Fig. 7. A model for ROS-induced apoptosis in cells devoid of selD/sps1. We propose that the increase in ROS caused by the selD^ptuf mutation leads to stabilization of Dmp53 and activation of Rpr caspase-dependent apoptosis. We cannot discount the possibility that other pathways such Ras/MAPK downregulation or a ROS-induced caspase-independent pathway may have a minor contribution to selD^ptuf apoptosis.

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