Zhang Feng, Pan Zhijian, Han Chenyang, Dong Huizhen, Lin Likun, Qiao Qinghai, Zhao Keke, Wu Juyou, Tao Shutian, Zhang Shaoling, Huang Xiaosan
College of Horticulture, State Key Laboratory of Crop Genetics and Germplasm Enhancement and Utilization, Nanjing Agricultural University, No.1 Weigang, Tongwei Road, Nanjing 210095, China.
Hortic Res. 2024 Mar 30;11(5):uhae090. doi: 10.1093/hr/uhae090. eCollection 2024 May.
Environmental disasters like drought reduce agricultural output and plant growth. Redox management significantly affects plant stress responses. An earlier study found that PbPIP1;4 transports HO and promotes HO downstream cascade signaling to restore redox equilibrium. However, this regulatory mechanism requires additional investigation. In this search, the AP2 domain-containing transcription factor was isolated by screening Y1H from the wild pear () cDNA library, named PbERF3. The overexpression of PbERF3 in pear callus and enhanced plant resistance to drought and re-established redox balance. The transcripts of the gene were upregulated under drought stress. The drought stress-related abscisic acid (ABA) signaling pathway modulates PbERF3. PbERF3 silencing lowered drought tolerance. Furthermore, yeast 2-hybrid, luciferase, bimolecular fluorescence complementation, and co-immunoprecipitation assays verified that PbERF3 physically interacted with PbHsfC1a. The PbERF3-PbHsfC1a heterodimer coordinately bound to and promoter, therefore activating both the HO and the ABA signaling pathway. This work revealed a novel PbERF3-PbHsfC1a-- regulatory module, in which PbERF3 interacts with PbHsfC1a to trigger the expression of target genes. This module establishes an interaction between the HO signaling component and the ABA pathways component , enabling a response to drought.
干旱等环境灾害会降低农业产量和植物生长。氧化还原管理显著影响植物的应激反应。早期研究发现,PbPIP1;4转运过氧化氢并促进过氧化氢下游级联信号传导以恢复氧化还原平衡。然而,这种调控机制需要进一步研究。在此研究中,通过从野生梨()cDNA文库中筛选酵母单杂交分离出含AP2结构域的转录因子,命名为PbERF3。PbERF3在梨愈伤组织中的过表达增强了植物对干旱的抗性并重新建立了氧化还原平衡。该基因的转录本在干旱胁迫下上调。干旱胁迫相关的脱落酸(ABA)信号通路调节PbERF3。PbERF3沉默降低了耐旱性。此外,酵母双杂交、荧光素酶、双分子荧光互补和免疫共沉淀试验证实PbERF3与PbHsfC1a发生物理相互作用。PbERF3-PbHsfC1a异源二聚体协同结合到和启动子上,从而激活过氧化氢和ABA信号通路。这项工作揭示了一种新的PbERF3-PbHsfC1a--调控模块,其中PbERF3与PbHsfC1a相互作用以触发靶基因的表达。该模块在过氧化氢信号成分和ABA途径成分之间建立了相互作用,从而实现对干旱的响应。