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The SL–MdDWARF53–MdbHLH1 module regulates MdAT1 -mediated redox homeostasis and alkaline salt tolerance mechanism in apple

2026/03/11 by Xiaomin Zhu, Yuqing Zhu, Xiaoyu Zhou +8 · 1 voice · 1 citation
Agricultural and Biological Sciences · #Arabidopsis #Homeostasis #Hydrogen peroxide #Oxidative stress #Plant Parasitism and Resistance #Plant Stress Responses and Tolerance #Plant and Biological Electrophysiology Studies #Reactive oxygen species #Repressor #Signal transduction #Strigolactone #Transcription factor

paper · doi:10.1093/hr/uhag089

published in Horticulture Research 13(7), uhag089 (Nature Portfolio)

openalex publication_date 2026/03/11 · openalex created_date 2026/03/13 · openalex updated_date 2026/08/05

Abstract

Abstract Alkaline salt stress is a key environmental factor restricting the sustainable development of the apple industry, significantly affecting the yield and quality of apple. In recent years, strigolactone (SLs) has been proven to play a central regulatory role in plant stress responses. However, its role and mechanism under alkaline salt stress remain unknown. Based on this, we found that exogenous application of the SL analog GR245DS can significantly enhance the adaptability of apple to alkaline salt stress. To elucidate the underlying molecular mechanisms, RNA sequencing (RNA-seq) analysis identified the key transcription factor MdbHLH1, whose expression was strongly induced by alkaline salt stress. Overexpression of MdbHLH1 conferred a salt-alkali tolerant phenotype. Further investigation demonstrated that MdbHLH1 directly binds to and activates the promoter of MdAT1 (Alkali Tolerance 1), a crucial alkali-tolerance gene. The MdbHLH1-MdAT1 module enhances alkaline salt stress resistance by promoting hydrogen peroxide (H2O2) efflux and alleviating oxidative damage. More in-depth studies revealed that MdbHLH1 interacts with MdD53 (MdDWARF53), a repressor in the SL signaling pathway. SL signaling induces ubiquitination and degradation of MdD53, thereby releasing MdbHLH1 to activate MdAT1 expression and ultimately improving alkaline stress tolerance in apple. This study elucidates a key SL–MdD53–MdbHLH1-MdAT1 regulatory pathway that enhances saline-alkali tolerance in apple by mitigating oxidative stress, thereby providing mechanistic insights into apple’s adaptation to saline-alkali environments.

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