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脱水素蛋白TaCOR410通过自噬作用提高小麦的抗旱性。

Dehydrin Protein TaCOR410 Improves Drought Resistance of Wheat Through Autophagy.

作者信息

Yan Mei, Song Hua-Dong, Wei Jia-Lian, Fu Kai-Yong, Li Gang, Li Yong-Bo, Li Cheng

机构信息

Agricultural College, Shi He Zi University, Shihezi 832000, China.

Shandong Luyan Seed Co., Ltd., Jinan 250100, China.

出版信息

Plants (Basel). 2025 Sep 2;14(17):2726. doi: 10.3390/plants14172726.

Abstract

Drought seriously affects wheat yield; it is therefore important to study the molecular mechanism of wheat resistance to drought stress to ensure national food security. Plants can remove harmful substances through autophagy, thus improving their drought resistance. The results of previous studies have shown that autophagy is involved in the drought stress response; however, the molecular mechanism of autophagy in response to drought stress has yet to be elucidated. In this study, molecular biological methods such as immunohistochemistry, Co-Immunoprecipitation (Co-IP), and pull-down were used to explain the molecular mechanism of autophagy in response to drought stress at the protein level. We found that a dehydrin protein called cold-regulated 410 (TaCOR410) interacts with autophagy-related 8 (TaATG8, a key protein of wheat autophagy). TaCOR410 interacted with TaATG8 through its ATG8-interacting motif (AIM), and interaction was inhibited after mutation of the AIM. Interference with inhibited autophagy and reduced the drought resistance of wheat. In contrast, transient transfection of promoted autophagy. In wheat, overexpression of improved the drought resistance of wheat. Following interference with , inhibited autophagy and reduced the drought resistance of wheat. From the above results, it is evident that autophagy can improve the drought resistance of wheat and can respond to drought stress through the interaction of TaCOR410 with TaATG8.

摘要

干旱严重影响小麦产量;因此,研究小麦抗旱胁迫的分子机制对于确保国家粮食安全至关重要。植物可以通过自噬清除有害物质,从而提高其抗旱性。先前的研究结果表明自噬参与干旱胁迫响应;然而,自噬响应干旱胁迫的分子机制尚待阐明。在本研究中,采用免疫组织化学、免疫共沉淀(Co-IP)和下拉等分子生物学方法,在蛋白质水平上解释自噬响应干旱胁迫的分子机制。我们发现一种名为冷调节蛋白410(TaCOR410)的脱水蛋白与自噬相关蛋白8(TaATG8,小麦自噬的关键蛋白)相互作用。TaCOR410通过其ATG8相互作用基序(AIM)与TaATG8相互作用,AIM突变后相互作用受到抑制。干扰TaCOR410会抑制自噬并降低小麦的抗旱性。相反,瞬时转染TaCOR410会促进自噬。在小麦中,过表达TaCOR410提高了小麦的抗旱性。干扰TaATG8后,TaCOR410抑制自噬并降低小麦的抗旱性。从上述结果可以明显看出,自噬可以提高小麦的抗旱性,并可通过TaCOR410与TaATG8的相互作用来响应干旱胁迫。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7ddb/12430722/0b1e7f2aa372/plants-14-02726-g001.jpg

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