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Differential role of transcription-coupled repair in UVB-induced G sub(2) arrest and apoptosis in mouse epidermis

van Oosten, M ; Rebel, H ; Friedberg, E C ; van Steeg, H ; van der H, TJ ; van Kranen, HJ ; Westerman, A ; van Zeeland, AA ; Mullenders, LHF ; de Gruijl, FR

Proceedings of the National Academy of Sciences - PNAS, 2000-10, Vol.97 (21), p.11268-11273 [Periódico revisado por pares]

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  • Título:
    Differential role of transcription-coupled repair in UVB-induced G sub(2) arrest and apoptosis in mouse epidermis
  • Autor: van Oosten, M ; Rebel, H ; Friedberg, E C ; van Steeg, H ; van der H, TJ ; van Kranen, HJ ; Westerman, A ; van Zeeland, AA ; Mullenders, LHF ; de Gruijl, FR
  • É parte de: Proceedings of the National Academy of Sciences - PNAS, 2000-10, Vol.97 (21), p.11268-11273
  • Notas: ObjectType-Article-2
    SourceType-Scholarly Journals-1
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    ObjectType-Feature-1
  • Descrição: Nucleotide excision repair (NER), apoptosis, and cell-cycle regulation are major defense mechanisms against the carcinogenic effects of UVB light. NER eliminates UVB-induced DNA photolesions via two subpathways: global genome repair (GGR) and transcription-coupled repair (TCR). Defects in NER result in the human disorders xeroderma pigmentosum (XP) and Cockayne syndrome (CS), displaying severe UV sensitivity and in the case of XP, cancer proneness. We investigated the impact of deficiencies in NER subpathways on apoptosis, hyperplasia, and cell cycle progression in the epidermis of UVB-exposed CS group B (Csb super(-/-)) mice (no TCR), XP group C (Xpc super(-/-)) mice (no GGR), and XP group A (Xpa super(-/-)) mice (no TCR and no GGR). On UVB treatment (250 J/m super(2)), Xpa super(-/-) and Csb super(-/-) mice revealed an extensive apoptotic response in the skin, a blockage of cell cycle progression of epidermal cells, and strong hyperplasia. Interestingly, the absence of this apoptotic response in the skin of wild-type and Xpc super(-/-) mice coincided with the ability of epidermal cells to enter the S phase. However, only epidermal cells of Xpc super(-/-) mice subsequently became arrested in the G sub(2) phase. Our data demonstrate that TCR (and/or restoration of UVB-inhibited transcription) enables damaged cells to progress through S phase and prevents the induction of apoptosis and hyperplasia. G sub(2) arrest is manifest only under conditions of proficient TCR in combination with deficient GGR, indicating that epidermal cells become arrested in the G sub(2) phase as a result of persisting damage in their genome.
  • Idioma: Inglês
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  • Realização: ABCD-USP USP   Logos de Redes Sociais: Freepik

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