Fig. 7: Model of ZmMYB98 controlled synergid cell functions and subsequent ZmRALF12 induced persistent synergid PCD after fertilization.
From: Fertilization-induced synergid cell death by RALF12-triggered ROS production and ethylene signaling
a Before fertilization, ZmMYB98 positively regulates most highly expressed synergid-specific/predominant genes required for pollen tube attraction and reception as well as cell wall modification. b After successful double fertilization, ZmMYB98 and its associated gene regulatory network (GRN) are downregulated, while a GRN is activated leading to RALF12 signaling culminating in high levels of mitochondrial ROS accumulation at the filiform apparatus adjacent region, oxidative stress, mitophagy, and synergid apoptosis. Activated ethylene biosynthesis further promotes sensitized synergid cell death. RALF12-mediated mitochondrial oxidative stress and ethylene biosynthesis can individually trigger synergid cell death, while they work synergistically to efficiently activate PCD TFs and PCD executors for persistent synergid nucleus and whole-cell elimination. Vacuole rupture as well as cell intercalation mediated by VPEγ and CEP1 likely contribute to synergid-endosperm (SE) fusion. c Schematic model of the GRN leading to persistent synergid PCD.
