Molecular interaction of charcoal rot pathogenesis in soybean: a complex interaction

Charcoal rot (CR) is a major disease of soybean, which is caused by Macrophomina phaseolina (Mp). Increasing temperatures and low rainfall in recent years have immensely benefitted the pathogen. Hence, the search for genetically acquired resistance to this pathogen is essential. The pathogen is a hemibiotroph, which germinates on the root surface and colonizes epidermal tissue. Several surface receptors initiate pathogenesis, followed by the secretion of various enzymes that provide entry to host tissue. Several enzymes and other converging cascades in the pathogen participate against host defensive responses. β-glucan of the fungal cell wall is recognized as MAMPs (microbe-associated molecular patterns) in plants, which trigger host immune responses. Kinase receptors, resistance, and pathogenesis-related genes correspond to host defense response. They work in conjunction with hormone-mediated defense pathway especially, the systemic acquired resistance, calcium-signaling, and production of phytoalexins. Due to its quantitative nature, limited QTLs have been identified in soybean for CR resistance. The present review attempts to provide a functional link between M. phaseolina pathogenicity and soybean responses. Elucidation of CR resistance responses would facilitate improved designing of breeding programs, and may help in the selection of corresponding genes to introgress CR resistant traits.