Growth of Colletotrichum gloeosporioides in pectolytic enzyme-inducing medium (PEIM) increased the pH of the medium from 3.8 to 6.5. Pectate lyase (PL) secretion was detected when the pH reached 5.8, and the level of secretion increased up to pH 6.5. PL gene (pel) transcript production began at pH 5.0 and increased up to pH 5.7. PL secretion was never detected when the pH of the inducing medium was lower than 5.8 or when C. gloeosporioides hyphae were transferred from PL-secreting conditions at pH 6.5 to pH 3.8. This behavior differed from that of polygalacturonase (PG), where pg transcripts and protein secretion were detected at pH 5.0 and continued up to 5.7. Under in vivo conditions, the pH of unripe pericarp of freshly harvested avocado (Persea americana cv. Fuerte) fruits, resistant to C. gloeosporioides attack, was 5.2, whereas in ripe fruits, when decay symptoms were expressed, the pericarp pH had increased to 6.3. Two avocado cultivars, Ardit and Ettinger, which are resistant to C. gloeosporioides attack, had pericarp pHs of less than 5.5, which did not increase during ripening. The present results suggest that host pH regulates the secretion of PL and may affect C. gloeosporioides pathogenicity. The mechanism found in avocado may have equivalents in other postharvest pathosystems and suggests new approaches for breeding against and controlling postharvest diseases.Colletotrichum gloeosporioides (Penz.) Penz. & Sacc [teleomorph Glomerella cingulata (Stonem). Spauld et Schrenk] infects avocado fruits, via spore germination, appressorium formation, and penetration. The pathogen attacks fruits early in their development and remains as a germinated appressorium during fruit growth (quiescent infection) (17). After harvest and fruit ripening, fast-developing brown-black spots on the pericarp and soft rot in the mesocarp, the symptoms of anthracnose, appear (17). Prusky (17) has suggested several hypotheses to explain the resistance mechanism of unripe fruits: (i) nutrients available to the pathogen may be limited in unripe hosts, (ii) preformed antifungal compounds present in unripe fruits decline during ripening, (iii) inducible antifungal compounds in unripe fruits decline during ripening, and (iv) fungal pathogenicity factors may be activated mainly in ripening fruits. Antifungal compounds are implicated in the resistance of avocado fruits to C. gloeosporioides (19), but no reports have described the role of enzyme secretion as a factor in fungal attack.C. gloeosporioides produces an array of pectolytic enzymes, including polygalacturonase (PG) (20), pectin lyase (2), pectin methyl esterase (15), and pectate lyase (PL) (28). No reports regarding the involvement of PG or pectin methyl esterase in C. gloeosporioides attack have been published. However, targeted disruption of pectin lyase from C. gloeosporioides did not reduce virulence (2). The importance of PL secretion during C. gloeosporioides attack in avocado fruits has been suggested by the inhibition of decay development during coinoculation of C. glo...

Penicillium expansum, the causal agent of blue mold rot, causes severe postharvest fruit maceration through secretion of D-gluconic acid (GLA) and secondary metabolites such as the mycotoxin patulin in colonized tissue. GLA involvement in pathogenicity has been suggested but the mechanism of patulin accumulation and its contribution to P. expansum pathogenicity remain unclear. The roles of GLA and patulin accumulation in P. expansum pathogenicity were studied using i) glucose oxidase GOX2-RNAi mutants exhibiting decreased GOX2 expression, GLA accumulation, and reduced pathogenicity; ii) IDH-RNAi mutants exhibiting downregulation of IDH (the last gene in patulin biosynthesis), reduced patulin accumulation, and no effect on GLA level; and iii) PACC-RNAi mutants exhibiting downregulation of both GOX2 and IDH that reduced GLA and patulin production. Present results indicate that conditions enhancing the decrease in GLA accumulation by GOX2-RNAi and PACC-RNAi mutants, and not low pH, affected patulin accumulation, suggesting GLA production as the driving force for further patulin accumulation. Thus, it is suggested that GLA accumulation may modulate patulin synthesis as a direct precursor under dynamic pH conditions modulating the activation of the transcription factor PACC and the consequent pathogenicity factors, which contribute to host-tissue colonization by P. expansum.

BackgroundThe mango belongs to the genus Mangifera, consisting of numerous tropical fruiting trees in the flowering plant family, Anacardiaceae. Postharvest treatment by hot water brushing (HWB) for 15–20 s was introduced commercially to improve fruit quality and reduce postharvest disease. This treatment enabled successful storage for 3–4 weeks at 12°C, with improved color and reduced disease development, but it enhanced lenticel discoloration on the fruit peel. We investigated global gene expression induced in fruit peel by HWB treatment, and identified key genes involved in mechanisms potentially associated with fruit resistance to pathogens, peel color improvement, and development of lenticel discoloration; this might explain the fruit’s phenotypic responses.ResultsThe mango transcriptome assembly was created and characterized by application of RNA-seq to fruit-peel samples. RNA-seq-based gene-expression profiling identified three main groups of genes associated with HWB treatment: 1) genes involved with biotic and abiotic stress responses and pathogen-defense mechanisms, which were highly expressed; 2) genes associated with chlorophyll degradation and photosynthesis, which showed transient and low expression; and 3) genes involved with sugar and flavonoid metabolism, which were highly expressed.ConclusionsWe describe a new transcriptome of mango fruit peel of cultivar Shelly. The existence of three main groups of genes that were differentially expressed following HWB treatment suggests a molecular basis for the biochemical and physiological consequences of the postharvest HWB treatment, including resistance to pathogens, improved color development, and occurrence of lenticel discoloration.Electronic supplementary materialThe online version of this article (doi:10.1186/1471-2164-15-957) contains supplementary material, which is available to authorized users.

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