数字农科院2.0

Enhancing pepper resistance to MEAM1 whiteflies: the role of BABA as a chemical priming agent

文献类型： 外文期刊

作者： Zhang, Helong;Guo, Haobo;Wen, Yaqi;Wu, Qingjun;Zhang, Youjun;Jiao, Xiaoguo

作者机构：

关键词： Beta-aminobutyric acid;Bemisia tabaci;Induced defense;Phytohormone;Phenylpropanoid pathway;Defense priming

期刊名称： JOURNAL OF PEST SCIENCE

ISSN： 1612-4758

年卷期： 2025 年

页码：

收录情况： SCIE（2025版）

摘要： Plants can acquire an enhanced resistance against pathogen by application of natural or artificial compounds. Application of these compounds results in earlier, faster and/or stronger responses of plant to the subsequent pathogen attacks, a process called chemical priming. Beta-aminobutyric acid (BABA) is recognized for its inducing and priming ability to enhance plant resistance against a broad spectrum of pathogens. However, BABA potential to induce and prime pepper plant (Capsicum annuum) resistance against the invasively polyphagous MEAM1 whitefly remains understudied. In the present study, we sprayed pepper plants with 20 mM BABA to assess its defense responses, as well as the host preference and performance of MEAM1. We found that MEAM1 showed a substantial preference for settling and laying eggs and a significantly higher performance on untreated plants in comparison with those treated with BABA. Compared with the control plants, BABA-treated pepper plants significantly increased the contents of total phenols and flavonoids, which coincided with the increased expression of the genes in the phenylpropanoid pathway. These results suggest that induced resistance of pepper by BABA application reduced MEAM1 host preference and performance. Furthermore, MEAM1 infestation on BABA-treated pepper plants significantly increased the contents of total phenols and flavonoids, and their expression of the genes in the phenylpropanoid biosynthesis pathway. Collectively, our findings suggest that BABA is a potent chemical inducer and priming agent, capable of bolstering pepper resistance against MEAM1. The resistance mechanism is partly due to the activation of the salicylic acid (SA) signaling and the phenylpropanoid metabolic pathways.

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