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Endo-1,4-β-glucanase (EG) is involved in the metabolism

Superficial scald of pear fruit is a physiological disorder that easily occurs during cold storage and seriously affects pear eating quality and commodity value. It is important to study the mechanism of superficial scald disorder. Our previous study reported that the incidence of superficial scald of calcium chloride (CaCl2)-treated pear fruit during storage was significantly lower than that of untreated fruit. In this study, we found that the accumulation of lignin in CaCl2-treated fruit was significantly lower than that of untreated fruit. The expression of the Pb4CL2 gene in the lignin synthesis pathway was downregulated in the CaCl2-treated fruit. The lignification level of the fruit overexpressing Pb4CL2 was significantly higher than that of the empty vector fruit. Therefore, we speculate that downregulation of Pb4CL2 after CaCl2 treatment plays an important role in CaCl2 inhibiting superficial scald disorder by affecting lignin accumulation in pear fruit.

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The hard-end is a disorder of pear fruit, however, the mechanisms underlying its development remain unknown. In this study, we found that the hard-end fruit contained a higher transcript abundance level of ethylene-response factor 1b-like (PpERF1b-like) and released more ethylene compared to normal pear. In the ethephon treated normal fruit, flesh tissues accumulated more lignin together with elevated expression of PpERF1b-like. Overexpressing PpERF1b-like transiently in fruit and stably in callus increased lignin accumulation and the expression of lignin biosynthesis genes; the opposite results were observed in fruit showing repressed expression of PpERF1b-like. These results confirmed the role of PpERF1b-like in promoting hard-end formation through promoting lignin synthesis. This study provided valuable information for further clarifying the regulation of hard-end formation in pear.