Evidence That PbrSAUR72 Contributes to Iron Deficiency Tolerance in Pears by Facilitating Iron Absorption

Iron is an essential trace element for plants; however, low bioactive Fe in soil continuously places plants in an Fe-deficient environment, triggering oxidative damage. To cope with this, plants make a series of alterations to increase Fe acquisition; however, this regulatory network needs further investigation. In this study, we found notably decreased indoleacetic acid (IAA) content in chlorotic pear (<i>Pyrus bretschneideri</i> Rehd.) leaves caused by Fe deficiency. Furthermore, IAA treatment slightly induced regreening by increasing chlorophyll synthesis and Fe²⁺ accumulation. At that point, we identified <i>PbrSAUR72</i> as a key negative effector output of auxin signaling and established its close relationship to Fe deficiency. Furthermore, the transient <i>PbrSAUR72</i> overexpression could form regreening spots with increased IAA and Fe²⁺ content in chlorotic pear leaves, whereas its transient silencing does the opposite in normal pear leaves. In addition, cytoplasm-localized PbrSAUR72 exhibits root expression preferences and displays high homology to <i>AtSAUR40</i>/<i>72</i>. This promotes salt tolerance in plants, indicating a putative role for <i>PbrSAUR72</i> in abiotic stress responses. Indeed, transgenic plants of <i>Solanum lycopersicum</i> and <i>Arabidopsis thaliana</i> overexpressing <i>PbrSAUR72</i> displayed less sensitivity to Fe deficiency, accompanied by substantially elevated expression of Fe-induced genes, such as <i>FER</i>/<i>FIT</i>, <i>HA</i>, and <i>bHLH39</i>/<i>100</i>. These result in higher ferric chelate reductase and root pH acidification activities, thereby hastening Fe absorption in transgenic plants under an Fe-deficient condition. Moreover, the ectopic overexpression of <i>PbrSAUR72</i> inhibited reactive oxygen species production in response to Fe deficiency. These findings contribute to a new understanding of <i>PbrSAURs</i> and its involvement in Fe deficiency, providing new insights for the further study of the regulatory mechanisms underlying the Fe deficiency response.