The ZAT7-OTU11-DOA9-CYS13 module enhances salt resistance by suppressing NPF2.4-mediated chloride transport in
Chunyan Wang1, Miao Liu1, Changai Wu1
1State Key Laboratory of Wheat Improvement, College of Life Sciences, Shandong Agricultural University, Shandong, Tai'an 271018, China.
Abstract:
Salt stress causes concurrent sodium (Na+) and chloride (Cl-) toxicity that severely inhibits plant growth and reduces crop yield. Although Na+ homeostasis has been studied extensively, the molecular mechanisms that underlie Cl- homeostasis during salt stress remain to be fully characterized. Root-to-shoot Cl- translocation is tightly regulated to prevent excessive Cl- accumulation in the shoots. Here, we show that the zinc finger protein ZAT7 directly binds to the promoter of the Cl- transporter gene NRT1/PTR FAMILY 2.4 (NPF2.4) and represses its expression, thus inhibiting the upward transport of Cl- mediated by NPF2.4. Through yeast two-hybrid screening and functional validation, we identified three upstream regulators of ZAT7: DUF295 ORGANELLAR A 9 (DOA9), the deubiquitinase OVARIAN TUMOR 11 (OTU11), and CYSTATIN 13 (CYS13). Under normal growth conditions, OTU11 stabilizes DOA9 to promote the degradation of ZAT7, thereby maintaining NPF2.4 expression and basal Cl- translocation to the shoots. Upon Cl- stress, CYS13 is rapidly induced and inactivates the OTU11-DOA9 module, leading to ZAT7 accumulation, NPF2.4 suppression, and reduced Cl- translocation. These findings reveal that plants fine-tune the abundance of the core chloride-resistance regulator ZAT7 via CYS13 under salt stress to precisely control root-to-shoot Cl- delivery.
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