Aureobasidium pullulans strain Ach1-1 was selected for its effectiveness against blue mold caused by Penicillium expansum on stored apple fruit. The possible involvement of competition for nutrients in the biocontrol activity of this antagonistic strain was investigated both in vitro and in situ. For in vitro assays, the effect of strain Ach1-1 on germination percentages of P. expansum conidia was evaluated after a 24 h incubation period in the presence of increasing apple juice concentrations (0-5%) using a system allowing the physical separation of both agents. In the absence of strain Ach1-1, conidial germination was strongly promoted by apple juice whatever the concentration. However, germination was significantly reduced by the presence of strain Ach1-1 except at the highest juice concentration. For conidia previously inhibited at 0.5% juice, germination after 24 h of incubation was partially recovered in the presence of strain Ach1-1 when fresh juice was added to a final concentration of 5%, and completely restored at both 0.5 and 5% juice concentrations in the absence of strain Ach1-1. For in situ assays, strain Ach1-1 was very protective against P. expansum on postharvest wounded apples. However, the application of high concentrations of exogenous sugars, vitamins and most particularly amino acids, significantly reduced such protection. Time-course analysis of apple amino acids at the wound site revealed that these compounds were more depleted in wounds treated with strain Ach1-1 alone and especially in those treated with both agents (strain Ach1-1 and P. expansum) compared to wounds treated with P. expansum alone or to untreated ones. Exogenous amino acids, applied at high concentrations on apple wounds as a mixture of specific amino acid groups or as individuals, significantly decreased strain Ach1-1 efficacy against P. expansum. The present study provides in vitro and in situ evidence that competition for apple nutrients, most particularly amino acids, may be a main mechanism of the biocontrol activity of A. pullulans strain Ach1-1 against blue mold caused by P. expansum on harvested apple fruit.

Chickpea (Cicer arietinum L.) is an important food and rotation crop in many parts of the world. Cold (freezing and chilling temperatures) and Ascochyta blight (Didymella rabiei) are the major constraints in chickpea production. The effects of temperature stresses on chickpea susceptibility and pathogen aggressiveness are not well documented in the Cicer-Didymella pathosystem. Two experiments were conducted under controlled conditions using chickpea genotypes and pathogen isolates in 2011 and 2012. In Experiment 1, four isolates of D. rabiei (AR-01, AR-02, AR-03 and AR-04), six chickpea genotypes (Ghab-1, Ghab-2, Ghab-3, Ghab-4, Ghab-5 and ICC-12004) and four temperature regimes (10, 15, 20, and 25°C) were studied using 10 day-old seedlings. In Experiment 2, three chickpea genotypes (Ghab-1, Ghab-2, and ICC-12004) were exposed to 5 and 10 days of chilling temperature exposure at 5°C and non-exposed seedlings were used as controls. Seedlings of the three chickpea genotypes were inoculated with the four pathogen isolates used in Experiment 1. Three disease parameters (incubation period, latent period and disease severity) were measured to evaluate treatment effects. In Experiment 1, highly significant interactions between genotypes and isolates; genotypes and temperature; and isolate and temperature were observed for incubation and latent periods. Genotype x isolate and temperature x isolate interactions also significantly affected disease severity. The resistant genotype ICC-12004 showed long incubation and latent periods and low disease severity at all temperatures. The highly aggressive isolate AR-04 caused symptoms, produced pycnidia in short duration as well as high disease severity across temperature regimes, which indicated it is adapted to a wide range of temperatures. Short incubation and latent periods and high disease severity were observed on genotypes exposed to chilling temperature. Our findings showed that the significant interactions of genotypes and isolates with temperature did not cause changes in the rank orders of the resistance of chickpea genotypes and aggressiveness of pathogen isolates. Moreover, chilling temperature predisposed chickpea genotypes to D. rabiei infection; developing multiple stress resistance is thus a pre-requisite for the expansion of winter-sown chickpea in West Asia and North Africa.

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