cAMP Signaling in M. grisea
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cAMP Signaling in M. grisea

cAMP (Cyclic Adenosine 3,5-monophosphate) signaling regulates appressorium formation in the Rice Blast fungus M. grisea (Magnaporthe grisea). Both saprophytic and pathogenic growth of M. grisea is regulated by AC (Adenylate Cyclase)/Mac1 but different effectors of cAMP mediate downstream effects specific for either cell morphogenesis or pathogenesis. M. grisea causes a devasting fungal disease of rice plants known as Rice Blast through appressorium (or infection tube) formation. cAMP mediates its effect on appressorium formation through PKA (Protein Kinase-A). A well-characterized intracellular target of cAMP in eukaryotic cells is the Regulatory subunit of PKA (Ref.1). The cAMP signaling which is required for growth and pathogenesis in M. grisea diverges at the level of PKA regulation. How external inductive signals are perceived by M. grisea is not yet clear, but it is clear that a cAMP-dependent signal transduction pathway is involved in appressorium formation. cAMP induces M. grisea germinating conidia or vegetative mycelia to produce appressoria on non-inductive surfaces. In M. grisea, surface hydrophobicity and hardness, adhesion and other environmental factors regulate appressorium formation. Mpg1 (Hydrophobin-Like Protein-Mpg1) is a fungal hydrophobin that is abundantly expressed during appressorium formation, symptom development and conidiation. Mpg1 aids in attachment, infection site preparation or topological signaling (Ref.2). In M. grisea, the G-proteins Magb/GBA1 (Guanine Nucleotide-Binding Protein-Alpha Subunit) and Mgb1 (a heterotrimeric G-Protein-Beta Subunit) serve as critical transducers between activated cell surface receptors and intracellular effectors. The G-proteins are depicted activating AC/Mac1. AC/Mac1 helps the fungi to form appressoria on a hydrophobic surface of rice leaves by enhancing cAMP production from ATP (Adenosine Triphosphate) (Ref.3).

Binding of cAMP to the Regulatory Subunit, Sum1 (cAMP-Dependent Protein Kinase Regulatory Subunit)/RPKA (PKA Regulatory Subunit) releases the Catalytic kinase subunits (CpkA and Cpk2), to phosphorylate the target proteins involved in cAMP-regulated processes. Hence inactivation of the Regulatory subunit activates the two catalytic PKA subunits in M. grisea. PKA as well as the G-proteins of M. grisea, regulate the components involved in the MAPK (Mitogen-Activated Protein Kinase) cascade. M. grisea pathogenicity protein PMK1 (Pathogenicity MAP Kinase-1) is essential for pathogenicity and is also required for invasive growth and viability in the host. On a hydrophilic surface in response to cAMP, PMK1 and MKK1 (MAP Kinase Kinase-1) activation, functions in parallel with cAMP-dependent signaling. Another MAPK, Mps1 (MAP Kinase-Mps1) is involved in cell wall integrity and helps the pathogen penetrate plant cell surfaces (Ref.4). To penetrate the plant cuticle, M. grisea generates Turgor pressures in excess. Pathogenesis in the rice blast fungus M. grisea reveals that heterotrimeric GTP-binding proteins, MAPK and cAMP signaling elements play essential roles in pathogenic morphogenesis. Genetic experiments indicate that these elements are involved in multiple pathways. The interesting questions that remain are how the cell perceives the environmental signals and specifies the signaling responses. To address these issues, upstream components such as receptor(s) and downstream targets of these pathways need to be identified and characterized (Ref.5).