Potato leafroll virus (PLRV) concentration at 20-d interval in plants of fi ve Solanum tuberosum subsp. andigena and three controls during primary (50–110 d) and secondary infection (30–90 d). 

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... showed a range of virus concentrations between 179 and 2056 ng g −1 of † (P) denotes the as control. fresh leaf tissue ( Table 6). Two of the three ‡ Mean of three andigena cultivars (LOP-868 and HUA- § nt, not tested. 332) classifi ed as highly resistant to PLRV infection and showed mean concentrations signifi cantly lower than the remaining andigena cultivars, but statistically higher than the highly resistant control DW.84-1457. The third highly resistant andigena cultivar, OCH-7643, had a mean titer not statistically diff erent from the control Achirana-INTA (551 ng g −1 of leaf ), which is considered to possess moderate levels of resistance to PLRV multiplication (Huarte et al., 1990). Most cultivars showed a wide range of virus titers along their vegetative growth cycles, causing a high standard devi- ation and hence a lack of statistically signifi cant diff erences among their numerically diff erent mean concentrations (Table 6). Diff erent trends in evolution of virus concentrations during the primary infection cycle were observed among the cultivars (Fig. 4). Susceptible controls and cultivars rapidly reached high concentrations while resistant controls and cultivars showed a delay. The resistant control Achirana-INTA, as well as the three resistant andigena cultivars showed increases in titer by the end of their vegetative growth periods (90 d for Achirana-INTA and 110 d for andigena cultivars), though these were lower than those of susceptible controls and cultivars, in which titers tended to decrease by this stage. During secondary infection, almost all genotypes showed higher titers 30 or 50 d after planting, which then tended to decrease, but diff erences between resistant and susceptible genotypes were maintained. Special cases were those of Achirana-INTA, which reached titers as high as one of the susceptible controls 70 d after planting during the secondary infection trial, and the highly resistant-bred line DW.84-1457 in which the virus was not detected during primary infection and maintained very low titers during secondary infection (Fig. 4). All plants were colonized within 36 h after apterous aphids were released. Cultivars showed a mean range of 22 to 95 aphids per plant in the initial counting performed 36 h after infestation (Table 5). Analysis of variance on log transformation of the total number of aphids 72 h after infestation, revealed signifi cant diff erences among cultivars (including the control) ( P ≤ 0.001), but a Waller–Duncan test showed only the S. acaule accession OCH-13824, used ...

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... showed a range of virus concentrations between 179 and 2056 ng g −1 of † (P) denotes the as control. fresh leaf tissue ( Table 6). Two of the three ‡ Mean of three andigena cultivars (LOP-868 and HUA- § nt, not tested. 332) classifi ed as highly resistant to PLRV infection and showed mean concentrations signifi cantly lower than the remaining andigena cultivars, but statistically higher than the highly resistant control DW.84-1457. The third highly resistant andigena cultivar, OCH-7643, had a mean titer not statistically diff erent from the control Achirana-INTA (551 ng g −1 of leaf ), which is considered to possess moderate levels of resistance to PLRV multiplication (Huarte et al., 1990). Most cultivars showed a wide range of virus titers along their vegetative growth cycles, causing a high standard devi- ation and hence a lack of statistically signifi cant diff erences among their numerically diff erent mean concentrations (Table 6). Diff erent trends in evolution of virus concentrations during the primary infection cycle were observed among the cultivars (Fig. 4). Susceptible controls and cultivars rapidly reached high concentrations while resistant controls and cultivars showed a delay. The resistant control Achirana-INTA, as well as the three resistant andigena cultivars showed increases in titer by the end of their vegetative growth periods (90 d for Achirana-INTA and 110 d for andigena cultivars), though these were lower than those of susceptible controls and cultivars, in which titers tended to decrease by this stage. During secondary infection, almost all genotypes showed higher titers 30 or 50 d after planting, which then tended to decrease, but diff erences between resistant and susceptible genotypes were maintained. Special cases were those of Achirana-INTA, which reached titers as high as one of the susceptible controls 70 d after planting during the secondary infection trial, and the highly resistant-bred line DW.84-1457 in which the virus was not detected during primary infection and maintained very low titers during secondary infection (Fig. 4). All plants were colonized within 36 h after apterous aphids were released. Cultivars showed a mean range of 22 to 95 aphids per plant in the initial counting performed 36 h after infestation (Table 5). Analysis of variance on log transformation of the total number of aphids 72 h after infestation, revealed signifi cant diff erences among cultivars (including the control) ( P ≤ 0.001), but a Waller–Duncan test showed only the S. acaule accession OCH-13824, used ...

