Fig. 8

Model for ROS in cell death regulation. Intracellular H₂O₂ production caused by the cat2 mutation lead to increased concentration of hormones (SA and JA, through SID2 and JAR1) and activation of multiple signaling pathways. The balance and timing of biosynthesis of auxin, SA and JA is one important determinant of cell death. In parallel, MPK signaling and other unknown signaling pathways may directly target TFs and regulate their activity and interaction with DNA with a subsequent change in gene expression. Other mechanisms in the nucleus also provide a suitable environment for accurate gene expression, including RCD1 that interacts with TFs. A yet to be identified regulator of cell death is farnesylated for proper function by ERA1. Extensive cross-talk between hormone signaling pathways allow fine tuning of the signal. Controlled ROS production via BAK1 and RBOHs may provide a signal to neighboring cells leading to propagation of cell death