Journal article
Defective Hfp-dependent transcriptional repression of dMYC is fundamental to tissue overgrowth in Drosophila XPB models
JEA Lee, NC Mitchell, O Zaytseva, A Chahal, P Mendis, A Cartier-Michaud, LM Parsons, G Poortinga, DL Levens, RD Hannan, LM Quinn
Nature Communications | NATURE PUBLISHING GROUP | Published : 2015
DOI: 10.1038/ncomms8404
Abstract
Nucleotide excision DNA repair (NER) pathway mutations cause neurodegenerative and progeroid disorders (xeroderma pigmentosum (XP), Cockayne syndrome (CS) and trichothiodystrophy (TTD)), which are inexplicably associated with (XP) or without (CS/TTD) cancer. Moreover, cancer progression occurs in certain patients, but not others, with similar C-terminal mutations in the XPB helicase subunit of transcription and NER factor TFIIH. Mechanisms driving overproliferation and, therefore, cancer associated with XPB mutations are currently unknown. Here using Drosophila models, we provide evidence that C-terminally truncated Hay/XPB alleles enhance overgrowth dependent on reduced abundance of RNA rec..
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Awarded by National Cancer Institute
Funding Acknowledgements
We thank M. Fuller and M. Zurita for the Haywire strains. We are grateful to the Bloomington and VDRC stock centres for Drosophila strains and to the DSHB for antibodies. This work was funded by Project Grants and a Senior Research Fellowship from the National Health and Medical Research Council of Australia. This work was also supported by the Cancer Council of Victoria.