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... by ELISA during the secondary infection trial allowed us to defi ne clear-cut diff erences in the levels of resistance of cultivars using controls that were previously reported as resistant to PLRV infection. The three controls, DW.84- 1547, Achirana-INTA, and Perricholi, reacted in agree- ment with their levels of reported resistance, which made them useful as standard cultivars for comparison across diff erent environments or diff erent isolates of the virus. A scale was built based on the performance of these controls, which allowed us to classify the tested cultivars into resistance categories. LOP-868 was classifi ed as highly resistant ; the other two putatively resistant parents (ZIM- 440 and CCC-4932) were classifi ed as susceptible , because all plants representing them became infected under both aphid pressures. Only four of the 13 putatively resistant cultivars tested showed some level of resistance, of which two (OCH- 7643 and HUA-332) were as highly resistant as LOP-868, with no plants infected under any aphid pressure. Despite the fact that a high ratio of escapes seems to have occurred in the preliminary screening of 2518 cultivars, this initial screening was helpful in discarding the more susceptible accessions. The eff ectiveness of PLRV resistance to infection depends on inoculum pressure (Barker and Harrison, 1985), however, there is no consensus on the minimum number of aphids per plant that qualifi es as high aphid pressure. We found that the application of 50 or 100 aphids per plant was adequate for infection, because under this pressure 100% of inoculated plants of moderately resistant and susceptible cultivars became infected. Aphid pressures beyond these levels would present more of a concern in terms of pest damage than virus infection. With regard to the level of resistance to infection of the 25 uninfected selections from one of the LOP-868 progenies, 24 were classifi ed as highly resistant and one as moderately resistant . This shows that the seedling screening method used to assess the resistance of progenies was also eff ective in selecting the most resistant individuals. Even though a previous study has showed the effi ciency of this method for identifying the more resistant progenies (Chuquillanqui and Jones, 1980); concerns about its use- fulness for selecting the most resistant individuals within progeny have also been raised (Solomon-Blackburn et al., 1994). These authors found that some uninfected seedlings selected after primary infection became infected under clonal fi eld evaluations. They also observed little or no correlation in the number of resistant clones (i.e., clones without any infected plants) between selected and unselected clones, that is, those not previously subjected to seedling screening, of the same cross in fi eld exposure trials, even though they found a greater number of resistant clones in R (resistant) × R and R × S (susceptible) crosses. In contrast, we do not expect all plants from these selected individuals to remain uninfected under clonal evaluation, but rather that they will have a low number of infected plants. In fact, two of the 24 clones classifi ed as highly resistant and the one classifi ed as moderately resistant showed one infected plant with 50- or 100-aphid pressure and two with 25 aphids per plant, respectively. Assessment of OP progenies from andigena cultivars based on resistance to PLRV infection at the seedling stage, showed that those cultivars classifi ed as resistant in the clonal assessment trial yielded a low frequency of infected individuals while a high frequency was found for those classifi ed as susceptible. The fact that phenotypic performance was refl ected in progeny performance sup- ports the previous statement about the potential for good progress in PLRV resistance through selection based on clonal performance of parents. Evaluation of resistance to PLRV infection does not provide information on the other components of PLRV resistance, such as resistance to PLRV accumulation, resistance to virus movement from foliage to tubers, or indirect resistance through aphid nonpreference or antixenosis (Barker and Harrison, 1985). PLRV accumulation was measured in the resistant andigena cultivars LOP-868, HUA-332, and OCH-7643, and a sample of susceptible cultivars at diff erent growth stages in graft inoculated plants and in their progeny plants obtained from harvested tubers. Surprisingly, the three cultivars with high levels of infection resistance were also those with lower mean virus titers. The same was true for the highly resistant bred line DW.84-1457 used as control. Two important features were observed in the trends of virus accumulation among these resistant cultivars. First, there was a delay in virus multiplication as compared with susceptible cultivars. Second, at certain points in their development, one or two of the fi ve plants tested showed high virus titers, increasing