethesda, MD, USA. koonin@ncbi.nlm.nih.gov
Eugene V
EV
Koonin
D000818:Animals; D016923:Cell Death; D018899:CpG Islands; D053903:DNA Breaks, Double-Stranded; D019175:DNA Methylation; D005786:Gene Expression Regulation; D007372:Interferons / Q000235:genetics* / Q000378:metabolism; D051379:Mice; D012330:RNA, Double-Stranded; D034741:RNA, Small Interfering / Q000235:genetics / Q000378:metabolism; D012091:Repetitive Sequences, Nucleic Acid; D015398:Signal Transduction; D016159:Tumor Suppressor Protein p53 / Q000235:genetics* / Q000378:metabolism
D012330:RNA, Double-Stranded; D034741:RNA, Small Interfering; D016159:Tumor Suppressor Protein p53; D007372:Interferons
DNA methylation; SINE repeats; interferon response; p53; transposable elements