Download or read book Genetic and Functional Characterization of the Host-Pathogen Interactions Underlying the Barley-Net Form Net Blotch Pathosystem written by Karl Martin Effertz and published by . This book was released on 2023 with total page 0 pages. Available in PDF, EPUB and Kindle. Book excerpt: Net blotch is a disease of barley that causes significant yield and quality loss throughout global barley growing regions. This disease is caused by the necrotrophic fungal pathogen Pyrenophora teres and presents in two distinct forms that differ in genetic structure and macroscopic lesion patterns: net form net blotch (NFNB) caused by Pyrenophora teres f. teres (Ptt), and spot form net blotch (SFNB) caused by Pyrenophora teres f. maculata (Ptm). While predominantly known as diseases of barley, multiple populations of both Ptt and Ptm have been recently found to infect wheat, representing a host jump that could impact wheat production in the future. The data presented here focuses on the host-pathogen interactions underlying resistance and susceptibility to Ptt, with a particular emphasis on the resistance to Pyrenophora teres 5 (Rpt5) - susceptibility to Pyrenophora teres 1 (Spt1) locus that has been previously shown to be highly important in this pathosystem. Association mapping of Ptt resistance in the wild barley diversity collection (WBDC) identified 18 unique loci associated with resistance to four distinct Ptt isolates, three of which are novel loci that were previously unmapped. High-resolution mapping of the Rpt5 locus resulted in the identification of a strong candidate gene encoding a receptor-like protein (RLP), which was subsequently validated as the first resistance gene cloned in this pathosystem. Functional characterization of this RLP identified an interaction with a putative effector, Ptt nuclear localization signal 1 (PttNLS1), which was found to suppress the expression of host pathogenesis-related (PR) genes and is a strong candidate for the Rpt5 avirulence protein (Avr-Rpt5). High-resolution mapping data across multiple independent populations reveals that Rpt5 and Spt1 map to the same genomic location, and allele analysis suggests that perhaps these two distinct phenotypes are caused by the same RLP encoding gene in an allele specific manner. Finally, we propose a functional model suggesting that the Rpt5/Spt1 locus evolved as a PR protein monitoring system and an evolutionary model revealing the host-pathogen co-evolutionary arms race underlying this economically important pathosystem.