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Enhanced SA and Ca2+ signaling results in PCD-mediated spontaneous leaf necrosis in wheat mutant wsl
Molecular Genetics and Genomics ( IF 2.3 ) Pub Date : 2021-08-23 , DOI: 10.1007/s00438-021-01811-z
Huijuan Li 1 , Zhixin Jiao 1 , Peipei Zhang 1 , Ting Wang 1 , Jing Zhang 1 , Junchang Li 1 , Yumei Jiang 1 , Xiwen Yang 1 , Lei Li 1 , Ziping Yao 1 , Jishan Niu 1 , Dexian He 1 , Yongjing Ni 2
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Leaf is the major photosynthesis organ and the key source of wheat (Triticum aestivum L.) grain. Spotted leaf (spl) mutant is a kind of leaf lesion mimic mutants (LMMs) in plants, which is an ideal material for studying the mechanisms of leaf development. In this study, we report the leaf abnormal development molecular mechanism of a spl mutant named white stripe leaf (wsl) derived from wheat cultivar Guomai 301 (WT). Histochemical observation indicated that the leaf mesophyll cells of the wsl were destroyed in the necrosis regions. To explore the molecular regulatory network of the leaf development in mutant wsl, we employed transcriptome analysis, histochemistry, quantitative real-time PCR (qRT-PCR), and observations of the key metabolites and photosynthesis parameters. Compared to WT, the expressions of the chlorophyll synthesis and photosynthesis-related homeotic genes were repressed; many genes in the WRKY transcription factor (TF) families were highly expressed; the salicylic acid (SA) and Ca2+ signal transductions were enhanced in wsl. Both the chlorophyll contents and the photosynthesis rate were lower in wsl. The contents of SA and reactive oxygen species (ROS) were significantly higher, and the leaf rust resistance was enhanced in wsl. Based on the experimental data, a primary molecular regulatory model for leaf development in wsl was established. The results indicated that the SA accumulation and enhanced Ca2+ signaling led to programmed cell death (PCD), and ultimately resulted in spontaneous leaf necrosis of wsl. These results laid a solid foundation for further research on the molecular mechanism of leaf development in wheat.



中文翻译:

增强的 SA 和 Ca2+ 信号导致小麦突变体 wsl 中 PCD 介导的自发性叶片坏死

叶是主要的光合作用器官,是小麦(Triticum aestivum L.)籽粒的主要来源。斑点叶(spl)突变体是一种植物叶片损伤模拟突变体(LMMs),是研究叶片发育机制的理想材料。在这项研究中,我们报告了来自小麦品种国麦301(WT)的白色条纹叶wslspl突变体的叶片异常发育分子机制。组织化学观察表明wsl的叶肉细胞在坏死区被破坏。探索突变体wsl叶片发育的分子调控网络,我们采用转录组分析、组织化学、定量实时 PCR (qRT-PCR) 以及关键代谢物和光合作用参数的观察。与WT相比,叶绿素合成和光合作用相关同源基因的表达受到抑制;WRKY 转录因子 (TF) 家族中的许多基因高度表达;水杨酸 (SA) 和 Ca 2+信号转导在wsl中增强。wsl的叶绿素含量和光合作用速率均较低。wsl中SA和活性氧(ROS)含量显着升高,叶锈病抗性增强。基于实验数据,建立了叶发育的主要分子调控模型wsl成立。结果表明,SA 积累和增强的 Ca 2+信号导致程序性细胞死亡 (PCD),并最终导致wsl 的自发性叶片坏死这些结果为进一步研究小麦叶片发育的分子机制奠定了坚实的基础。

更新日期:2021-08-25
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