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Title: Gene expression profiling describes the genetic regulation of Meloidogyne arenaria resistance in Arachis hypogaea and reveals a candidate gene for resistance

Author
item CLEVENGER, JOSH - University Of Georgia
item CHU, YE - University Of Georgia
item GUIMARAES, LARISSA - University Of Georgia
item MAIA, THIAGO - University Of Georgia
item BERTIOLI, DAVID - University Of Georgia
item LEAL-BERTIOLI, SORAYA - University Of Georgia
item Timper, Patricia - Patty
item Holbrook, Carl - Corley
item OZIAS-AKINS, PEGGY - University Of Georgia

Submitted to: Scientific Reports
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 3/20/2017
Publication Date: 5/21/2017
Citation: Clevenger, J., Chu, Y., Guimaraes, L., Maia, T., Bertioli, D., Leal-Bertioli, S., Timper, P., Holbrook Jr, C.C., Ozias-Akins, P. 2017. Gene expression profiling describes the genetic regulation of Meloidogyne arenaria resistance in Arachis hypogaea and reveals a candidate gene for resistance. Scientific Reports. 7:1317. doi:10.1038/s41598-017-00971-6.

Interpretive Summary: Resistance to root-knot nematode was bred into cultivated peanut from a wild peanut relative. The location of the resistance genes was previously mapped to chromosome A09. Two inbred peanut lines were developed (RIL 46 and RIL 4) from a cross between cv. Gregory (susceptible) and Tifguard (resistant). Each inbred line contains a unique resistance gene with RIL 46 being highly resistant and RIL 48 being moderately resistant to nematodes. Differential gene expression analysis was performed on the two inbred lines plus their parents using root tissue harvested from root-knot nematode infected plants at 0, 3, 7 days after inoculation. Differential gene expression analysis provides evidence that root-knot nematodes modulate biological pathways involved in plant hormone, defense, cell signaling, and cell wall metabolism in a susceptible reaction. Corresponding to the resistance reaction, an immune response induced by chemical signals from the nematode and mediated by the resistance gene was identified in Tifguard. Mapping of chromosome A09 indicated that 92% of the chromosome in Tifguard originated from the wild species. RIL46 and RIL 48 possessed 3.6% and 83.5% of wild species DNA on A09, respectively. Within the small region of wild DNA carried by RIL 46, a gene was identified as the candidate for nematode resistance. Potential defense pathways against root-knot nematodes include sequestering the chemical signals that the nematode uses to initiate its feeding site in the plant, triggering the native immune response in the plant, and production of mucilage which hinders the formation of the nematode feeding site.

Technical Abstract: Resistance to root-knot nematode was introgressed into cultivated peanut Arachis hypogaea from a wild peanut relative, A. cardenasii and previously mapped to chromosome A09. The highly resistant recombinant inbred RIL 46 and moderately resistant RIL 48 were selected from a population with cv. Gregory (susceptible) and Tifguard (resistant) as female and male parents, respectively. RNAseq analysis was performed on these four genotypes using root tissue harvested from root-knot nematode infected plants at 0, 3, 7 days after inoculation. Differential gene expression analysis provides evidence that root-knot nematodes modulate biological pathways involved in plant hormone, defense, cell signaling, cytoskeleton and cell wall metabolism in a susceptible reaction. Corresponding to resistance reaction, an effector-induced-immune response mediated by R-gene was identified in Tifguard. Mapping of the introgressed region indicated that 92% of linkage group A09 was of A. cardenasii origin in Tifguard. RIL46 and RIL 48 possessed 3.6% and 83.5% of the introgression on A09, respectively. Within the small introgressed region carried by RIL 46, a constitutively expressed TIR-NBSLRR gene was identified as the candidate for nematode resistance. Potential defense responsive pathways include effector endocytosis through clathrin-coated vesicle trafficking, defense signaling through membrane lipid metabolism and mucilage production.