RNAseq analysis reveals the role of secondary metabolism in the response of URS 21, a race‐nonspecific resistant cultivar, to crown rust

Abstract

Crown rust (Puccinia coronata f. sp. avenae) can devastate oats (Avena sativa). Plants possessing durable resistance are desirable and they may contain mechanisms that differ from those underlying genes with specific effects. Gathering information about the molecular mechanisms involved, especially those not associated with the hypersensitive reaction, and combining those acting at different infection stages may increase the ability to defeat the pathogen. The cultivar URS 21 has strongly reduced the intensity and growth of crown rust for the last 14 years, demonstrating durable racenonspecific resistance expressed at adult and seedling stages. The main objective of this study was to identify, by deep sequencing, oat transcripts induced by P. coronata in the URS 21 cultivar inoculated at seedling stage. Two important reactions to inoculation, secondary metabolism and the oxidative response, were studied further. The expression of specific genes associated with biosynthesis of secondary metabolites was evaluated in adult plants by RT-PCR, as well as the accumulation of saponins and avenanthramides, found to be important in other pathosystems, and comparisons were made with the susceptible cultivar URS 22. The URS 21 resistance mechanism probably involves several components including the biosynthesis of avenanthramides and steroid saponins; also, several genes related to antioxidative stress were down-regulated. A large number of oat sequences were generated by RNA-seq analysis in this study, which will help in the search for genes involved in the race-nonspecific resistance; they may also be useful in the development of markers to search for QTLs associated with race-nonspecific resistance.

Crown rust on oat genotypes with different levels of resistance: damages and losses

“…URS 22, released in 2001 as immune, had its resistance overcame in a short time, exhibiting high susceptibility since. Similarly, URS 21, released at the same year as immune, kept that immunity for only a few years but, in contrast to URS 22, showed a high level of race-non-specific resistance, which was durable, sensu JOHNSON (1981), in the field for at least 14 years (FIGUEIRÓ et al, 2017).…”