Xiaoyan Tao

Tomato fruit malformation causes substantial yield and economic losses, but its molecular mechanisms are not well understood. This study compared floral traits of WT ‘QT57’ and malformed-fruit mutant ‘QT2’, integrated transcriptomic data, and qRT-PCR analysis to screen key candidate genes, and analyzed the pectinase gene family. The results found the ‘QT2’ mutant differed from WT ‘QT57’ in flower and fruit development. Expression analysis of CLAVATA-WUSCHEL pathway genes preliminarily validated the compensatory mechanism of SlCRCa and SlCRCb in ‘QT2’ malformed fruit. Six pectinase genes were identified as key candidates via RNA-seq and qRT-PCR analysis. Transcriptomic and qRT-PCR analyses of the pectinase gene family revealed their potential role in regulating tomato fruit malformation. Family analysis showed 34 pectinase genes distributed unevenly across 12 chromosomes. Subcellular localization confirmed SlPL7 in the nucleus and SlPME9 in the cell membrane/endoplasmic reticulum. The PL and PME genes were evolutionarily close, suggesting a potential functional overlap. Gibberellin-responsive elements were found in most pectinase genes. Pectinase genes may regulate tomato fruit malformation through the gibberellin-WUS pathway, carbohydrate metabolism, or cell wall metabolic disorder. This pathway provides new targets gene for the precise regulation of fruit malformation and offers significant reference value for practical production.