E2F1 controls alternative splicing pattern of genes involved in apoptosis through upregulation of the splicing factor SC35. - Institut Albert Bonniot Accéder directement au contenu
Article Dans Une Revue Cell Death and Differentiation Année : 2008

E2F1 controls alternative splicing pattern of genes involved in apoptosis through upregulation of the splicing factor SC35.

Résumé

The transcription factor E2F1 has a key function during S phase progression and apoptosis. It has been well-demonstrated that the apoptotic function of E2F1 involves its ability to transactivate pro-apoptotic target genes. Alternative splicing of pre-mRNAs also has an important function in the regulation of apoptosis. In this study, we identify the splicing factor SC35, a member of the Ser-Rich Arg (SR) proteins family, as a new transcriptional target of E2F1. We demonstrate that E2F1 requires SC35 to switch the alternative splicing profile of various apoptotic genes such as c-flip, caspases-8 and -9 and Bcl-x, towards the expression of pro-apoptotic splice variants. Finally, we provide evidence that E2F1 upregulates SC35 in response to DNA-damaging agents and show that SC35 is required for apoptosis in response to these drugs. Taken together, these results demonstrate that E2F1 controls pre-mRNA processing events to induce apoptosis and identify the SC35 SR protein as a key direct E2F1-target in this setting.
Fichier principal
Vignette du fichier
Merdzhanova et al.doc révisée.pdf (157.03 Ko) Télécharger le fichier
Origine : Fichiers produits par l'(les) auteur(s)

Dates et versions

inserm-02337603 , version 1 (29-10-2019)

Identifiants

Citer

Galina Merdzhanova, Valérie Edmond, Sandrine de Seranno, Arnaud van den Broeck, Laurent Corcos, et al.. E2F1 controls alternative splicing pattern of genes involved in apoptosis through upregulation of the splicing factor SC35.. Cell Death and Differentiation, 2008, 15 (12), pp.1815-1823. ⟨10.1038/cdd.2008.135⟩. ⟨inserm-02337603⟩
68 Consultations
79 Téléchargements

Altmetric

Partager

Gmail Facebook X LinkedIn More