Search

With 2 figures and 2 tables The purpose of this research was to identify the genetic basis of foliar and tuber resistance to Phytophthora infestans in a potato breeding population developed from a cross between two tetraploid Solanum tuberosum lines, NY121 and NY115. The parent with high foliar resistance, NY121, was highly susceptible to tuber blight. Foliar resistance was assessed in field trials, while tuber blight was assessed both in the field and in the laboratory. A quantitative trait locus (QTL) explaining ca. 50% of the phenotypic variance for foliar resistance was located on the lower arm of linkage group V, and was loosely associated with tuber blight resistance (significantly in one of two trials). This QTL was confirmed in a separate sample from the same population. Tuber blight detected via laboratory assays was not correlated with tuber blight incidence in the field. Most markers associated with tuber blight resistance were not associated with foliar resistance and most markers associated with foliar resistance were not associated with tuber blight resistance. [ABSTRACT FROM AUTHOR]

Abstract: Several phosphonate biopesticides were evaluated in three field trials over 2 years for efficacy in suppressing tuber infections caused by Phytophthora infestans. Tuber disease was assessed at harvest and (for two trials) after 2 months in storage; foliar disease was assessed during the growing season. The phosphonates were dipotassium phosphonate–dipotassium phosphate; mono- and dipotassium phosphorous acid, potassium phosphite; mono- and dibasic sodium, potassium and ammonium phosphites; and aluminum tris O-ethyl phosphonate. Each phosphonate was applied at weekly intervals to the foliage. Additionally some phosphonates were applied in combination with, or in alternation with a conventional fungicide. Although tuber blight was highly variable in these small plots, tubers from plots treated with phosphonates generally had less tuber blight relative to tubers from plots treated with chlorothalonil. The effect on tuber blight was particularly visible after 2 months in storage. All phosphonates applied alone or in combination with chlorothalonil suppressed foliar disease. [Copyright &y& Elsevier]

Phytophthora infestans, the causal agent of late blight, threatens potato production worldwide. An important tool in the management of the disease is the use of resistant varieties. Eleven major resistance genes have been identified and introgressed from Solanum demissum. However, new sources of resistance are continually sought. Here, we report the characterization and refined genetic localization of a resistance gene previously identified as Rber in a backcross progeny of Solanum tuberosum and Solanum berthaultii. In order to further characterize Rber, we developed a set of P. infestans isolates capable of identifying each of the 11 R-genes known to confer resistance to late blight in potato. Our results indicate that Rber is a new resistance gene, different from those recognized in S. demissum, and therefore, it has been named R Pi-ber according to the current system of nomenclature. In order to add new molecular markers around R Pi-ber , we used a PCR-based mapping technique, named MASP-map, which located R Pi-ber in a 3.9 cM interval between markers CT240 and TG63 on potato chromosome X. The location of R Pi-ber coincides with an area involved in resistance to different pathogens of potato and tomato. [ABSTRACT FROM AUTHOR]

Ten institutions in nine countries joined together to test the stability of resistance of 14 potato genotypes to the oomycete pathogenPhytophthora infestansin three separate trials. Seven of the genotypes were tested in one trial involving seven locations, and all 14 were tested in two subsequent trials, each involving eight locations. Stability of resistance was tested with nonparametric tests and with an additive main effects and multiplicative interaction (AMMI) model. Overall, resistance toP. infestanswas robust; resistant genotypes were consistently resistant in all locations and trials. The nonparametric analysis indicated that specific genotypes were basically stable across sites for resistance. In trial 3, theZstatistic for overall stability was significant at 0·05%, indicating a significant level of interaction across the trial, but there were no significant interactions for specific genotypes in this trial. The genotype by environment (G × E) effect of the AMMI model was highly significant in both trials, but the mean square of G × E was less than 10% of the genotype effect in each trial. The first two principal components (PCA1 and PCA2) of the AMMI analyses together explained 75 and 80% of the interaction effects in trials 2 and 3, respectively. Based on both nonparametric and AMMI analyses, Ecuador and Argentina were locations of relatively high interaction effects for both trials 2 and 3, although in Ecuador this interaction was not associated with any particular potato genotype. Other locations also had high interaction effects, but these occurred in only one trial. The genotypes Chata Blanca and, to a lesser extent, Torridon were relatively unstable in trials 2 and 3, but in the case of Torridon, resistant, this did not represent a significant loss of resistance. [ABSTRACT FROM AUTHOR]