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我校在植物硼营养机制研究方面取得新进展

核心提示: 近日,我校植物营养生物学团队研究揭示了油菜素甾醇(BRs)和茉莉酸(JA)参与植物响应缺硼胁迫的分子调控机制。

南湖新闻网讯(通讯员 张成)植物激素在植物生长发育、抵抗生物和非生物胁迫中发挥着重要的调控作用。近日,我校植物营养生物学团队研究揭示了油菜素甾醇(BRs)和茉莉酸(JA)参与植物响应缺硼胁迫的分子调控机制。

油菜素甾醇(brassinosteroids, BRs)是一类多羟基的甾醇类植物激素,因首先从油菜花粉中发现提取而得名,广泛分布在植物的根、茎、叶片、花、种子和幼嫩的生长组织中,调控植物的生长发育。植物缺硼会严重抑制主根的生长,该团队通过研究分析拟南芥响应缺硼和BR的RNA-seq结果,发现两者共表达的基因数高达45.9%(图1c),且这些共表达的基因大部分呈现相反的表达趋势。与野生型相比,BR的受体突变体bri1-119和bri1-301表现出对低硼胁迫不敏感,而BR信号增强突变体bes1-D对缺硼胁迫则表现出显著高的抗性(图1a)。此外,外源添加24-表油菜素内酯(eBL)能显著缓解根的生长抑制(图1b),而添加BR合成抑制剂BRZ会加重根生长的抑制,且缺硼减少了BES1的核信号,但在缺硼条件下添加eBL则能增加BES1的核信号。进一步研究发现缺硼通过抑制BR合成基因BR6ox1和BR6ox2的表达而减少了油菜素内酯(BL)的合成(图1d)。

油菜素甾醇(BR)参与拟南芥缺硼胁迫的反应

油菜素甾醇(BR)参与拟南芥缺硼胁迫的反应

茉莉酸(JA)是调节植物生长发育、抵御逆境胁迫的一种植物激素。植物营养生物学团队研究发现缺硼条件下拟南芥地上部和根中积累JA达到正常硼条件下的7.9倍和2.8倍,生长受严重抑制,外源添加JA合成抑制剂DIECA则可以缓解缺硼对生长的抑制。团队进一步鉴定到一个缺硼诱导的乙烯转录因子ERF018,通过作用于JA合成基因AOCs的启动子区域,上调了JA合成基因的表达,使JA合成增多。在茉莉酸氨基酸结合酶JAR1的作用下,增多的JA进一步转变为有生物活性形式的茉莉酸-异亮氨酸JA-Ile。JA-Ile与受体复合物SCFCOI1结合激活JA下游信号,参与缺硼对拟南芥生长的抑制。同时,研究发现缺硼上调了乙烯(ET)合成基因的表达,使ET积累,并负调主根生长。JA通过抑制jar1-1突变体中乙烯信号转录因子EIN3的蛋白水平,从而实现JA与ET协同作用于缺硼对主根生长的抑制。JA并不直接调控硼的吸收转运,而是通过影响缺硼时根系构型而影响硼的吸收。

上述研究获得了国家自然科学基金、国家重点研发计划和中央高校基本科研业务费专项基金资助,团队成员汪社亮副研究员、王创研究员,丁广大副教授,蔡红梅副教授和石磊教授等参与了研究工作。

审核人:徐芳森

【英文摘要】

Brassinosteroids (BRs) are pivotal phytohormones involved in dominating root development. Boron (B) is an essential micronutrient for plants, and root growth is rapidly inhibited under B‐deficiency conditions. However, the mechanisms underlying this inhibition are still unclear. Here, we identified BR‐related processes underlying B deficiency at the physiological, genetic, molecular/cell biological and transcriptomic levels and found strong evidence that B deficiency can affect BR biosynthesis and signalling, thereby altering root growth. RNA sequencing analysis revealed strong co‐regulation between BR‐regulated genes and B deficiency‐responsive genes. We found that the BR receptor mutants bri1‐119 and bri1‐301 were more insensitive to decreased B supply, and the gain‐of function mutants bes1‐D and pBZR1‐bzr1‐D lines exhibited insensitivity to low‐B stress. Under B‐deficiency conditions, exogenous 24‐epibrassinolide (eBL) rescued the inhibition of root growth, and application of the BR biosynthesis inhibitor BRZ exacerbated this inhibitory effect. The nuclear‐localized signal of BES1 was reduced under low‐B conditions compared with B‐sufficiency conditions. We further found that B deficiency hindered the accumulation of brassinolide (BL) to downregulate BR signalling and modulate root elongation, which may occur through a reduction in BR6ox1 and BR6ox2 mRNA levels. Taken together, our results reveal a role of BR signalling in root elongation under B deficiency.

The essential micronutrient boron (B) has key roles in cell wall integrity and B deficiency inhibits plant growth. The role of jasmonic acid (JA) in plant growth inhibition under B deficiency remains unclear. Here, we report that low B elevates JA biosynthesis in Arabidopsis thaliana by inducing the expression of JA biosynthesis genes. Treatment with JA inhibited plant growth and, a JA biosynthesis inhibitor enhanced plant growth, indicating that the JA induced by B deficiency affects plant growth. Furthermore, examination of the JA signaling mutants jasmonate resistant1coronatine insensitive1‐2, and myc2 showed that JA signaling negatively regulates plant growth under B deficiency. We identified a low‐B responsive transcription factor, ERF018, and used yeast one‐hybrid assays and transient activation assays in Nicotiana benthamiana leaf cells to demonstrate that ERF018 activates the expression of JA biosynthesis genes. ERF018 overexpression (OE) lines displayed stunted growth and up‐regulation of JA biosynthesis genes under normal B conditions, compared to Col‐0 and the difference between ERF018 OE lines and Col‐0 diminished under low B. These results suggest that ERF018 enhances JA biosynthesis and thus negatively regulates plant growth. Taken together, our results highlight the importance of JA in the effect of low B on plant growth.

论文链接

https://onlinelibrary.wiley.com/doi/10.1111/tpj.15311

https://academic.oup.com/jxb/article/72/8/3108/6126775 

https://onlinelibrary.wiley.com/doi/10.1111/jipb.13048

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