Time Course RNA-seq Reveals Soybean Responses against Root-Lesion Nematode and Resistance Players.
Valéria Stefania Lopes-Caitar, Rafael Bruno Guayato Nomura, Suellen Mika Hishinuma-Silva, Mayra Costa da Cruz Gallo de Carvalho, Ricardo Vilela Abdelnoor, Waldir Pereira Dias, Francismar Corrêa Marcelino-Guimarães
Author Information
Valéria Stefania Lopes-Caitar: Department of Biological Sciences, Universidade Estadual de Londrina (UEL), Londrina 86057-970, PR, Brazil.
Rafael Bruno Guayato Nomura: Brazilian Agricultural Research Corporation-Embrapa Soja, Londrina 86001-970, PR, Brazil.
Suellen Mika Hishinuma-Silva: Brazilian Agricultural Research Corporation-Embrapa Soja, Londrina 86001-970, PR, Brazil.
Mayra Costa da Cruz Gallo de Carvalho: Department of Biological Sciences, Universidade Estadual do Norte do Paraná (UENP), Bandeirantes 86360-000, PR, Brazil.
causes serious damage to soybean production and other crops worldwide. Plant molecular responses to RLN infection remain largely unknown and no resistance genes have been identified in soybean. In this study, we analyzed molecular responses to RLN infection in moderately resistant BRSGO (Chapadões-BRS) and susceptible TMG115 RR (TMG) genotypes. Differential expression analysis revealed two stages of response to RLN infection and a set of differentially expressed genes (DEGs) in the first stage suggested a pattern-triggered immunity (PTI) in both genotypes. The divergent time-point of DEGs between genotypes was observed four days post-infection, which included the activation of mitogen-activated protein kinase (MAPK) and plant-pathogen interaction genes in the BRS, suggesting the occurrence of an effector-triggered immunity response (ETI) in BRS. The co-expression analyses combined with single nucleotide polymorphism (SNP) uncovered a key element, a transcription factor phytochrome-interacting factor (PIF7) that is a potential regulator of moderate resistance to RLN infection. Two genes for resistance-related leucine-rich repeat (LRR) proteins were found as BRS-specific expressed genes. In addition, alternative splicing analysis revealed an intron retention in a myo-inositol oxygenase (MIOX) transcript, a gene related to susceptibility, may cause a loss of function in BRS.
