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The Functional Verification of <i>CmSMXL6</i> from <i>Chrysanthemum</i> in the Regulation of Branching in <i>Arabidopsis thaliana</i>
oleh: Fenglan Wang, Zhiren Hu, Honghui Luo, Qing Wu, Xiuzhe Chen, Shuang Wen, Zihang Xiao, Xiaoxiao Ai, Yanhong Guo
| Format: | Article |
|---|---|
| Diterbitkan: | MDPI AG 2024-07-01 |
Deskripsi
The development of branching plays a pivotal role in the cultivation of ornamental chrysanthemums, as it dictates the ultimate morphology and quality of the plants. Strigolactones (SLs) are associated with apical dominance to indirectly inhibit shoot branching. <i>Chrysanthemum morifolium</i> ‘Baltasar’ in this study was subjected to treatment with three hormones: auxin (IAA), 6-BA, and GR24. Following the exogenous application of GR24 and IAA, a significant reduction in both the length and quantity of lateral buds on chrysanthemums was observed. Additionally, there was a notable down-regulation in the expression levels of <i>CmPIN1</i> (associated with auxin transport) and <i>CmIPT3</i>, which is involved in cytokinin (CK) synthesis. After the application of 6-BA, there was a significant increase in both the length and quantity of lateral buds on chrysanthemums. Subsequently, the separate application of IAA and 6-BA to <i>C. morifolium</i> ‘Baltasar’ notably induced the expression of <i>CmMAX1</i>, a gene involved in the biosynthesis of strigolactones, and <i>CmSMXL6</i>, a gene associated with the signaling pathway of SLs, suggesting a negative regulatory role for SLs and auxin in chrysanthemum lateral buds, while CK demonstrated positive regulation. Cloning and expression analysis of <i>CmSMXL6</i>, a member of the <i>D53/SMXL</i> gene family in chrysanthemum, revealed its up-regulation following GR24 treatment, peaking at 9 h. The overexpression of <i>CmSMXL6</i> in <i>Arabidopsis thaliana</i> promoted increased numbers of primary and secondary branches. In transgenic lines, genes associated with SLs synthesis (<i>AtMAX1</i>, <i>AtMAX2</i>, and <i>AtMAX3</i>) exhibited varying degrees of down-regulation, while the branching-inhibitory gene <i>AtBRC1</i> also displayed decreased expression levels. These findings suggest that <i>CmSMXL6</i> plays a role in promoting branching.