Abstract
BackgroundMeloidogyne chitwoodi commonly known as Columbia root-knot nematode or CRKN is one of the most devastating pests of potato in the Pacific Northwest of the United States of America. In addition to the roots, it infects potato tubers causing internal as well as external defects, thereby reducing the market value of the crop. Commercial potato varieties with CRKN resistance are currently unavailable. Race specific resistance to CRKN has been introgressed from the wild, diploid potato species Solanum bulbocastanum into the tetraploid advanced selection PA99N82–4 but there is limited knowledge about the nature of its resistance mechanism. In the present study, we performed histological and differential gene expression profiling to understand the mode of action of introgressed CRKN resistance in PA99N82–4 in comparison to the CRKN susceptible variety Russet Burbank.ResultsHistological studies revealed that the nematode juveniles successfully infect both resistant and susceptible root tissue by 48 h post inoculation, but the host resistance response restricts nematode feeding site formation in PA99N82–4. Differential gene expression analysis shows that 1268, 1261, 1102 and 2753 genes were up-regulated in PA99N82–4 at 48 h, 7 days, 14 days and 21 days post inoculation respectively, of which 61 genes were common across all the time points. These genes mapped to plant-pathogen interaction, plant hormonal signaling, antioxidant activity and cell wall re-enforcement pathways annotated for potato.ConclusionThe introgressed nematode resistance in PA99N82–4 is in the form of both pattern-triggered immune response and effector-triggered immune response, which is mediated by accumulation of reactive oxygen species and hypersensitive response (HR). Salicylic acid is playing a major role in the HR. Polyamines and suberin (a component of the Casperian strip in roots) also play an important role in mediating the resistance response. The present study provides the first ever comprehensive insights into transcriptional changes among M. chitwoodi resistant and susceptible potato genotypes after nematode inoculation. The knowledge generated in the present study has implications in breeding for CRKN resistance in potato.
Highlights
Meloidogyne chitwoodi commonly known as Columbia root-knot nematode or CRKN is one of the most devastating pests of potato in the Pacific Northwest of the United States of America
In PA99N82–4, the nematodes entered the roots between 24 hpi and 48 dpi, but they did not progress in their life cycle beyond the J2 stage
When we searched our transcriptome data for Resistance gene (R-gene) and their signaling partners, we found RPM1, RSP2, SGT1, PIK1, EDS1, HSP90 upregulated in PA99N82–4
Summary
Meloidogyne chitwoodi commonly known as Columbia root-knot nematode or CRKN is one of the most devastating pests of potato in the Pacific Northwest of the United States of America. Meloidogyne chitwoodi Golden, O’Bannon, Santo & Finley commonly known as the Columbia root-knot nematode (CRKN) is one of the most severe pests of potato in the Pacific Northwest (PNW). This nematode was first reported in several areas in the PNW in 1977 [1] and populations flourish in the sandy soils of this major potato production region of the United States. Host genetic resistance is viewed as a more sustainable approach to control CRKN, but to date, there has been no commercial potato variety available with genetic resistance to CRKN
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