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

dc.contributor.authorLee, Jue Er Amanda
dc.contributor.authorMitchell, Naomi
dc.contributor.authorZaytseva, Olga
dc.contributor.authorChahal, Arjun
dc.contributor.authorMendis, Peter
dc.contributor.authorCartier-Michaud, Amandine
dc.contributor.authorParsons, Linda M.
dc.contributor.authorPoortinga, Gretchen
dc.contributor.authorLevens, David
dc.contributor.authorHannan, Ross
dc.contributor.authorQuinn, Leonie
dc.date.accessioned2018-11-29T22:56:34Z
dc.date.available2018-11-29T22:56:34Z
dc.date.issued2015
dc.date.updated2018-11-29T08:13:02Z
dc.description.abstractNucleotide 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
dc.format.mimetypeapplication/pdfen_AU
dc.identifier.issn2041-1723
dc.identifier.urihttp://hdl.handle.net/1885/153564
dc.provenance© 2015 Macmillan Publishers Limited. http://www.sherpa.ac.uk/romeo/issn/2041-1723/..."Publisher's version/PDF may be used. On author's personal website, institutional repository or open access repository" from SHERPA/RoMEO site (as at 2/02/16).
dc.publisherMacmillan Publishers Ltd
dc.sourceNature Communications
dc.titleDefective Hfp-dependent transcriptional repression of dMYC is fundamental to tissue overgrowth in Drosophila XPB models
dc.typeJournal article
dcterms.accessRightsOpen Accessen_AU
local.bibliographicCitation.issue15
local.bibliographicCitation.startpage7404
local.contributor.affiliationLee, Jue Er Amanda, University of Melbourne
local.contributor.affiliationMitchell, Naomi, University of Melbourne
local.contributor.affiliationZaytseva, Olga, University of Melbourne
local.contributor.affiliationChahal, Arjun, The University of Melbourne
local.contributor.affiliationMendis, Peter, University of Melbourne
local.contributor.affiliationCartier-Michaud, Amandine, Aix-Marseille University
local.contributor.affiliationParsons, Linda M., University of Melbourne
local.contributor.affiliationPoortinga, Gretchen, Peter MacCallum Cancer Centre
local.contributor.affiliationLevens, David, National Cancer Institute
local.contributor.affiliationHannan, Ross, College of Health and Medicine, ANU
local.contributor.affiliationQuinn, Leonie, College of Health and Medicine, ANU
local.contributor.authoremailu1000203@anu.edu.au
local.contributor.authoruidHannan, Ross, u1000203
local.contributor.authoruidQuinn, Leonie, u1037504
local.description.notesImported from ARIES
local.identifier.absfor110999 - Neurosciences not elsewhere classified
local.identifier.ariespublicationu5192707xPUB10
local.identifier.ariespublicationU3488905xPUB6746
local.identifier.citationvolume6
local.identifier.doi10.1038/ncomms8404
local.identifier.scopusID2-s2.0-84935874480
local.identifier.thomsonID000357175700006
local.identifier.uidSubmittedByu5192707
local.type.statusPublished Version

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