Suppression of the soybean (Glycine max) Phytoglobin GmPgb1 improves tolerance to iron stress

Iron is an important microelement implicated in a variety of processes including chlorophyll synthesis and chloroplast development. Iron deprivation alters nitric oxide (NO) homeostasis, and depresses antioxidant responses leading to the toxic accumulation of reactive oxygen species (ROS) which damage photosynthetic components compromising plant growth. This study evaluated how the NO scavengers Phytoblobins (Pgbs) influence plant response to iron deficiency. Commercial varieties of soybean (Glycine max) characterized by low GmPgb1 expression in leaves, and transgenic plants down-regulating GmPgb1 were more tolerant to iron deficiency and exhibited a higher retention of chlorophyll relative to WT plants and plants with high GmPgb1 levels. Suppression of GmPgb1 alleviated the accumulation of ROS and ROS-induced damage caused by iron deficit as a result of elevated activities of superoxide dismutase (SOD) and catalase (CAT). The same plants also exhibited a higher activity of monodehydroascorbate reductase (MDHAR) and an elevated pool of ascorbic acid (ASC) facilitating the reduction of Fe(III) to the more soluble and mobile Fe(II) and utilization of foliar iron. This was in contrast to plants over-expressing GmPgb1 which were characterized by higher levels of ROS and ROS-induced damage, as well as lower cellular ASC, associated to a diminished ability to reduce Fe(III) to Fe(II). Pharmacological treatments revealed that the observed effects were mediated by NO, in a model consistent with the NO scavenging function of GmPgb1. Collectively this work demonstrates that manipulation of GmPgb1 can be used as a reliable tool to enhance tolerance to iron deficiency.