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E2F1 controls alternative splicing pattern of genes involved in apoptosis through upregulation of the splicing factor SC35
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E2F1 controls alternative splicing pattern of genes involved in apoptosis through upregulation of the splicing factor SC35
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Journal Article
E2F1 controls alternative splicing pattern of genes involved in apoptosis through upregulation of the splicing factor SC35
2008
Overview
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.
Publisher
Nature Publishing Group UK,Nature Publishing Group
Subject
/ Alternative Splicing - drug effects
/ Alternative Splicing - genetics
/ Animals
/ Biochemistry, Molecular Biology
/ Biomedical and Life Sciences
/ CASP8 and FADD-Like Apoptosis Regulating Protein
/ CASP8 and FADD-Like Apoptosis Regulating Protein - metabolism
/ Cyclophosphamide - pharmacology
/ E2F1 Transcription Factor - metabolism
/ Gene Expression Regulation - drug effects
/ Genes
/ Humans
/ Ligands
/ Mice
/ Nuclear Proteins - metabolism
/ Protein Binding - drug effects
/ Proteins
/ Ribonucleoproteins - genetics
/ Ribonucleoproteins - metabolism
/ Serine-Arginine Splicing Factors
/ Transcription, Genetic - drug effects
