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首页> 外文期刊>Plant Growth Regulation: An International Journal on Natural and Synthetic Regulators >Branching gene expression during chrysanthemum axillary bud outgrowth regulated by strigolactone and auxin transport
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Branching gene expression during chrysanthemum axillary bud outgrowth regulated by strigolactone and auxin transport

机译:分枝基因表达在枯草酮和生长素转运中调节的菊花腋芽产芽中的表达

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摘要

Shoot branching is essential in ornamental chrysanthemum production and determines final plant shape and quality. Auxin is associated with apical dominance to indirectly inhibit bud outgrowth. Two non-mutually exclusive models exist for indirect auxin inhibition. Basipetal auxin transport inhibits axillary bud outgrowth by limiting auxin export from buds to stem (canalization model) or by increasing strigolactone levels (second messenger model). Here we analyzed bud outgrowth in treatments with auxin (IAA), strigolactone (GR24) and auxin transport inhibitor (NPA) using a split-plate bioassay with isolated chrysanthemum stem segments. Besides measuring bud length, dividing cell percentage was measured with flow cytometry and RT-qPCR was used to monitor expression levels of genes involved in auxin transport (CmPIN1) and signaling (CmAXR2), bud dormancy (CmBRC1, CmDRM1) and strigolactone biosynthesis (CmMAX1, CmMAX3). Treatments over a 5-day period showed bud outgrowth in the control and inhibition with IAA and IAA + GR24. Bud outgrowth in the control coincided with high dividing cell percentage, decreased expression of CmBRC1 and CmDRM1 and increased CmPIN1 expression. Inhibition by IAA and IAA + GR24 coincided with low dividing cell percentage and unchanged or increased expressions of CmBRC1, CmDRM1 and CmPIN1. Treatment with GR24 showed restricted bud outgrowth that was counteracted by NPA. This restricted bud outgrowth was still concomitant with a high dividing cell percentage and coincided with decreased expression of dormancy genes. These results indicate incomplete inhibition of bud outgrowth by GR24 treatment and suggest involvement of auxin transport in the mechanism of bud inhibition by strigolactones, supporting the canalization model.
机译:拍摄分支是观赏菊花生产的必需品,并确定最终的植物形状和质量。植物素与间接抑制芽外的顶端优势相关。存在两个非相互排斥的模型,用于间接养蛋白抑制。通过限制芽孢杆菌从茎(运用模型)或增加血清内酯水平(第二信使模型)来抑制腋芽芽孢杆菌抑制腋芽过度。在这里,我们使用分离板生物测定与分离的菊花锡段分析芽蛋白(IAA),杂霉酮(GR24)和生长素传输抑制剂(NPA)的治疗中的芽源性。除了测量芽长,通过流式细胞术测量分割细胞百分比,使用RT-QPCR监测疾病转运(CMPIN1)和信号传导(CMBAXR2),芽休眠(CMBRC1,CMDRM1)和滴度生物合成中所涉及的基因的表达水平(CMMAX1 ,cmmax3)。治疗在5天的时间内显示出对照和抑制IAA和IAA + GR24的芽外。控制中的芽外生长在控制中恰好具有高分性细胞百分比,降低CMBRC1和CMDRM1的表达,并增加CMPIN1表达。 IAA和IAA + GR24的抑制作用与CMBRC1,CMDRM1和CMPIN1的低分割细胞百分比和不变或增加的表达。用GR24治疗表现出限制的芽外生长,由NPA抵消。这种受限制的芽外生长仍然伴随着高分子细胞百分比并恰逢休眠基因的表达降低。这些结果表明GR24治疗的芽外产生的不完全抑制,并表明毒素转运在滴漏抑制作用机制中的抑制,支持分布溶液。

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