HEMIBIOTROPHIC INFECTION OF SUNFLOWER ROOT CELLS BY THE PARASITE OROBANCHE CUMANA WALLR

The process of infection of different sunflower hybrids by Orobanche cumana was studied according to the way the pathogen interacts with the components of root cells. The study of the behavior of sunflower root cells during the penetration of Gaustoria showed not biotrophic, but hemibiotrophic process of infection of hybrids with the pathogen. In the hemibiotrophic mixed type of sunflower infection, broomrape initially develops as a biotrophic pathogen and, with the help of effectors, suppresses the course of immune reactions and forms multicellular haustoria, which at a certain stage of growth break the membrane bags of cells, leading to cytoplasmic leakage and causing the death of root cells as a necrotrophic pathogen. The discovery of the hemibiotrophic process of sunflower broomrape infection opens a new promising direction in reducing the infection of hybrids with the parasite through the induction of systemic acquired resistance (SAR) by drugs that cause the formation of reactive oxygen species and trigger plant defense responses through programmed cell death at the sites of infection and cause pathogen necrosis. The process of infection of cells and the emergence of reverse immune responses in plants when infected with pathogens has similar features and a similar course of protective responses. In the interaction between broomrape and sunflower, resistance mechanisms may act to stop the pathogen in the root cortex, in the entodermis, or after reaching the central cylinder. The cell wall is the first obstacle that pathogens have to overcome. The cell membranes of growing cells have a “primary” structure. Cell walls are composed of cellulose and matrix substances (hemicelluloses, pectins, and proteins). In cells that have already formed, the cell walls are reinforced with lignin, suberin, and kalose. Sunflower’s defense reactions against broomrape consist of strengthening the cell wall through the deposition of lignin, suberin, accumulation of callose, protective proteins and cross-linking of proteins that prevent the parasite from penetrating and communicating with the host vascular system. Lignin, suberin and callose polymers strengthen the cell wall structure by increasing its stiffness at the site of infection to limit the penetration of the parasite.