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Physiopathology
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User name	Arndt Benecke
Email	arndt@ihes.fr
Phone / Fax number	+33160926665 / +33160926609
Location	Institut des Hautes Etudes Scientifiques (Integrative Biology) - 35, route de Chartres - 91440 Bures sur Yvette, France

Scientific description

Notch pathway controls multiple cellular processes, such as differentiation, cell proliferation and apoptosis. Its activation is based on the ligand binding to a Notch receptor after which, the Notch intracellular active domain (NIC) is released through cleavage mediated by ?-secretase. Upon cleavage, NIC translocate to the nucleus where it binds the CSL-complex and actives the transcription of its target genes, like Hes1. TAF6 is a subunit of the TFIID basal transcription complex that plays an important role in the regulation of RNA polymerase II transcription. TAF6? is a specialized isoform of TAF6 that can induce apoptosis and induces the expression of Notch target genes. This study aims to explore the potential crosstalk between TAF6? and Notch signalling pathways and its impact on apoptosis.
Our data shows, for the first time that the Notch pathway is activated by TAF6? in several models of cancer and that association, contributes to apoptosis in cervical cancer.

Technical description

To validate the impact of TAF6? expression on the Notch pathway, we performed microarray analysis. TAF6? induction, mediated through transfection of SSO (Splice-Switching oligonucleotides), revealed a ?-secretase–dependent induction of Notch target genes in HeLa cells. Flow cytometry analysis further showed that TAF6?-dependent apoptosis is reduced by treatment with ?-secretase inhibitors. Immunofluorescence analysis revealed that TAF6? induced translocation of NIC-2 to the nucleus. Finally, qPCR showed that Notch target gene expression is increased in several cancer cell lines in response to TAF6? induction.

Reference

Edith M. Alvarado, Emanuelle Wilhelm, Hélène Léger, Arndt G. Benecke, Brendan Bell. Crosstalk between TAF6 and Notch signaling pathways. Submitted.