mean readings temporarily (Fig. 4). According to Barker and Harrison (1985), three possible mechanisms might result in a restriction of virus accumulation: a decrease in virus synthesis, an enhancement of virus breakdown, or a restriction in virus movement. Using fl uo- rescent antibody staining, these authors showed that the lat- ter mechanism was most likely, because diff erences in virus accumulation between resistant and susceptible genotypes depended on the number of PLRV-containing companion cells. This mechanism would account better for what might be occurring in graft-inoculated plants of resistant genotypes. The continuous supply of virus particles by infected scions would facilitate a greater number of initially infected cells than would be expected by aphid-borne inoculum, accounting for the ready detection of the virus in graft- inoculated plants compared with that in plants of resistant genotypes inoculated by aphids. It seems that the amount of viral particles has a great eff ect on the success of the virus in overcoming this mechanism of restricted virus movement, causing new infected cells and hence increasing virus accumulation and facilitating its movement to tubers. Marked diff erences in virus titers encountered among plants of the same resistant genotype might support this statement. On the other hand, lack of virus detection in progeny plants of some graft-inoculated mother plants of resistant genotypes would support the idea that inhibition of virus movement operated effi ciently in those cases. We were not able to detect the virus in progeny plants of three, two, and one graft-inoculated mother plants of DW.84-1457, HUA-332, and OCH-7643, respectively, for which mean concentrations in each occasion were estimated only from infected progeny plants. In contrast, the virus was detected in all tuber progeny from graft-inoculated plants of the resistant cultivar LOP-868, but their concentrations were signifi cantly lower than in the mother plants at all growth stages. Our results showed that three components of PLRV resistance—that is, resistance to infection, to accumulation, and in some extent to virus movement from foliage to tubers—seem to be present in the three resistant andigena cultivars identifi ed. A test for antixenosis ruled out nonpreference as a confounding feature of the resistance to infection we describe, since in all tested cultivars, no evidence was found of aphids moving away from plants, but instead the number of aphids was observed to increase through time. Barker and Harrison (1986) suggested that resistance to infection of potato genotypes could have the same cause as decreased virus accumulation in infected plants. In this case, the same mechanism aff ecting transport within the phloem could be preventing the virus from moving out of initially inoculated or initially infected cells, causing the virus to fail to become established systematically and hence to be detected serologi- cally. Swiezynski et al. (1989) also found that resistance to infection was associated with resistance to PLRV accumulation in the diploid line DW.84-1457 used as control in this work, and in additional diploid lines. By contrast, other reports maintain that this association is not always found, as some clones that restrict virus accumulation appeared to be susceptible to infection (Solomon-Blackburn and Barker, 1993). We did not identify any andigena cultivar susceptible to PLRV infection expressing resistance to virus accumulation. Our results support a previous hypothesis suggesting that multiple components of resistance in a single genotype could be the result of a common mechanism controlled by several genes (Barker, 1987). Infl uence of the genetic background on resistance expression was studied in a factorial mating design involving crosses between the highly resistant andigena cultivars identifi ed in this study and known commercial cultivars. Com- mercial potatoes belong to S. tuberosum subsp. tuberosum, which share a common evolutionary origin with this native cultivated subspecies from the Andean region. This explains the ease of crossability between these two tetra- ploid subspecies, whereas the divergent selection applied to them in recent history accounts for several distinctive features and likely for the heterosis found in some of their hybrids (Hawkes, 1990; Tarn and Tai, 1983). The subspecies tuberosum is well adapted to temperate areas and the subspecies andigena to short daylength latitudes. PLRV resistance of some commercial varieties adapted to temperate zones decreases in tropical areas where higher temperatures and aphid populations are present (Beemster and Rozendaal, 1972), hence the importance of increasing levels of resistance. It is well known that GCA may be diff erent depending on the genetic constitution of alternative parents used to develop the progenies. This could be due to modifi cation or even suppression of the resistance in off spring, depending on which germplasm the ...