Disassembly of the fruit cell wall by the ripening-associated polygalacturonase and expansin influences tomato cracking

Fangling Jiang,Zhen Wu,Shengke Tian,Elizabeth Mitcham,Qinghui Yu,Ann L T Powell,John M Labavitch,Shinjae Jeon,Sergio Tonetto De Freitas,Alfonso Lopez

doi:10.1038/s41438-018-0105-3

Abstract

Fruit cracking is an important problem in horticultural crop production. Polygalacturonase (SlPG) and expansin (SlEXP1) proteins cooperatively disassemble the polysaccharide network of tomato fruit cell walls during ripening and thereby, enable softening. A Golden 2-like (GLK2) transcription factor, SlGLK2 regulates unripe fruit chloroplast development and results in elevated soluble solids and carotenoids in ripe fruit. To determine whether SlPG, SlEXP1, or SlGLK2 influence the rate of tomato fruit cracking, the incidence of fruit epidermal cracking was compared between wild-type, Ailsa Craig (WT) and fruit with suppressed SlPG and SlEXP1 expression (pg/exp) or expressing a truncated nonfunctional Slglk2 (glk2). Treating plants with exogenous ABA increases xylemic flow into fruit. Our results showed that ABA treatment of tomato plants greatly increased cracking of fruit from WT and glk2 mutant, but not from pg/exp genotypes. The pg/exp fruit were firmer, had higher total soluble solids, denser cell walls and thicker cuticles than fruit of the other genotypes. Fruit from the ABA treated pg/exp fruit had cell walls with less water-soluble and more ionically and covalently-bound pectins than fruit from the other lines, demonstrating that ripening-related disassembly of the fruit cell wall, but not elimination of SlGLK2, influences cracking. Cracking incidence was significantly correlated with cell wall and wax thickness, and the content of cell wall protopectin and cellulose, but not with Ca2+ content.

Highlights

Cracking of the epidermis of harvested fruit destroys the appearance and increases the susceptibility of fruit to infections by opportunistic pathogens
In 2012, there was no difference in the size of the pg/exp fruit (52.7 mm in abscisic acid (ABA) treated plants and 52.2 mm in water treated plants) compared to the glk[2] mutant fruit (54.1 mm in ABA treated plants and 52.8 mm in water treated plants)
As cell wall networks weaken with fruit ripening[41,42], even as cell turgor falls, resistance to stresses at the fruit surface may require a greater contribution from wax and cuticle layer structures than they can provide; and cell turgor pushing the plasmalemma against the cell wall creates some stress on the cell wall polysaccharide networks that may be accommodated by the elasticity of the wall "fabric"; this leading to cracking

Summary

Introduction

Cracking of the epidermis of harvested fruit destroys the appearance and increases the susceptibility of fruit to infections by opportunistic pathogens. Fruit with cracks are not marketable, and, have reduced economic value. The predisposition to form cracks has been correlated with heredity, various fruit traits (shape, size, firmness, strength and components of pericarp, anatomical structure, water absorbing capacity of the pericarp, number and distribution of stomates, growth period) and external causes, such as cultivation practices (irrigation, nutrition, hormone applications) and growing environment (humidity, temperature, wind, and light)[1,3,4,5,6,7,8,9,10]. Fruit that are susceptible to cracking often have high levels of soluble solids and produce juice with elevated concentrations of osmotically active compounds[17]

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Discussion

Conclusion