DNA mismanagement leads to immune system oversight.
Trex1, a major 3' DNA exonuclease in mammalian cells, has been thought to act primarily in DNA replication or repair. Surprisingly, the major phenotype resulting from Trex1 deficiency in humans and mice is a chronic inflammatory disease. In this issue, Yang et al. (2007) report that Trex1 deficiency causes chronic activation of the ATM-dependent DNA-damage checkpoint and accumulation of a discrete single-stranded DNA species in the cytoplasm, either of which could contribute to chronic inflammation.
Department of Molecular and Cell Biology and Cancer Research Laboratory, Life Sciences Addition, University of California at Berkeley, Berkeley, CA 94720, USA. lcoscoy@berkeley.edu
Laurent
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Coscoy
David H
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Raulet
D000818:Animals; D015551:Autoimmunity / Q000235:genetics*; D004249:DNA Damage / Q000502:physiology*; D005090:Exodeoxyribonucleases / Q000235:genetics / Q000502:physiology; D006801:Humans; D007107:Immune System / Q000502:physiology*; D051379:Mice; D008954:Models, Biological; D009205:Myocarditis / Q000235:genetics; D010750:Phosphoproteins / Q000235:genetics / Q000502:physiology
D010750:Phosphoproteins; D005090:Exodeoxyribonucleases; C429526:three prime repair exonuclease 1