Defective Hfp-dependent transcriptional repression of dMYC is fundamental to tissue overgrowth in Drosophila XPB models

Jue Er Amanda Lee, Naomi C. Mitchell, Olga Zaytseva, Arjun Chahal, Peter Mendis, Amandine Cartier-Michaud, Linda M. Parsons, Gretchen Poortinga, David L. Levens, Ross D. Hannan and Leonie M. Quinn ()
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Jue Er Amanda Lee: University of Melbourne
Naomi C. Mitchell: University of Melbourne
Olga Zaytseva: University of Melbourne
Arjun Chahal: University of Melbourne
Peter Mendis: University of Melbourne
Amandine Cartier-Michaud: Aix-Marseille University
Linda M. Parsons: University of Melbourne
Gretchen Poortinga: Peter MacCallum Cancer Centre, St Andrews Place
David L. Levens: Center for Cancer Research, National Cancer Institute, NIH
Ross D. Hannan: Peter MacCallum Cancer Centre, St Andrews Place
Leonie M. Quinn: University of Melbourne

Nature Communications, 2015, vol. 6, issue 1, 1-12

Abstract: 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 recognition motif protein Hfp/FIR, which transcriptionally represses the MYC oncogene homologue, dMYC. The data demonstrate that dMYC repression and dMYC-dependent overgrowth in the Hfp hypomorph is further impaired in the C-terminal Hay/XPB mutant background. Thus, we predict defective transcriptional repression of MYC by the Hfp orthologue, FIR, might provide one mechanism for cancer progression in XP/CS.

Date: 2015
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DOI: 10.1038/ncomms8404

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