Open Access Highly Accessed Research article

TAF6δ orchestrates an apoptotic transcriptome profile and interacts functionally with p53

Emmanuelle Wilhelm1, Mara Kornete1, Brice Targat2, Jimmy Vigneault-Edwards2, Mattia Frontini3, Laszlo Tora4, Arndt Benecke2 and Brendan Bell1*

Author Affiliations

1 RNA Group. Département de microbiologie et d'infectiologie, Faculté de médecine et sciences de la santé, Université de Sherbrooke, 3001 12e ave Nord, Sherbrooke, Québec J1H 5N4, Canada

2 Institut des Hautes Études Scientifiques & Institut de Recherche Interdisciplinaire - CNRS/USTL; 35 route de Chartres; 91440 Bures sur Yvette, France

3 Clinical Science Center, Hammersmith Hospital Campus, Du Cane Road, W12 0NN, London, UK

4 Department of Functional Genomics Institut de Génétique et de Biologie Moléculaire et Cellulaire (IGBMC), UMR 7104 CNRS, UdS, INSERM U964, BP 10142, F-67404 ILLKIRCH Cedex, CU de Strasbourg, France

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BMC Molecular Biology 2010, 11:10  doi:10.1186/1471-2199-11-10

Published: 22 January 2010



TFIID is a multiprotein complex that plays a pivotal role in the regulation of RNA polymerase II (Pol II) transcription owing to its core promoter recognition and co-activator functions. TAF6 is a core TFIID subunit whose splice variants include the major TAF6α isoform that is ubiquitously expressed, and the inducible TAF6δ. In contrast to TAF6α, TAF6δ is a pro-apoptotic isoform with a 10 amino acid deletion in its histone fold domain that abolishes its interaction with TAF9. TAF6δ expression can dictate life versus death decisions of human cells.


Here we define the impact of endogenous TAF6δ expression on the global transcriptome landscape. TAF6δ was found to orchestrate a transcription profile that included statistically significant enrichment of genes of apoptotic function. Interestingly, gene expression patterns controlled by TAF6δ share similarities with, but are not equivalent to, those reported to change following TAF9 and/or TAF9b depletion. Finally, because TAF6δ regulates certain p53 target genes, we tested and demonstrated a physical and functional interaction between TAF6δ and p53.


Together our data define a TAF6δ-driven apoptotic gene expression program and show crosstalk between the p53 and TAF6δ pathways.