Hours after watering plants with 75 mM NaCl, the water potential of reproductive structures precipitously decreases. In flowers with mature gametes, this change in water potential did not alter the rate of fertilization but caused 37% of the fertilized ovules to abort. We hypothesize that the accumulation of reactive oxygen species (ROS) in ovules is an early physiological manifestation associated with seed failure. In this study, we characterize ROS scavengers that were differentially expressed in stressed ovules to determine whether any of these genes regulate ROS accumulation and/or associate with seed failure. Mutants in an iron-dependent superoxide dismutase (FSD2), ascorbate peroxidase (APX4), and three peroxidases (PER17, PER28, and PER29) were evaluated for changes in fertility. Fertility was unchanged in apx4 mutants, but the other mutants grown under normal conditions averaged a 140% increase in seed failure. In pistils, PER17 expression increases three-fold after stress, while the other genes decreased two-fold or more following stress; this change in expression accounts for differences in fertility between healthy and stressed conditions for different genotypes. In pistils, H2O2 levels rose in per mutants, but only in the triple mutant was there a significant increase, indicating that other ROS or their scavengers be involved in seed failure.
Keywords: fertility; ovules; plant stress; reactive oxygen; seed formation.