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Ultra-high α-linolenic acid accumulating developmental defective embryo was rescued by lysophosphatidic acid acyltransferase 2.
The Plant Journal ( IF 7.2 ) Pub Date : 2020-06-23 , DOI: 10.1111/tpj.14889
Yongtai Yin 1, 2 , Zhenyi Guo 1 , Kang Chen 1 , Tian Tian 1 , Jiajun Tan 1 , Xinfeng Chen 1 , Jing Chen 1 , Bing Yang 1 , Shuyan Tang 1 , Kangfu Peng 1 , Si Liu 1 , Yu Liang 1 , Kai Zhang 1 , Longjiang Yu 1 , Maoteng Li 1, 2
Affiliation  

For decades, genetic engineering approaches to produce unusual fatty acids (UFAs) in crops has reached a bottleneck, including reduced seed oil production and seed vigor. Currently, plant models in the field of research are primarily used to investigate defects in oil production and seedling development, while the role of UFAs in embryonic developmental defects remains unknown. In this study, we developed a transgenic Arabidopsis plant model, in which the embryo exhibits severely wrinkled appearance owing to α‐linolenic acid (ALA) accumulation. RNA‐sequencing analysis in the defective embryo suggested that brassinosteroid synthesis, FA synthesis and photosynthesis were inhibited, while FA degradation, endoplasmic reticulum stress and oxidative stress were activated. Lipidomics analysis showed that ultra‐accumulated ALA is released from phosphatidylcholine as a free FA in cells, inducing severe endoplasmic reticulum and oxidative stress. Furthermore, we identified that overexpression of lysophosphatidic acid acyltransferase 2 rescued the defective phenotype. In the rescue line, the pool capacity of the Kennedy pathway was increased, and the esterification of ALA indirectly to triacylglycerol was enhanced to avoid stress. This study provides a plant model that aids in understanding the molecular mechanism of embryonic developmental defects and generates strategies to produce higher levels of UFAs.

中文翻译:

溶血磷脂酸酰基转移酶2挽救了累积发育缺陷胚胎的超高α-亚麻酸。

几十年来,用于在农作物中产生不常见脂肪酸(UFA)的基因工程方法已成为瓶颈,包括降低种子油产量和种子活力。当前,研究领域中的植物模型主要用于调查石油生产和幼苗发育中的缺陷,而UFA在胚胎发育缺陷中的作用仍然未知。在这项研究中,我们开发了一种转基因拟南芥植物模型,其中的胚胎由于α-亚麻酸(ALA)的积累而呈现出严重皱纹的外观。有缺陷的胚胎中的RNA测序分析表明,油菜素甾醇合成,FA合成和光合作用受到抑制,而FA降解,内质网应激和氧化应激被激活。脂质组学分析表明,超积累的ALA作为细胞中的游离FA从磷脂酰胆碱中释放出来,引起严重的内质网和氧化应激。此外,我们发现溶血磷脂酸酰基转移酶2的过表达挽救了缺陷表型。在救援线中,肯尼迪途径的库容量增加,并且ALA间接酯化为三酰基甘油的酯化作用得以增强,从而避免了压力。这项研究提供了一种植物模型,有助于理解胚胎发育缺陷的分子机制,并产生产生更高水平UFA的策略。在救援线中,肯尼迪途径的库容量增加,并且ALA间接酯化为三酰基甘油的酯化作用得以增强,从而避免了压力。这项研究提供了一种植物模型,有助于理解胚胎发育缺陷的分子机制,并产生产生更高水平UFA的策略。在救援线中,肯尼迪途径的库容量增加,并且ALA间接酯化为三酰基甘油的酯化作用得以增强,从而避免了压力。这项研究提供了一种植物模型,有助于理解胚胎发育缺陷的分子机制,并产生产生更高水平UFA的策略。
更新日期:2020-06-23
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