Journal of Integrative Agriculture ›› 2024, Vol. 23 ›› Issue (10): 3487-3505.DOI: 10.1016/j.jia.2024.03.036

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棉花和拟南芥中的果胶甲基酯酶抑制因子GhPMEI53和AtPMEI19通过调节细胞壁可塑性促进种子萌发

  

  • 收稿日期:2023-10-16 接受日期:2024-02-01 出版日期:2024-10-20 发布日期:2024-09-11

Pectin methylesterase inhibitors GhPMEI53 and AtPMEI19 improve seed germination by modulating cell wall plasticity in cotton and Arabidopsis

Yayue Pei1*, Yakong Wang1*, Zhenzhen Wei1*, Ji Liu2, Yonghui Li3, Shuya Ma3Ye Wang3Fuguang Li1, 2#, Jun Peng2, 3#, Zhi Wang1, 2, 3#   

  1. 1 Zhengzhou Research Base, State Key Laboratory of Cotton Bio-breeding and Integrated Utilization, Zhengzhou University, Zhengzhou 450001, China
    2 National Nanfan Research Institute (Sanya), Chinese Academy of Agricultural Sciences, Sanya 572024, China
    3 National Key Laboratory of Cotton Bio-breeding and Integrated Utilization/Institute of Cotton Research, Chinese Academy of Agricultural Sciences, Anyang 455000, China
  • Received:2023-10-16 Accepted:2024-02-01 Online:2024-10-20 Published:2024-09-11
  • About author:#Correspondence Zhi Wang, E-mail: wangzhi01@caas.cn; Jun Peng, E-mail: jun_peng@126.com; Fuguang Li, E-mail: aylifug@caas.cn * These authors contributed equally to this study.
  • Supported by:
    This study was funded by the National Natural Science Foundation of China (32072022), the Nanfan Special Project, CAAS (YBXM07), and the Hainan Yazhou Bay Seed Laboratory, China (B23CJ0208). 

摘要:

果胶甲酯酶(PME)和果胶甲酯酶抑制子(PMEI)通过拮抗方式调控果胶甲酯化程度,在种子萌发中发挥了重要作用,但其中的具体调控机制尚不明晰。我们的研究表明,棉花GhPMEI53的过表达导致PME活性降低,果胶甲酯化程度增加,进而使种子细胞壁软化,最终促进了种子的萌发。GhPMEI53在拟南芥中的同源基因AtPMEI19在种子萌发过程中具有相似的作用,这说明PMEI在种子萌发中的功能和调控机制具有一定的保守性。进一步研究表明GhPMEI53和AtPMEI19促使细胞壁变软,降低其机械强度,从而直接促进胚根突破和种子萌发。通过转录组测序发现,转基因材料中ABA和GA的信号通路发生了显著变化,表明GhPMEI53和AtPMEI19介导的果胶甲酯化过程影响了种子萌发中的激素信号转导。综上所述,GhPMEI53及其同源基因AtPMEI19不仅通过调控果胶甲酯化程度改变细胞壁的力学特性影响胚根突破胚乳和种皮的过程,还通过调控激素信号通路(如ABA, GA)影响种子萌发。这些结果丰富了我们对果胶甲酯化在植物细胞形态动力学和激素信号转导中的认识,也有助于对植物PME/PMEI超基因家族作用机制的全面了解。

Abstract:

The germination process of seeds is influenced by the interplay between two opposing factors, pectin methylesterase (PME) and pectin methylesterase inhibitor (PMEI), which collectively regulate patterns of pectin methylesterification.  Despite the recognized importance of pectin methylesterification in seed germination, the specific mechanisms that govern this process remain unclear.  In this study, we demonstrated that the overexpression of GhPMEI53 is associated with a decrease in PME activity and an increase in pectin methylesterification.  This leads to seed cell wall softening, which positively regulates cotton seed germination.  AtPMEI19, the homologue in Arabidopsis thaliana, plays a similar role in seed germination to GhPMEI53, indicating a conserved function and mechanism of PMEI in seed germination regulation.  Further studies revealed that GhPMEI53 and AtPMEI19 directly contribute to promoting radicle protrusion and seed germination by inducing cell wall softening and reducing mechanical strength.  Additionally, the pathways of abscicic acid (ABA) and gibberellin (GA) in the transgenic materials showed significant changes, suggesting that GhPMEI53/AtPMEI19-mediated pectin methylesterification serves as a regulatory signal for the related phytohormones involved in seed germination.  In summary, GhPMEI53 and its homologs alter the mechanical properties of cell walls, which influence the mechanical resistance of the endosperm or testa.  Moreover, they impact cellular phytohormone pathways (e.g., ABA and GA) to regulate seed germination.  These findings enhance our understanding of pectin methylesterification in cellular morphological dynamics and signaling transduction, and contribute to a more comprehensive understanding of the PME/PMEI gene superfamily in plants.


Key words: seed germination ,  cell wall ,  pectin demethylesterification ,  PMEI ,  ABA