Calmodulin-like protein MdCML15 interacts with MdBT2 to modulate iron homeostasis in apple
文献类型： 外文期刊
作者： Liu, Xiao-Juan 1 ; Liu, Xin 1 ; Zhao, Qiang 1 ; Dong, Yuan-Hua 1 ; Liu, Qiangbo 5 ; Xue, Yuan 2 ; Yao, Yu-Xin 1 ; You, Chun-Xiang 1 ; Kang, Hui 1 ; Wang, Xiao-Fei 1 ;
作者机构： 1.Shandong Agr Univ, Coll Hort Sci & Engn, Apple Technol Innovat Ctr Shandong Prov, Shandong Green Fertilizer Technol Innovat Ctr,Natl, Tai An 271018, Shandong, Peoples R China
2.Chinese Acad Forestry, State Key Lab Genet & Breeding, Beijing 100091, Peoples R China
3.Beijing Acad Agr & Forestry Sci, Inst Forestry & Pomol, Beijing 100093, Peoples R China
4.Qingdao Agr Univ, Coll Hort, Qingdao 266109, Peoples R China
5.Shandong Agr Univ, Natl Key Lab Wheat Improvement, Coll Life Sci, Tai An 271018, Peoples R China
期刊名称：HORTICULTURE RESEARCH （ 影响因子：7.6； 五年影响因子：8.2 ）
ISSN： 2662-6810
年卷期： 2024 年 11 卷 5 期
页码：
收录情况： SCI
摘要： BTB and TAZ domain proteins (BTs) function as specialized adaptors facilitating substrate recognition of the CUL3-RING ubiquitin ligase (CRL3) complex that targets proteins for ubiquitination in reaction to diverse pressures. Nonetheless, knowledge of the molecular mechanisms by which the apple scaffold protein MdBT2 responds to external and internal signals is limited. Here we demonstrate that a putative Ca 2+ sensor, calmodulin-like 15 (MdCML15), acts as an upstream regulator of MdBT2 to negatively modulate its functions in plasma membrane H+-ATPase regulation and iron deficiency tolerance. MdCML15 was identified to be substantially linked to MdBT2, and to result in the ubiquitination and degradation of the MdBT2 target protein MdbHLH104. Consequently, MdCML15 repressed the MdbHLH104 target, MdAHA8's expression, reducing levels of a specific membrane H+-ATPase. Finally, the phenotype of transgenic apple plantlets and calli demonstrated that MdCML15 modulates membrane H+-ATPase-produced rhizosphere pH lowering alongside iron homeostasis through an MdCML15-MdBT2-MdbHLH104-MdAHA8 pathway. Our results provide new insights into the relationship between Ca2+ signaling and iron homeostasis.
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