4.7 Article

MdBZR1 regulates ABA response by modulating the expression of MdABI5 in apple

期刊

PLANT CELL REPORTS
卷 40, 期 7, 页码 1127-1139

出版社

SPRINGER
DOI: 10.1007/s00299-021-02692-7

关键词

Apple (malus domestica); Brassinosteroids; MdBZR1; ABA sensitivity; MdABI5

资金

  1. National Key R&D Program of China [2018YFD1000100]
  2. National Natural Science Foundation of China [32030097, 31772288]
  3. Shandong Province Program [TSCY20190126]
  4. Open funds of the State Key Laboratory of Crop Genetics and Germplasm Enhancement [ZW202008]
  5. Agricultural Variety Improvement Project of Shandong Province [2019LZGC007]

向作者/读者索取更多资源

In this study, MdBZR1 was identified as a negative regulator of ABA signaling by directly binding to the promoter of MdABI5 and suppressing its expression. This finding contributes to a better understanding of the crosstalk between BR and ABA signaling pathways.
Key message MdBZR1 directly binds to the promoter of MdABI5 and suppresses its expression to mediate ABA response. The plant hormones brassinosteroids (BRs) and abscisic acid (ABA) antagonistically regulate various aspects of plant growth and development. However, the association between BR and ABA signaling is less clear. Here, we identified MdBZR1 in apple (Malus domestica) and demonstrated that it was activated by BRs and could respond to ABA treatment. Overexpression of MdBZR1 in apple calli and Arabidopsis reduced ABA-hypersensitive phenotypes, suggesting that MdBZR1 negatively regulates ABA signaling. Subsequently, we found that MdBZR1 directly bound to the promoter region of MdABI5 and suppressed its expression. MdABI5 was significantly induced by ABA treatment. And overexpression of MdABI5 in apple calli increased sensitivity to ABA. Ectopic expression of MdABI5 in Arabidopsis inhibited seed germination and seedling growth. In addition, overexpression of MdBZR1 partially attenuated MdABI5-mediated ABA sensitivity. Taken together, our data indicate that MdBZR1 directly binds to the promoter of MdABI5 and suppresses its expression to antagonistically mediate ABA response. Our work contributes to the functional studies of BZR1 and further broadens the insight into the between BR and ABA signaling.

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