HyPRP1, A Tomato Multipotent Regulator, Negatively Regulates Tomato Resistance to Sulfur Dioxide Toxicity and Can Also Reduce Abiotic Stress Tolerance of Escherichia coli and Tobacco

Abstract

Abiotic stresses have led to an extensive decline in global crop production and quality. As one of the abiotic stress factors, sulfur dioxide (SO2) causes severe oxidative damage to plant tissues. Based on our previous study, a tomato hybrid-proline-rich protein 1 (HyPRP1) was found to be involved in abiotic stress and SO2 metabolism, though the gene functions remained largely unknown. In this study, the function analysis of the HyPRP1 gene was extended, and DNA methylation analysis, subcellular localization, and cis-element analysis were performed to investigate the features of this gene. The DNA methylation analysis implied that the HyPRP1 gene was hypermethylated and the methylation density in the leaf differed from that in the flower and fruit. Subcellular localization analysis identified HyPRP1 localized in the cytoplasm and plasma membrane in vivo. The E. coli cells harboring SlHyPRP1 showed reduced salt and drought resistance. In tomato, when SO2 toxicity occurred, the HyPRP1 RNAi knockdown lines accumulated more sulfates and less hydrogen peroxide (H2O2) and showed minimal leaf necrosis and chlorophyll bleaching. In tobacco, the overexpression of HyPRP1 reduced tolerance against salt stresses exerted by NaCl. We conclude that the heterologous expression of tomato HyPRP1 in E. coli and tobacco reduces abiotic stress tolerance and negatively regulates the resistance to sulfur dioxide toxicity by scavenging H2O2 and sulfite in tomato.