Abstract
BackgroundPhytophthora root and stem rot (PRR) of soybean, caused by Phytophthora sojae, is controlled by Rps genes. However, little is known regarding the Rps-induced molecular responses to P. sojae and how they actually overlap. We thus sequenced, analyzed, and compared the transcriptomes of 10 near isogenic lines (NILs), each with a unique Rps gene/allele, and the susceptible parent Williams, pre- and post-inoculation with the pathogen.ResultsA total of 4,330 differentially expressed genes (DEGs) were identified in Williams versus 2,014 to 5,499 DEGs in individual NILs upon inoculation with the pathogen. Comparisons of the DEGs between the NILs and Williams identified incompatible interaction genes (IIGs) and compatible interaction genes (CIGs). Hierarchical cluster and heatmap analyses consistently grouped the NILs into three clusters: Cluster I (Rps1-a), Cluster II (Rps1-b, 1-c and 1-k) and Cluster III (Rps3-a, 3-b, 3-c, 4, 5, and 6), suggesting an overlap in Rps-induced defense signaling among certain NILs. Gene ontology (GO) analysis revealed associations between members of the WRKY family and incompatible reactions and between a number of phytohormone signaling pathways and incompatible/compatible interactions. These associations appear to be distinguished according to the NIL clusters.ConclusionsThis study characterized genes and multiple branches of putative regulatory networks associated with resistance to P. sojae in ten soybean NILs, and depicted functional “fingerprints” of individual Rps-mediated resistance responses through comparative transcriptomic analysis. Of particular interest are dramatic variations of detected DEGs, putatively involved in ethylene (ET)-, jasmonic acid (JA)-, (reactive oxygen species) ROS-, and (MAP-kinase) MAPK- signaling, among these soybean NILs, implicating their important roles of these signaling in differentiating molecular defense responses. We hypothesize that different timing and robustness in defense signaling to the same pathogen may be largely responsible for such variations.
Highlights
Phytophthora root and stem rot (PRR) of soybean, caused by Phytophthora sojae, is controlled by Rps genes
Symptom development in 10 near isogenic lines (NILs) and the recurrent susceptible parent inoculated with P. sojae The 10 soybean NILs carrying Rps1-a, Rps1-b, Rps1-c, Rps1-k, Rps3-a, Rps3-b, Rps3-c, Rps4, Rps5, or Rps6, within the Williams background, provided a unique resource for investigating the common and specific defense responses mediated by individual Rps genes against P. sojae (Additional file 1)
NILs containing Rps3-a, Rps3-b, Rps3-c, Rps5 and Rps6 showed a slight variation in the proportion of surviving seedlings across the three replicates, which may be attributed to minor differences in environmental conditions
Summary
Phytophthora root and stem rot (PRR) of soybean, caused by Phytophthora sojae, is controlled by Rps genes. PRR is caused by the soil-borne, hemibiotrophic pathogen Phytophthora sojae, and is most effectively controlled by Rps (Resistance to P. sojae) genes. Like most resistance (R) genes, the Rps gene family encodes, or is predicted to encode nucleotide binding leucine rich repeat (NB-LRR)-type proteins [6,7,8], which are able to recognize the Avr effector proteins of pathogens directly or indirectly to induce the appropriate defense response [9,10]. In these cases, the R protein appears to require the existence of a ‘guard protein’ or ‘decoy’ in order to recognize an Avr protein [12,13]. SYRINGAE 2) proteins in Arabidopsis [14,15]
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