Nectarine [Prunus persica (L.) Batsch var.] fruits are highly susceptible to cracking during the ripening process, which significantly decreases their commercial value. In this study, we investigated the underlying mechanism of nectarine fruit-cracking using two nectarine varieties, namely, "Qiannianhong" (cracking-susceptible) and "CR1012" (cracking-resistant). Our findings indicate that nectarine fruit-cracking occurs during the second stage of fruit expansion. Despite no differences in epicarp cell size between "Qiannianhong" and "CR1012", the mesocarp cells of "Qiannianhong" were larger than those of "CR1012". Moreover, a comparison of starch hydrolysis between the two varieties revealed that "CR1012" had higher starch content in the mesocarp but lower soluble sugar content compared to "Qiannianhong". Additionally, by testing the α-amylase and β-amylase activity of the mesocarp, our results showed a difference only in α-amylase activity between the two varieties. Furthermore, qRT-PCR detection indicated a higher expression level of the PpAmy1 (α-amylase synthesis gene) in "Qiannianhong" compared to "CR1012". To further investigate the role of PpAmy1, we employed RNAi technology to suppress its expression in "Qiannianhong" fruits. The results showed a significant reduction in α-amylase activity, starch hydrolysis, soluble sugar content, cell size of the mesocarp, and fruit-cracking. These findings underscore the pivotal role of PpAmy1 in the occurrence of nectarine fruit cracking.
Keywords: PpAmy1; fruit-cracking; mesocarp; nectarine; starch hydrolysis.