tae-miR399-UBC24 Module Enhances Freezing Tolerance in Winter Wheat via a CBF Signaling Pathway

被引：19

作者：

Peng, Kankan ^{[1
]}

Tian, Yu ^{[1
]}

Sun, Xianze ^{[1
]}

Song, Chunhua ^{[1
]}

Ren, Zhipeng ^{[1
]}

Bao, Yuzhuo ^{[1
]}

Xing, Jinpu ^{[1
]}

Li, Yuanshan ^{[1
]}

Xu, Qinghua ^{[1
]}

Yu, Jing ^{[1
]}

Zhang, Da ^{[1
]}

Cang, Jing ^{[1
]}

机构：

[1] Northeast Agr Univ, Coll Life Sci, Harbin 150030, Peoples R China

来源：

JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY | 2021年 / 69卷 / 45期

基金：

中国国家自然科学基金;

关键词：

miR399; freezing stress; CBF signaling pathway; starch degradation; ROS scavenging; AGROBACTERIUM-MEDIATED TRANSFORMATION; PHOSPHATE-STARVATION RESPONSE; TRANSCRIPTION FACTOR; LOW-TEMPERATURE; ARABIDOPSIS-THALIANA; GENE-EXPRESSION; CBF3/DREB1A EXPRESSION; NEGATIVE REGULATOR; COLD-ACCLIMATION; STRESS TOLERANCE;

D O I：

10.1021/acs.jafc.1c04316

中图分类号：

S [农业科学];

学科分类号：

09 ;

摘要：

Although the regulation of Pi homeostasis by miR399 has been studied in various plant species, its underlying molecular mechanism in response to freezing stress is still poorly understood. In this work, we found that the expression of tae-miR399 and its target gene TaUBC24 in the tillering nodes of the strong cold-resistant winter wheat cultivar Dongnongdongmail (Dn1) was not only significantly altered after severe winters but also responsive to short-term freezing stress. TaUBC24 physically interacted with TaICE1. Enhanced freezing tolerance was observed for tae-miR399-overexpressing Arabidopsis lines. Under freezing stress, overexpression of tae-miR399 ultimately decreased the expression of AtUBC24, inhibiting the degradation of AtICE1, which increased the expression of genes involved in the CBF signaling pathway and starch metabolism and promoted the activities of antioxidant enzymes. These results will improve our understanding of the molecular mechanism through which the miR399-UBC24 module plays a cardinal role in regulating plant freezing stress tolerance through mediation of downstream pathways.

引用

页码：13398 / 13415

页数：18