|MAHNAZ, RASHIDI - University Of Idaho|
|Novy, Richard - Rich|
|RASHED, ARASH - University Of Idaho|
Submitted to: Phytopathology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 8/15/2017
Publication Date: 9/1/2017
Citation: Mahnaz, R., Novy, R.G., Wallis, C.M., Rashed, A. 2017. Characterization of host plant resistance to zebra chip disease from species-derived potato genotypes and the identification of new sources of zebra chip resistance. Phytopathology. 12(8): e0183283.
Interpretive Summary: Zebra chip disease (ZC), caused by ‘Candidatus Liberibacter solanacearum’(Lso), is a major threat to potato production in North America, Central America, and New Zealand. Long-term management requires the use of Lso-infection tolerant or resistant potato cultivars, although none are yet commercially available. This study assessed 11 potato breeding lines for relative expression of tolerance and resistance, as measured by reduced symptom development or Lso titers, respectively, compared to a highly susceptible commercial cultivar Russet Burbank. Three of these breeding lines, all with the A07781 background, had relative lower symptom expression and lower Lso titers than Russet Burbank. Therefore, these could be used to impart increased ZC resistance in future potato cultivars.
Technical Abstract: ‘Candidatus Liberibacter solanacearum’ (Lso), an uncultivable phloem-limited phytopathogenic bacterium, is known to be associated with Zebra Chip disease (ZC), which represents a major threat to potato production in the US and elsewhere. This pathogen is transmitted by the phloem-feeding potato psyllid, Bactericera cockerelli Sulc (Hem. Triozidae). Currently, there are no reports of resistance to ZC in cultivated potatoes. This greenhouse study was conducted to evaluate ZC susceptibility of 11 potato breeding clones, representing diverse genetic background, to ZC, in relation to a susceptible commercial cultivar, Russet Burbank.Individual plants were exposed to two Lso-positive potato psyllids for 48 hours. The percentage of successful Lso transmission varied across genotypes, ranging between 7 and 57%. Freshly-cut and fried tubers showed significant variation in ZC symptom severity among the breeding clones, with several genotypes expressing relative tolerance when compared to Russet Burbank. None of the evaluated clones showed statistically lower Lso titers than Russet Burbank with the exception of one genotype in the second year of the study. However, the presence of a non-significant relationship between average symptom severity and Lso titer indicated variations in phenotypic responses (i.e., tolerance) to Lso existed among evaluated breeding lines. Breeding clones A07781-3LB, A07781-4LB and A07781-10LB had relatively lower Lso titer (low susceptibility) and tuber symptom expression (high tolerance) among the tested genotypes. These three clones represent full siblings, indicative of a possible genetic basis of resistance/tolerance to ZC. Findings provide a better understanding of resistance/tolerance to ZC, and contribute to continued efforts in breeding for resistance to this disease.