Page 194 - PC2019 Program & Proceedings
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PLANT CANADA 2019

               S173. Implication of major tuber flesh proteins in common scab resistance in Russet Burbank
               somaclonal variant adapted to thaxtomin A
                          *
               Isayenka, I. ; N. Beaudoin
               University of Sherbrooke

               Potato common scab is a widely spread disease of potato tubers inducing significant economic losses.
               Mechanism of potato resistance to common scab is not understood. Common scab is caused by the
               actinobacterium Streptomyces scabies. Pathogenicity of S. scabies depends on its ability to produce a
               phytotoxin thaxtomin A (TA). TA mode of action remains unknown although it was described as a
               cellulose biosynthesis inhibitor that induces programmed cell death. The somaclone variant RB9, which
               was produced by the adaptation of the Russet Burbank cultivar to TA, is more resistant to common scab.
               LC-MS/MS analysis showed that increased resistance was associated with changes in the RB9 tuber
               proteome. Changes included increased accumulation of major tuber proteins: storage proteins (patatins),
               proteins implicated in lipid metabolism (9-lipoxygenases, 9-LOX) and serine protease inhibitors (Kunitz-
               type, KTI). Gene expression analysis (qPCR) showed significantly higher expression of the KTI coding
               DrTI-like gene in RB9. Higher abundance of patatin in RB9 was associated with enhanced expression of
               PATB1 gene and of different RB9 patatin coding loci. 9-LOX protein accumulation was not associated
               with increased 9-LOX gene expression, suggesting regulation at the protein level. During infection of RB
               and RB9 young developing tubers, we detected a significant decrease in patatin and KTI abundance in the
               parental cultivar comparing to RB9. At the same time, 9-LOX was highly accumulated in infected RB and
               RB9 tubers.


               Iauhenia Isayenka (Iauhenia.Isayenka@USherbrooke.ca)


               S174. Biosynthesis of the thaxtomin A phytotoxin in the potato common scab pathogen
               Streptomyces scabies: role of the MbtH-like protein TxtH
               Li, Y.; J. Liu; D. Adekunle; L. Bown; K. Tahlan; Bignell, D.
               Memorial University of Newfoundland

               Common scab (CS) is a disease that negatively impacts the quality and market value of seed, processing
               and table stock potatoes. The disease is caused by Streptomyces soil bacteria, of which
               Streptomyces scabies is the first described and best characterized pathogenic species. The principle
               pathogenicity determinant produced by S. scabies is a phytotoxic metabolite called thaxtomin A (ThxA),
               which functions as a plant cellulose biosynthesis inhibitor. The enzymes requires for the biosynthesis of
               ThxA are all encoded within a biosynthetic gene cluster in S. scabies. In addition, the gene cluster
               encodes a small protein called TxtH, which belongs to the MbtH-like protein (MLP) family. The
               objective of this study was to investigate the role of TxtH in the biosynthesis of ThxA in S. scabies.
               Biochemical studies in Escherichia coli revealed that TxtH functions as a chaperone that is required for
               the proper function of the megasynthase enzymes which synthesize the ThxA backbone. Deletion of the
               txtH gene significantly reduced ThxA production in S. scabies, while deletion of two other MLP-encoding
               genes in the S. scabies genome abolished ThxA production completely. The txtH single mutant and the
               MLP triple mutant were reduced in virulence in a potato tuber bioassay compared to the wild-type strain.
               Overall, the results our study demonstrate that TxtH plays a key role in ThxA biosynthesis and plant
               pathogenicity in S. scabies.

               Dawn Bignell (dbignell@mun.ca)









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