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UV damage causes uncontrolled DNA breakage in cells from patients with combined features of XP-D and Cockayne syndrome (Articolo in rivista)

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UV damage causes uncontrolled DNA breakage in cells from patients with combined features of XP-D and Cockayne syndrome (Articolo in rivista) (literal)

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Berneburg M.; Lowe J.E.; Nardo T.; Araujo S.; Fousteri M.I.; Green M.H.L.; Krutmann J.; Wood R.D.; Stefanini M.; Lehmann A.R. (2000)
UV damage causes uncontrolled DNA breakage in cells from patients with combined features of XP-D and Cockayne syndrome
in EMBO journal (Print)
(literal)

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Berneburg M.; Lowe J.E.; Nardo T.; Araujo S.; Fousteri M.I.; Green M.H.L.; Krutmann J.; Wood R.D.; Stefanini M.; Lehmann A.R. (literal)

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MRC Cell Mutation Unit, Sussex University, Falmer, Brighton BN1 9RR, United Kingdom; Clin. and Exp. Photodermatology, Heinrich-Heine-Universität, Moorenstrasse 5, 40225 Düsseldorf, Germany; Sch. of Pharm. and Biomol. Sciences, University of Brighton, Cockcroft Building, Brighton BN2 4GJ, United Kingdom; Ist. Genet. Biochim. E., Via Abbiategrasso 207, Pavia, Italy; Imperial Cancer Research Fund, Clare Hall Laboratories, South Mimms, Herts EN6 3LD, United Kingdom (literal)

Titolo

UV damage causes uncontrolled DNA breakage in cells from patients with combined features of XP-D and Cockayne syndrome (literal)

Abstract

Nucleotide excision repair (NER) removes damage from DNA in a tightly regulated multiprotein process. Defects in NER result in three different human disorders, xeroderma pigmentosum (XP), trichothiodystrophy (TTD) and Cockayne syndrome (CS). Two cases with the combined features of XP and CS have been assigned to the XP-D complementation group. Despite their extreme UV sensitivity, these cells appeared to incise their DNA as efficiently as normal cells in response to UV damage. These incisions were, however, uncoupled from the rest of the repair process. Using cell-free extracts, we were unable to detect any incision activity in the neighbourhood of the damage. When irradiated plasmids were introduced into unirradiated XP-D/CS cells, the ectopically introduced damage triggered the induction of breaks in the undamaged genomic DNA, XP-D/CS cells thus have a unique response to sensing UV damage, which results in the introduction of breaks into the DNA at sites distant from the damage. We propose that it is these spurious breaks that are responsible for the extreme UV sensitivity of these cells. (literal)

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