Abstract
Resistance genes are an effective means for disease control in plants. They predominantly function by inducing a hypersensitive reaction, which results in localized cell death restricting pathogen spread. Some resistance genes elicit an atypical response, termed extreme resistance, where resistance is not associated with a hypersensitive reaction and its standard defense responses. Unlike hypersensitive reaction, the molecular regulatory mechanism(s) underlying extreme resistance is largely unexplored. One of the few known, naturally occurring, instances of extreme resistance is resistance derived from the soybean Rsv3 gene, which confers resistance against the most virulent Soybean mosaic virus strains. To discern the regulatory mechanism underlying Rsv3-mediated extreme resistance, we generated a gene regulatory network using transcriptomic data from time course comparisons of Soybean mosaic virus-G7-inoculated resistant (L29, Rsv3-genotype) and susceptible (Williams82, rsv3-genotype) soybean cultivars. Our results show Rsv3 begins mounting a defense by 6 hpi via a complex phytohormone network, where abscisic acid, cytokinin, jasmonic acid, and salicylic acid pathways are suppressed. We identified putative regulatory interactions between transcription factors and genes in phytohormone regulatory pathways, which is consistent with the demonstrated involvement of these pathways in Rsv3-mediated resistance. One such transcription factor identified as a putative transcriptional regulator was MYC2 encoded by Glyma.07G051500. Known as a master regulator of abscisic acid and jasmonic acid signaling, MYC2 specifically recognizes the G-box motif (“CACGTG”), which was significantly enriched in our data among differentially expressed genes implicated in abscisic acid- and jasmonic acid-related activities. This suggests an important role for Glyma.07G051500 in abscisic acid- and jasmonic acid-derived defense signaling in Rsv3. Resultantly, the findings from our network offer insights into genes and biological pathways underlying the molecular defense mechanism of Rsv3-mediated extreme resistance against Soybean mosaic virus. The computational pipeline used to reconstruct the gene regulatory network in this study is freely available at https://github.com/LiLabAtVT/rsv3-network.
Highlights
Soybean is a crop of global importance, and the Soybean mosaic virus (SMV)-soybean pathosystem provides an opportunity to study the extreme resistance (ER) response, a type of resistance unique from the typical hypersensitive reaction (HR) response in that it is triggered earlier and cell death is not observed [1]
This was accomplished by implementing machine learning inference algorithms on a gene regulatory networks (GRNs) constructed from time course RNA sequencing (RNA-seq) data from leaves of SMV-G7 inoculated resistant and susceptible soybean cultivars, L29 and Williams82, respectively
1128 genes were differentially expressed between two cultivars, at one or more time points between 2 and 8 hpi (S1 Table); differentially expressed genes (DEGs) identified at 0 hpi were excluded, as they were considered effects from differences in genetic backgrounds between the two cultivars
Summary
Soybean is a crop of global importance, and the Soybean mosaic virus (SMV)-soybean pathosystem provides an opportunity to study the extreme resistance (ER) response, a type of resistance unique from the typical hypersensitive reaction (HR) response in that it is triggered earlier and cell death is not observed [1]. Comparative sequence analysis has revealed that Glyma.14g204700 is highly polymorphic in the LRR domain of soybean lines carrying Rsv. Comparative sequence analysis has revealed that Glyma.14g204700 is highly polymorphic in the LRR domain of soybean lines carrying Rsv3 This suggests Rsv3-mediated resistance is initiated by the LRR domain’s recognition of an effector, the SMV cylindrical inclusion protein (CI) [12, 14]. The events directly following recognition remain undefined It is hypothesized in [15] that the abscisic acid (ABA) signaling pathway is triggered during later stages of the Rsv3-mediated ER response. A large gap remains in our understanding of the Rsv3-mediated ER response, as the initial molecular events occurring prior to activation of the ABA signaling pathway are still unknown
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