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 (Pyrus bretschneideriRehd.) leaves caused by Fe deficiency. Furthermore, IAA treatment slightly induced regreening by increasing chlorophyll synthesis and Fe2+accumulation. At that point, we identifiedPbrSAUR72as a key negative effector output of auxin signaling and established its close relationship to Fe deficiency. Furthermore, the transientPbrSAUR72overexpression 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 toAtSAUR40/72. This promotes salt tolerance in plants, indicating a putative role forPbrSAUR72in abiotic stress responses. Indeed, transgenic plants ofSolanum lycopersicumandArabidopsis thalianaoverexpressingPbrSAUR72displayed less sensitivity to Fe deficiency, accompanied by substantially elevated expression of Fe-induced genes, such asFER/FIT,HA, andbHLH39/100. 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 ofPbrSAUR72inhibited reactive oxygen species production in response to Fe deficiency. These findings contribute to a new understanding ofPbrSAURsand its involvement in Fe deficiency, providing new insights for the further study of the regulatory mechanisms underlying the Fe deficiency response.