The sequencing of many different eukaryotic genomes revealed that genes represent only a small part of each genome compared with intergenic and repeated sequences (e.g. satellites, microsatellites, transposable elements). For instance, up to 45% of the human genome consists of transposable elements (TEs). Active TEs are able to replicate by inserting new copies elsewhere in the host genome, which can dramatically impact genome structure and function. However, diverse defense mechanisms (including piRNA-mediated transcriptional silencing) restrain mobilization of integrated TEs to low levels compatible with host survival. Indeed, depending on their insertion site, TEs can lead to the destruction, inactivation, or deregulation of coding genes. TEs can also affect the epigenetic landscape in the vicinity of the insertion site and the three-dimensional (3D) chromatin structure. Moreover, TE sequences are able to recruit the host transcription machinery to express their own products and promote transposition. This capacity is kept long after they have lost the ability to transpose, suggesting that TEs have significantly contributed to the evolution of transcription regulation. Indeed, selection tends to co-opt positive insertions and eliminate harmful insertions. Altogether, this gives rise to a delicate equilibrium which, when disrupted, leads to pathologies or sterility (when germ cells are concerned by transposition).
The three following projects aim to understand these genetic conflicts and their eventual resolution at both the lab and evolutionary time scales.
Project 1 : What are the impacts of TE insertions on the genome structure and function?
Project 2 : What are the transcriptional roles of piRNAs on TEs and piRNA source loci ?
Project 3 : What are the chromatin effectors of TE transcriptional repression ?
Mourdas Mohamed, Nguyet Thi-Minh Dang, Yuki Ogyama, Nelly Burlet, Bruno Mugat, Matthieu Boulesteix, Vincent Mérel, Philippe Veber, Judit Salces-Ortiz, Dany Severac, Alain Pélisson, Cristina Vieira, François Sabot, Marie Fablet, Séverine Chambeyron
Bruno Mugat, Simon Nicot, Carolina Varela-Chavez, Christophe Jourdan, Kaoru Sato, Eugenia Basyuk, François Juge, Mikiko C. Siomi, Alain Pélisson & Séverine Chambeyron
Barckmann B, El-Barouk M, Pélisson A, Mugat B, Li B, Franckhauser C, Fiston Lavier AS, Mirouze M, Fablet M, Chambeyron S
Romero-Soriano V, Modolo L, Lopez-Maestre H, Mugat B, Pessia E, Chambeyron S, Vieira C, Garcia Guerreiro MP
Akkouche, A., Mugat, B., Barckmann, B., Varela-Chavez, C., Li, B., Raffel, R., Pelisson, A., Chambeyron, S.
Lopez-Maestre H, Carnelossi EA, Lacroix V, Burlet N, Mugat B, Chambeyron S, Carareto CM, Vieira C
Barckmann,B., Pierson,S., Dufourt, J., Papin, C., Armenise, C., Port, F., Grentzinger, T., Chambeyron, S., Baronian, G., Desvignes, JP., Curk, T., Simonelig, M.
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Régulation des ARNm et Développement
Mugat B, Akkouche A, Serrano V, Armenise C, Li B, Brun C, Fulga TA, Van Vactor D, Pélisson A, Chambeyron S
Grentzinger T, Armenise C, Pelisson A, Brun C, Mugat B, Chambeyron S.
Chambeyron, S., Seitz, H.
Grentzinger T, Chambeyron S.
Grentzinger T, Armenise C, Pelisson A, Brun C, Mugat B, Chambeyron S
Brasset E, Chambeyron S.
Akkouche A, Grentzinger T, Fablet M, Armenise C, Burlet N, Braman V, Chambeyron S. §, Vieira C§ (co-dernier auteur)
Grentzinger T, Armenise C, Brun C, Mugat B, Serrano V, Pelisson A, Chambeyron S.
Soutenue par Marianne El Barouk le 16-12-2016
illustration page équipe Sylvaine Jenny
