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Pathogen attacks affect tree health, causing considerable economic losses as well as serious damage to the surrounding environment. Understanding the disease resistance mechanisms of trees is important for tree breeding. In previous studies on birch (Betula platyphylla × B. pendula), we identified a lesion mimic mutant called lmd. We found that reduced expression of BpEIL1 was responsible for the phenotype in lmd. Following cloning, we acquired several BpEIL1 overexpression and suppression lines in birch. In this study, we cloned the BpEIL1 promoter and found that BpEIL1 was primarily expressed in leaves, particularly in veins. We further studied the traits of transgenic lines and the function of BpEIL1 in disease resistance in birch using the BpEIL1 overexpression line OE9, the suppression line SE13 and the non-transgenic line NT. We found that hydrogen peroxide accumulated in SE13 leaves. Ascorbate peroxidase and catalase activity significantly increased in SE13. SE13 was more resistant to the fungal pathogens Alternaria alternata and Rhizoctonia solani than were the OE9 and NT lines. RNA-seq indicated that pathways related to signal transduction, disease resistance and plant immunity were enriched in SE13. BpEIL1 is thus a negative regulatory transcription factor for disease resistance in birch. This study provides a reference for disease resistance of birch and other trees.

genes and genetic systems

&lt;i&gt;BpEIL1&lt;/i&gt; negatively regulates resistance to &lt;i&gt;Rhizoctonia solani&lt;/i&gt; and &lt;i&gt;Alternaria alternata&lt;/i&gt; in birch