Genetic control of tomato fruit cracking through SlPMEI27-dependent pectin modification.

Abstract

Fruit cracking severely affects tomato quality and yield. By utilizing genetic transformation, knockout of the SlPMEI27 gene can enhance the activity of pectin methylesterases (PMEs). Here, by conducting an immunofluorescence analysis, we observed that the pectin methylation rate decreased by approximately 46% (versus approximately 70% in the overexpression line), while calcium-mediated pectin cross-linking enhancement increased fruit hardness by 1.8-fold. In contrast, SlPMEI27 overexpression inhibits PME activity, resulting in highly methyl-esterified pectin. Transmission electron microscopy analysis demonstrated that SlPMEI27 overexpression significantly reduced cell-to-cell adhesion and increased intercellular space expansion. These factors contribute significantly to susceptibility to cracking. Additional evidence, such as enzyme activity and the expression levels of related genes, shows that the interaction between SlPMEI27 and SlGAUT7 regulates pectin modification and biosynthesis. Transcriptomic analysis revealed that SLPMEI27 is associated with altered expression of downstream cell wall hydrolases, such as pectate/pectin lyases (PL), polygalacturonases (PG), and β-galactosidases (β-Gal), as well as ripening-related transcription factors (bHLH, ERF, and MYB). This study demonstrates that SlPMEI27 regulates cracking by directly modulating pectin methylesterification and cell wall mechanical properties. These findings establish pectin methylesterification status as a crucial determinant of cell wall integrity during fruit development, offering a theoretical foundation for breeding crack-resistant tomatoes.