Small RNAs from the plant pathogenic fungus Sclerotinia sclerotiorum highlight host candidate genes associated with quantitative disease resistance

Abstract

Summary Fungal plant pathogens secrete effector proteins and metabolites to cause disease. Additionally, some species transfer small RNAs (sRNAs) into plant cells to silence host mRNAs through complementary base pairing and suppress plant immunity. The fungus Sclerotinia sclerotiorum infects over 600 plant species, but little is known about the molecular processes that govern interactions with its many hosts. In particular, evidence for the production of sRNAs by S. sclerotiorum during infection is lacking. We sequenced sRNAs produced by S. sclerotiorum in vitro and during infection of two host species, Arabidopsis thaliana and Phaseolus vulgaris . We found that S. sclerotiorum produces at least 374 distinct highly abundant sRNAs during infection, mostly originating from repeat‐rich plastic genomic regions. We predicted the targets of these sRNAs in A. thaliana and found that these genes were significantly more down‐regulated during infection than the rest of the genome. Predicted targets of S. sclerotiorum sRNAs in A. thaliana were enriched for functional domains associated with plant immunity and were more strongly associated with quantitative disease resistance in a genome‐wide association study (GWAS) than the rest of the genome. Mutants in A. thaliana predicted sRNA target genes SERK2 and SNAK2 were more susceptible to S. sclerotiorum than wild‐type, suggesting that S. sclerotiorum sRNAs may contribute to the silencing of immune components in plants. The prediction of fungal sRNA targets in plant genomes can be combined with other global approaches, such as GWAS, to assist in the identification of plant genes involved in quantitative disease resistance.

Small RNAs and extracellular vesicles: New mechanisms of cross-species communication and innovative tools for disease control

“…A panel of sRNAs from Verticillium dahliae , which causes Verticillium wilt in many plant hosts, also move into plant cells and associate with the host AGO1 protein to silence host genes involved in plant defense [4]. A genome-wide association study shows that the white mold fungal pathogen Sclerotinia sclerotiorum produces sRNAs that, to facilitate infection, can target plant genes associated with quantitative disease resistance [5]. A miRNA-like sRNA from Puccinia striiformis , the causal agent of the destructive wheat stripe rust, targets wheat pathogenesis-related genes and suppresses host immunity to achieve successful infection [3].…”

Application of small RNAs for plant protection

“…Известно, что на 5'-конце таких молекул присутствует уридин, который является важным элементом функционирования малых РНК патогенов в организмах растений [30][31][32][33][34][35]. Уридин, по-видимому, принимает участие в связывании малых РНК с определенным белком семейства Argonaut -AGO1 [36]. P. Baldrich и соавт.…”

“…Один из таких механизмов -синтез эффекторов, специфических белковых молекул, которые направленно действуют на определенные молекулярные структуры организма хозяина [46][47][48]. Недавно было открыто, что кроме белков схожими функциями могут обладать молекулы малых РНК, которые при попадании в организм хозяина подавляют экспрессию некоторых генов [36]. Вероятно, РНК-эффекторы в большинстве своем действуют против тех генов, которые являются ключевыми элементами врожденной иммунной системы хозяина.…”

“…Derbyshire и соавт. [36] отмечали, что гриб Sclerotinia sclerotiorum (Lib.) de Bary, поражающий огромное количество сельскохозяйственных культур, продуцирует в высокой концентрации малые РНК, направленные на подавление некоторых иммунных и сигнальных процессов в растениях.…”

Differential Alternative Splicing Genes and Isoform Regulation Networks of Rapeseed (Brassica napus L.) Infected with Sclerotinia sclerotiorum

“…Current research into SSR is mainly focused on the pathogenicity and resistance mechanisms involved. The outcome of SSR is the product of the interaction of multiple factors in both B. napus and S. sclerotiorum, resulting in a gradient of resistance phenotypes termed quantitative disease resistance [7][8][9]. The resistance strategy has been frequently explored using approaches such as genome-wide association studies [10], quantitative trait locus mapping [11], RNA sequencing (RNA-seq) [12] and the identification of relevant noncoding RNAs [13], resulting in the discovery of rare but highly effective factors.…”