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ARS Home » Northeast Area » Beltsville, Maryland (BARC) » Beltsville Agricultural Research Center » Molecular Plant Pathology Laboratory » Research » Publications at this Location » Publication #337812

Title: Rhizoctonia resistance conferred by a sugar beet polygalacturonase-inhibiting protein gene

item Li, Haiyan
item Hanson, Linda
item Smigocki, Anna

Submitted to: American Society of Sugar Beet Technologists
Publication Type: Research Technical Update
Publication Acceptance Date: 2/3/2017
Publication Date: 6/3/2017
Citation: Li, H., Hanson, L.E., Smigocki, A.C. 2017. Rhizoctonia resistance conferred by a sugar beet polygalacturonase-inhibiting protein gene. American Society of Sugar Beet Technologists.

Interpretive Summary: Rhizoctonia solani is a pathogenic fungus with a wide host range and worldwide distribution causing diseases in commercially important crops such as sugar beet, soybean, potato and rice. During plant attack, the fungus releases many degradative enzymes to macerate host tissues, among them endopolygalacturonase (PG) that breaks down plant cell walls. For self-protection, plants produce antimicrobial compounds such as polygalacturonase-inhibiting protein (PGIP) to inhibit fungal PGs. Role of sugar beet PGIP proteins in fungal resistance is not known. We isolated sugar beet PGIP genes and transferred them into tobacco plants to test PGIP function in fungal resistance. We determined that sugar beet PGIP proteins protected tobacco plants against two highly virulent fungal strains. We propose that sugar beet PGIPs may provide fungal disease control in plants. Scientists and breeders will use this information to develop improved crops with disease resistance that will increase yields, reduce usage of harmful pesticide and provide safer produce for the consumer.

Technical Abstract: Polygalacturonase-inhibiting proteins (PGIPs) are cell wall leucine-rich repeat (LRR) proteins recognized as having a role in plant defense. PGIPs inhibit fungal polygalacturonase (PG) enzymes that break down the polygalacturonate chain in plant cell walls to initiate disease development. The interaction between PGs and plant PGIPs favors the accumulation of oligogalacturonides which elicit a wide range of plant defense responses. We cloned sugar beet PGIP (BvPGIP) genes from F1016, a root maggot resistant germplasm, and F1010, a susceptible line in order to define their function in disease resistance mechanisms. BvPGIP1 was shown to be unique in F1016. BvPGIP2, cloned from F1016 and F1010, was shown to differ from BvPGIP1 in eight amino acids. BvPGIP1and BvPGIP2 were each reconstructed for constitutive expression and introduced separately into Nicotiana benthamiana. Independently derived transgenic plants were identified by genomic PCR, Southern blot and RT-PCR analyses. Plants exhibiting high levels of expression were infected with Rhizoctonia solani AG2-2 isolate R1 or AG4 isolate Rzc27, isolated from sugar beet . Two weeks post-inoculation with fungal-colonized barley grains, stem rot and seedling death were significantly reduced on transgenic BvPGIP1 and BvPGIP2 plants as compared to the controls. With AG2-2, seedling death was reduced by 70% - 82% on BvPGIP1 and BvPGIP2 , and with AG4, by 50% on BvPGIP1 plants. No enhanced resistance was seen with AG4 on BvPGIP2 plants. These initial results suggest that sugar beet BvPGIP genes play an important role in plant defense and could provide an approach for controlling fungal diseases in sugar beet and other crops.