Overexpression of MsGH3.5 inhibits shoot and root development through the auxin and cytokinin pathways in apple plants
Overexpression of MsGH3.5 inhibits shoot and root development through the auxin and cytokinin pathways in apple plants
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MsGH3.5 的过度表达通过生长素和细胞分裂素途径抑制苹果植物中芽和根的发育
DOI：
10.1111/tpj.14717
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发表时间：
2020
期刊：
影响因子：
7.2
通讯作者：
Li Tianhong
中科院分区：
文献类型：
--
作者：
Zhao Di;Wang Yantao;Feng Chen;Wei Yan;Peng Xiang;Guo Xiao;Guo Xinwei;Zhai Zefeng;Li Jian;Shen Xiaoshuai;Li Tianhong
植物激素相互作用对植物发育至关重要。生长素和细胞分裂素（CK）在植物生长发育中起着重要的调控作用，然而，这两种植物激素之间的相互作用是复杂的，并没有完全了解。本研究克隆了野生苹果（Malus sieversiiRoem）GRETCHEN HAGEN 3（GH 3）基因MsGH 3. 5，该基因编码吲哚-3-乙酸（IAA）-酰胺合成酶。MsGH3.5过表达显著降低了游离IAA含量，增加了部分IAA-氨基酸结合物的含量，并且MsGH3.5过表达株系比对照矮化，产生的不定根（AR）也较少。这种表型与GH 3在生长素体内平衡中将过量的游离活性IAA与氨基酸结合的作用一致。令人惊讶的是，MsGH3.5的过表达显著增加了整个植株中CK的浓度，并改变了参与CK生物合成、代谢和信号转导的基因的表达。此外，外源性CK应用通过CK B型反应调节因子MsRR 1a的活性诱导MsGH3.5表达，MsRR 1a介导CK初级反应。MsRR 1a通过直接与其启动子结合，连接生长素和CK信号通路，激活MsGH3.5的表达。过表达MsRR 1a的植株也显示较少的AR，这与MsRR 1a对MsGH3.5表达的调节一致。综上所述，我们揭示了MsGH3.5通过调节生长素和CK水平及信号通路影响苹果生长发育。这些发现提供了深入了解生长素和CK途径之间的相互作用，并可能对改善苹果结构的努力产生重大影响。
Phytohormonal interactions are crucial for plant development. Auxin and cytokinin (CK) both play critical roles in regulating plant growth and development; however, the interaction between these two phytohormones is complex and not fully understood. Here, we isolated a wild apple (Malus sieversiiRoem)GRETCHEN HAGEN3(GH3) gene,MsGH3.5, encoding an indole‐3‐acetic acid (IAA)‐amido synthetase. Overexpression ofMsGH3.5significantly reduced the free IAA content and increased the content of some IAA‐amino acid conjugates, andMsGH3.5‐overexpressing lines were dwarfed and produced fewer adventitious roots (ARs) than the control. This phenotype is consistent with the role ofGH3in conjugating excess free active IAA to amino acids in auxin homeostasis. Surprisingly, overexpression ofMsGH3.5significantly increased CK concentrations in the whole plant, and altered the expression of genes involved in CK biosynthesis, metabolism and signaling. Furthermore, exogenous CK application inducedMsGH3.5expression through the activity of the CK type‐B response regulator, MsRR1a, which mediates the CK primary response. MsRR1a activatedMsGH3.5expression by directly binding to its promoter, linking auxin and CK signaling. Plants overexpressingMsRR1aalso displayed fewer ARs, in agreement with the regulation ofMsGH3.5expression byMsRR1a. Taken together, we reveal thatMsGH3.5affects apple growth and development by modulating auxin and CK levels and signaling pathways. These findings provide insight into the interaction between the auxin and CK pathways, and might have substantial implications for efforts to improve apple architecture.