|WILLIAMSON-BENAVIDES, BRUCE - WASHINGTON STATE UNIVERSITY|
|SHARPE, RICHARD - WASHINGTON STATE UNIVERSITY|
|NELSON, GRANT - WASHINGTON STATE UNIVERSITY|
|BODAH, ELAINE - CONSULTANT|
|DHINGRA, AMIT - WASHINGTON STATE UNIVERSITY|
Submitted to: Frontiers in Genetics
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 7/29/2020
Publication Date: 8/18/2020
Citation: Williamson-Benavides, B.A., Sharpe, R., Nelson, G., Bodah, E.T., Porter, L.D., Dhingra, A. 2020. Identification of Fusaruim solani f. sp. pisi (Fsp) responsive genes in Pisum sativum. Frontiers in Genetics. 11. Article 950. https://doi.org/10.3389/fgene.2020.00950.
Interpretive Summary: Peas are a fast emerging, inexpensive and major contributor to the plant-based protein market. Due to the short life cycle of pea plants, the ability of pea roots to fix nitrogen and low water usage, pea is a useful rotation or cover crop that requires minimal inputs. Peas are critical for sustainable agriculture and future food security. Root rot of pea caused by the fungal pathogen Fusarium solani f. sp. pisi (Fsp) can result in a 15 to 60% reduction in yield. The identification and function of genes associated with resistance to Fsp needs to be understood to develop resistant cultivars. The present research determined how genes of Fsp-resistant and susceptible pea plants respond differently to infection over time and the difference in how genes involved in resistant or susceptible reaction are expressed. There were 42,905 genes differentially expressed between resistant and susceptible pea plants. Interestingly, the vast majority of gene expressions were in the susceptible lines at all sampling time points, rather than in resistant lines. Genes associated with susceptible responses to Fsp involved genes that function in cell absorbtion of metabolites, hormones and proteins; sugar transporters; the synthesis of salicylic acid, which is a common plant defense compound, and genes involved in cell death. In tolerant lines, genes involved in secretion of products from cells, and compounds involved in plant defense mechanisms, such as anthocyanins and defense proteins, were overexpressed. The research has identified a set of genes to evaluate for resistance in pea to Fusarium root rot.
Technical Abstract: Pisum sativum (pea) is fast emerging as an inexpensive and major contributor to the plant-derived protein market. Due to its nitrogen-fixing capability, short life cycle, and low water usage, pea is a useful cover-and-break crop that requires minimal external inputs. It is critical for sustainable agriculture and indispensable for future food security. Root rot of pea caused by the fungal pathogen, Fusarium solani f. sp. pisi (Fsp), results in a 15- 60% reduction in yield. The molecular basis of tolerance of pea to Fsp needs to be urgently understood to develop Fsp-tolerant or resistant cultivars. A complementary genetics and gene expression approach was undertaken in this study to identify Fsp-responsive genes in four tolerant and four susceptible pea genotypes. Time course RNA-seq was performed on both sets of genotypes after Fsp challenge. Analysis of the transcriptome data resulted in the identification of 42,905 differentially expressed contigs (DECs). Interestingly, the vast majority of DECs were overexpressed in the susceptible genotypes at all sampling time points, rather than in the tolerant genotypes. Gene expression and GO enrichment analysis revealed genes coding for receptor-mediated endocytosis, sugar transporters, salicylic acid synthesis and signaling, and cell death were overexpressed in the susceptible genotypes. In the tolerant genotypes, genes involved in exocytosis, and secretion by cell, the anthocyanin synthesis pathway as well as the DRR230 gene, a pathogenesis-related (PR) gene, were overexpressed. The complementary genetic and RNAseq approach has yielded a set of potential genes that could be targeted for improved tolerance against root rot in P. sativum. Fsp challenge produced a futile transcriptomic response in the susceptible genotypes. This type of response is hypothesized to be related to the speed at which the pathogen infestations advances in the susceptible genotypes, and the preexisting level of disease-preparedness in the tolerant genotypes.