Fig. 3: Model for the mechanism by which cAMP/PKA, Pmk1, and TOR signalling pathways regulate regulated cell death and appressorium-mediated plant infection by M. oryzae.

Appressorium initiation and conidium cell death are regulated by three core signalling pathways; the cAMP/PKA, Pmk1, and TOR signalling pathways. Surface cues, including hydrophobicity and surface hardness, are perceived by upstream components of the cAMP/PKA and Pmk1 signalling pathways, Pth11, Msb2, and Sho1. Activation of cAMP/CPKA is required for surface recognition and turgor generation. Pmk1 MAPK activation is necessary to initiate appressorium development, requiring an S-phase cell-cycle checkpoint. The absence of nutrients on the host surface suppresses TOR activity (TOROFF) via glucose- and glutamine-responsive Abl1 and Asd4, respectively. TOR inactivation arrests the cell cycle in G2 to initiate appressorium maturation and de-represses cargo-dependent autophagy. The autophagic breakdown and mobilization of conidial storage products into the appressorium cell supplies the structure with substrates for turgor generation. The autophagic-dependent release of iron (from an unknown source) then facilitates production of reactive oxygen species (ROS) which leads to generation of lipid peroxides to lethal concentrations, leading to ferroptotic cell death, which is necessary for appressorium function. Figure created with BioRender.com (https://BioRender.com/p83g790).