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水稻 SM1 突变增强了实心中脉的形成并增加了甲烷排放。

Mutation of rice SM1 enhances solid leaf midrib formation and increases methane emissions.

机构信息

Key Laboratory of High Magnetic Field and Ion Beam Physical Biology, Hefei Institutes of Physical Science, Chinese Academy of Sciences, Hefei, China; University of Science and Technology of China, Hefei, China.

Key Laboratory of High Magnetic Field and Ion Beam Physical Biology, Hefei Institutes of Physical Science, Chinese Academy of Sciences, Hefei, China.

出版信息

Plant Sci. 2025 Jan;350:112312. doi: 10.1016/j.plantsci.2024.112312. Epub 2024 Oct 29.

DOI:10.1016/j.plantsci.2024.112312
PMID:39481760
Abstract

The leaf midrib system is essential for plant growth and development, facilitating nutrient transport, providing structural support, enabling gas exchange, and enhancing resilience to environmental stresses. However, the molecular mechanism regulating leaf midrib development is still unclear.In this study, we reported a rice solid midrib 1 (sm1) mutant, exhibiting solid leaf aerenchyma and abaxial rolling leaves due to abnormal development of parenchyma and bulliform cells. Map-based cloning revealed that SM1 encodes a litter zipper protein (ZPR). SM1 was mainly expressed in the sheaths and basal midrib and was associated with the nucleus. Further experiments indicated that SM1 can interact with OSHB1, preventing the formation of OSHB:OSHB dimers and subsequently repressing the expression of OSH1 involved in the regulation and maintenance of apical stem meristem formation. The sm1 mutant reduced long-distance oxygen transport ability from shoot to root. The impaired oxygen transport in the sm1 mutant may have contributed to the increase in methanogens and elevated methane emissions. Collectively, our findings revealed that the SM1-OSHB1-OSH1 modules regulate leaf aerenchyma development in rice. These modules not only enhance our understanding of the molecular mechanism of rice leaf aerenchyma development but also offer insights for reducing methane emissions through genetic modification.

摘要

叶片中脉系统对植物的生长和发育至关重要,它有助于营养物质的运输,提供结构支撑,实现气体交换,并增强对环境胁迫的适应能力。然而,调控叶片中脉发育的分子机制尚不清楚。在这项研究中,我们报道了一个水稻实心中脉 1 突变体(sm1),由于薄壁组织和泡状细胞的异常发育,表现出实心叶通气组织和叶片内卷。基于图谱的克隆表明,SM1 编码一个丛生拉链蛋白(ZPR)。SM1 在叶鞘和基部中脉中主要表达,并与核相关联。进一步的实验表明,SM1 可以与 OSHB1 相互作用,防止 OSHB:OSHB 二聚体的形成,并随后抑制参与调控和维持顶端茎分生组织形成的 OSH1 的表达。sm1 突变体降低了从地上部到根部的远距离氧气运输能力。sm1 突变体中氧气运输的受损可能导致产甲烷菌的增加和甲烷排放的升高。总之,我们的研究结果揭示了 SM1-OSHB1-OSH1 模块在水稻叶片通气组织发育中的调控作用。这些模块不仅增强了我们对水稻叶片通气组织发育分子机制的理解,也为通过遗传修饰减少甲烷排放提供了新的思路。

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