Project description:Death-promoting transcription factor Btf has been reportedly implicated in the apoptotic signal triggered by ionizing radiation, DNA damage-inducing agents, and cyclic stretch. However, mechanisms for the regulation of Btf-mediated apoptosis remain largely unknown. In the present study, we performed genome-wide mRNA expression profiling from Btf-depleted Hela cells and identified SMAD3 as a potential downstream target of Btf. Btf interacted with the SMAD3 promoter and this interaction was associated with the activation of SMAD3 gene transcription. Furthermore, we provided evidence that SMAD3 is involved in the induction of apoptosis, and that the disruption of Btf-mediated SMAD3 expression leads to resistance to DNA damage-induced apoptosis
Project description:Here we show that depletion of the homologous non-classical serine-arginine-rich (SR) splicing factors Btf (BCLAF1) and TRAP150 causes mitotic defects. We propose that, in addition to their previously reported roles in maintaining mRNA distribution, Btf and TRAP150 control abundance of transcripts encoding mitotic regulators thereby affecting mitotic progression in human cells.
