The OPR gene family in watermelon: Genome-wide identification and expression profiling under hormone treatments and root-knot nematode infection.

The enzyme 12-oxo-phytodienoic acid reductase (OPR) is important in the jasmonic acid (JA) biosynthesis pathway and thus plays a vital role in plant defence. However, systematic and comprehensive analyses of OPR genes in watermelon and their roles in defence responses are extremely limited. The physicochemical properties, phylogenetic tree, gene structure and cis-acting elements of watermelon OPR genes were analysed using bioinformatics, and qRT-PCR and RNA-Seq were applied to assay expression of OPR genes in watermelon. A total of five OPR family genes were identified in watermelon, which were unevenly distributed across the four chromosomes. Phylogenetic analysis assigned OPR members from different plant species to five subfamilies (OPRI-OPRV). The motif compositions of OPR members were relatively conserved. Expression analysis using qRT-PCR revealed that ClOPR genes, except for ClOPR5, were highly expressed in the flower and fruit. RNA-seq analysis showed that the ClOPR genes had different expression patterns during flesh and rind development. Furthermore, the ClOPR genes, particularly ClOPR2 and ClOPR4, were significantly upregulated by exogenous JA, salicylic acid (SA) and ethylene (ET) treatments. In addition, red light induced expression of ClOPR2 and ClOPR4 in leaves and roots of root-knot nematode (RKN)-infected watermelon plants, suggesting their involvement in red light-induced defence against RKN. These results provide a theoretical basis for elucidating the diverse functions of OPR family genes in watermelon.

Carbon dioxide enrichment alleviates heat stress by improving cellular redox homeostasis through an ABA-independent process in tomato plants.

Plant responses to elevated CO2 and high temperature are critically regulated through a complex network of phytohormones and redox homeostasis. However, the involvement of abscisic acid (ABA) in plant adaptation to heat stress under elevated CO2 conditions has not been thoroughly studied. This study investigated the interactive effects of elevated CO2 (800 µmol·mol(-1) ) and heat stress (42 °C for 24 h) on the endogenous level of ABA and the cellular redox state of two genotypes of tomato with different ABA biosynthesis capacities. Heat stress significantly decreased maximum photochemical efficiency of PSII (Fv/Fm) and leaf water potential, but also increased levels of malondialdehyde (MDA) and electrolyte leakage (EL) in both genotypes. Heat-induced damage was more severe in the ABA-deficient mutant notabilis (not) than in its parental cultivar Ailsa Craig (Ailsa), suggesting that a certain level of endogenous ABA is required to minimise the heat-induced oxidative damage to the photosynthetic apparatus. Irrespective of genotype, the enrichment of CO2 remarkably stimulated Fv/Fm, MDA and EL in heat-stressed plants towards enhanced tolerance. In addition, elevated CO2 significantly strengthened the antioxidant capacity of heat-stressed tomato seedlings towards a reduced cellular redox state for a prolonged period, thereby mitigating oxidative stress. However, elevated CO2 and heat stress did not alter the endogenous level of ABA or the expression of its biosynthetic gene NCED2 in either genotype, indicating that ABA is not involved in elevated CO2 -induced heat stress alleviation. The results of this study suggest that elevated CO2 alleviated heat stress through efficient regulation of the cellular redox poise in an ABA-independent manner in tomato plants.