Abstract
Strawberry is a soft fruit with short postharvest life, due to a rapid loss of firmness. Pectin methylesterase (PME)-mediated cell wall remodeling is important to determine fruit firmness and softening. Previously, we have verified the essential role of FvPME38 in regulation of PME-mediated strawberry fruit softening. However, the regulatory network involved in PME-mediated fruit softening is still largely unknown. Here, we identified an R2R3-type MYB transcription factor FvMYB79, which activates the expression level of FvPME38, thereby accelerating fruit softening. During fruit development, FvMYB79 co-expressed with FvPME38, and this co-expression pattern was opposite to the change of fruit firmness in the fruit of ‘Ruegen’ which significantly decreased during fruit developmental stages and suddenly became very low after the color turning stage. Via transient transformation, FvMYB79 could significantly increase the transcriptional level of FvPME38, leading to a decrease of firmness and acceleration of fruit ripening. In addition, silencing of FvMYB79 showed an insensitivity to ABA-induced fruit ripening, suggesting a possible involvement of FvMYB79 in the ABA-dependent fruit softening process. Our findings suggest FvMYB79 acts as a novel regulator during strawberry ripening via transcriptional activation of FvPME38, which provides a novel mechanism for improvement of strawberry fruit firmness.
Highlights
Fruit softening is a major determinant of shelf life and commercial value
The strawberry Pectin methylesterase (PME), FvPME38 regulated fruit softening at the maturity stage of strawberry fruit, and the expression level of FvPME38 is positively regulated by abscisic acid (ABA) [12]
To further study whether FvMYB79 is involved in the regulation of fruit ripening, we examined the transcriptional level of well-known ripening marker genes, including pectin methylesterase (PME), expansin (EXP), beta-xylosidase (XYL), pectate lyase (PL), polygalacturonase (PG), and cellulose (CEL); the flavonoid biosynthesis genes chalcone synthase (CHS), chalconeisomerase (CHI), dihydroflavonol 4-reductase (DFR), UDP-glucose flavonoid 3-O-glycosyltransferase (UFGT) and phenylalanine ammonialyase (PAL)
Summary
Fruit softening is a major determinant of shelf life and commercial value. It is the consequence of multiple cellular processes, including changes in soluble sugar content, glycosylation of cellulose, and remodeling of cell wall structure. The strawberry PME, FvPME38 regulated fruit softening at the maturity stage of strawberry fruit, and the expression level of FvPME38 is positively regulated by abscisic acid (ABA) [12]. These results all indicated that PME-mediated cell wall modification is an essential process to control fruit rigidity and ripening. These studies help us to understand the biological function of PME in the control of fruit softening, the complex regulatory network involved in the PME-dependent module remains to be further explored.
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
