IGBMC, Illkirch, France
The seminar in brief:
Transcription mediated by RNA polymerase II (RNA Pol II) is responsible for the expression of protein-coding genes and many non-coding RNAs in all cells of the body. Disruption of RNA Pol II activity is thus associated with many diseases. Understanding the mechanisms that control transcription is therefore of fundamental but also medical interest. Our laboratory focuses on the protein complexes that are involved in RNA Pol II transcription initiation, the first step of the transcriptional cycle, in particular on the general transcription factor (GTF) TFIID. The TFIID complex is the first GTF to interact with DNA by recognizing the promoter and allows the nucleation of the pre-initiation transcription complex (PIC). TFIID is composed of TBP (TATA-binding protein) and 13 TAFs (TBP-associated factors) in higher eukaryotes.
This somewhat simplistic view has been challenged in metazoans, because the composition of TFIID is in fact more complex. Indeed, i) some subunits are not necessarily required in certain cellular contexts, ii) some TAFs have paralogs that are associated with developmental programs and that can be integrated into TFIID and iii) there are TBP-like proteins associated with gamete differentiation but it is not clear whether these TBP-like proteins are capable of integrating a TFIID complex. All these data indicate that there is potential diversity in the mechanisms of promoter recognition and transcription initiation and that this step can be considered as a new level of regulation of gene expression.
Our aim is to analyze the functional diversity of the protein complexes that recognize the promoters and initiate the formation of the PIC. We have identified a unique TFIID-independent basal transcription machinery during oocyte growth and analyzed the effects of deletion of genes encoding certain TAFs on TFIID composition and Pol II transcription during murine development and in embryonic stem cells.
INSERM U1239 (NorDic) IRIB, Université de Rouen-Normandie, Rouen
MRI, BioCampus Montpellier, UAR 3426 CNRS - US 09 INSERM - UM
Dept of Genetics, Blavatnik Institute, Harvard Medical School, Boston, Ms., USA
Séminaire en distanciel, un lien Zoom sera diffusé la semaine précédente
CRCL, INSERM U1052/CNRS UMR 5286, Centre Léon Bérard, Université Lyon 1
Immune Microenvironment and Immunotherapy Lab, UMR1135 Inserm, Hopital Pitié-Salpêtriere, Paris.
University of Gent, Experimental Cancer Research Lab, Belgium
Some more on the speaker:
Since his PhD, he has been working on cancer-associated fibroblasts (CAFs) in colon cancer progression (De Wever et al., FASEBJ 2004, J Pathol 2003, J Cell Science 2004 over 1000 cumulative WOS citations). I He expanded his research into adipose tissue during his post-doc (Lapeire et al., Cancer Res 2014) and the secretory mechanisms of pro-metastatic signals (Hendrix et al., JNCI 2010, Cancer Res 2010). His current lab woks on tumor-environment interactions including design of model systems (De Jaeghere et al., Biomaterials 2018), response to therapy of CAFs (Tommelein et al., Cancer Res 2018), and exploitation of CAFs as therapy (De Vlieghere et al., Biomaterials 2015) and extracellular vesicles with the Hendrix lab (De Wever and Hendrix EMBOJ 2019).
Institut de Génétique Humaine, CNRS/Université de Montpellier