Chrysanthemum white rust (CWR), caused by Puccinia horiana Henn., has been a significant obstacle for chrysanthemum growers, impacting both the ornamental and monetary value of the plant. Tapping disease resistance genes and breeding new disease-resistant cultivars are therefore essential. Our previous study identified CmPAL as a differentially expressed gene in response to CWR from the transcriptome database. However, the molecular mechanism of its response to P. horiana infection remains unclear. Here, CmPAL was identified from the chrysanthemum resistant cultivar “C029,” and its expression was strongly activated with P. horiana infection. We found that CmPAL positively regulated resistance to P. horiana. Silencing of CmPAL in “C029” resulted in an increased spore load on leaves. Conversely, overexpression of CmPAL reduced the spore growth rates and enhanced resistance to CWR after inoculating P. horiana. In addition, overexpression of CmPAL in susceptible cultivar “Jinba” promoted the synthesis of SA and lignin and activated the expression of SA pathway genes (CmPRs and CmNPR1) and lignin pathway genes (CmCAD and CmC4H). The opposite effects were observed in the silenced lines. The promoter sequence of CmPAL was found to contain a conserved W-box cis-element. We further identified that CmWRKY15-1 binds directly to the W-box cis-element in the CmPAL promoter. Based on our results, we demonstrated that CmPAL plays a critical role in chrysanthemum resistance to CWR by promoting SA and lignin synthesis.
Keywords:
CmPAL; chrysanthemum white rust (CWR); functional analysis; lignin; salicylic acid.
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