Abstract

Fruit firmness is an important economical trait in sweet cherry (Prunus avium L.) where the change of this trait is related to cell wall degradation. Xyloglucan endotransglycosylase/hydrolase (XTH) and polygalacturonases (PGs) are critical cell-wall-modifying enzymes that occupy a crucial position in fruit ripening and softening. Herein, we identified 18 XTHs and 45 PGs designated PavXTH1-18 and PavPG1-45 based on their locations in the genome of sweet cherry. We provided a systematical overview of PavXTHs and PavPGs, including phylogenetic relationships, conserved motifs, and expression profiling of these genes. The results showed that PavXTH14, PavXTH15 and PavPG38 were most likely to participated in fruit softening owing to the substantial increment in expression during fruit development and ripening. Furthermore, the phytohormone ABA, MeJA, and ethephon significantly elevated the expression of PavPG38 and PavXTH15, and thus promoted fruit softening. Importantly, transient expression PavXTH14, PavXTH15 and PavPG38 in cherry fruits significantly reduced the fruit firmness, and the content of various cell wall components including hemicellulose and pectin significantly changed correspondingly in the transgenic fruit. Taken together, these results present an extensive analysis of XTHs and PGs in sweet cherry and provide potential targets for breeding softening-resistant sweet cherry cultivars via manipulating cell wall-associated genes.

Highlights

  • Softening, which is one of the irreversible ripening results, is a major determinant of shelf life and commercial quality after harvest [1]

  • To determine the xyloglucan endotransglycosylase/hydrolase (XTH) and PG family members in sweet cherry, the Arabidopsis XTH and PG protein sequences were used as queries to search against the sweet cherry genome by BLAST

  • The molecular weight (MW) calculated by the ExPASy ranged from 17.43–73.43 kDa for XTHs and 17.15–175.36 kDa for PGs, while the PIs varied from 5.2–9.68 for XTHs and 5.38–9.83 for PGs

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Summary

Introduction

Softening, which is one of the irreversible ripening results, is a major determinant of shelf life and commercial quality after harvest [1]. Textural changes occur which result from modifications and disassembly of cell wall structure and composition. The primary cell wall is mainly composed of cellulose, hemicellulose, pectin, structural proteins and some phenolics [2]. The solubilization of pectin and depolymerization of xyloglucan is thought to be the main modifications in cell wall responsible for the softening process, which are mediated by a set of hydrolytic enzymes such as xyloglucan endotransglycosylase/hydrolase (XTH) and polygalacturonase (PG) [3,4]. Suppressing the expression of genes involved in cell wall metabolisms by genetic manipulation could be an effective way of delaying fruit softening and maintaining moderate firmness. Currently little is known regarding the role of cell wall-modification genes in sweet cherry, which severely hampers any attempt to breed softening-resistant sweet cherry cultivars

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