Rice (Oryza sativa) is a major staple crop providing both calories and essential microelements such as Zn for humans. Understanding the molecular mechanisms involved in the control of Zn homeostasis may aid in optimizing Zn levels to improve rice growth and maximize its nutritional value. In this study, we aimed to decipher the precise function of ZINC TRANSPORTER1 (OsZIP1) in Zn uptake and the signaling pathways through which OsZIP1 responds to fluctuations in Zn bioavailability. In contrast to other members of the OsZIP family, OsZIP1 did not respond to Zn deficiency through binding of BASIC LEUCINE ZIPPER TRANSCRIPTION FACTOR50/48 (bZIP50/48) to canonical ZDRE elements. However, OsZIP1 was induced by both depletion and excess of Zn. Excessive Zn triggered Fe deficiency signaling and induced the accumulation of POSITIVE REGULATOR OF IRON DEFICIENCY RESPONSE 2 (OsPRI2), which in turn activated ABSCISIC ACID INSENSITIVE5 (OsABI5) expression and drove the upregulation of OsZIP1. By contrast, Zn depletion upregulated the expression of OsZIP1 via unfolded protein response (UPR) signaling. The nuclear isoform of BASIC LEUCINE ZIPPER TRANSCRIPTION FACTOR74 (bZIP74) , which was generated by alternative splicing in response to Zn depletion, bound to the modified unfolded protein response element (mUPRE) in the promoter of OsZIP1 and enhanced its expression. Our study reveals a pivotal role of a low-affinity transporter in fine-tuning Zn homeostasis and provides an essential node in the control of cellular Zn homeostasis at fluctuating Zn bioavailability.
谭龙涛 et al. (Fri,) studied this question.