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<p><i>Camellia oleifera</i> is one of the three major woody oil plants worldwide, and the anthracnose caused by <i>Colletotrichum fructicola</i> is prevalent in its cultivation, causing serious losses each year. In a previous study, we found that CfGcn5-mediated H3 acetylation regulates the growth, development, and pathogenicity of <i>C. fructicola</i>. To understand the functional mechanism of CfGcn5, we performed affinity purification coupled with mass spectrometry analysis for CfGcn5-interacting proteins and identified the transcriptional adaptor CfAda2. Similar to CfGcn5, CfAda2 was localized in the nucleus and cooperated with CfGcn5 to regulate the acetylation of H3K18. Targeted gene deletion revealed that CfAda2 mediated the nuclear localization of CfGcn5. We further found that Δ<i>Cfada2</i> mutant is defective in growth, conidiation, and multiple responses to the environmental stresses. Importantly, we presented evidence showing that Δ<i>Cfada2</i> mutant exhibit accelerated autophagy flux, revealing the first link between this class of adaptor proteins and autophagy regulation. These combined effects result in its non-pathogenicity on <i>C. oleifera</i>. Furthermore, we found that the ZnF_ZZ and SANT domains of CfAda2 are essential for its interaction with CfGcn5 and that both of the domains are important for normal CfAda2 functions. Taken together, our study presents the multiple functions of CfAda2 in regulating fungal growth, development, and pathogenicity of <i>C. fructicola</i>.</p>

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The CfAda2 regulates growth, development, and pathogenicity of Colletotrichum fructicola

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年11月27日

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  • Yan Chen,
  • Yiling Wang,
  • Jing Luo,
  • Huimin Wang,
  • He Li,
  • Shengpei Zhang

摘要

Camellia oleifera is one of the three major woody oil plants worldwide, and the anthracnose caused by Colletotrichum fructicola is prevalent in its cultivation, causing serious losses each year. In a previous study, we found that CfGcn5-mediated H3 acetylation regulates the growth, development, and pathogenicity of C. fructicola. To understand the functional mechanism of CfGcn5, we performed affinity purification coupled with mass spectrometry analysis for CfGcn5-interacting proteins and identified the transcriptional adaptor CfAda2. Similar to CfGcn5, CfAda2 was localized in the nucleus and cooperated with CfGcn5 to regulate the acetylation of H3K18. Targeted gene deletion revealed that CfAda2 mediated the nuclear localization of CfGcn5. We further found that ΔCfada2 mutant is defective in growth, conidiation, and multiple responses to the environmental stresses. Importantly, we presented evidence showing that ΔCfada2 mutant exhibit accelerated autophagy flux, revealing the first link between this class of adaptor proteins and autophagy regulation. These combined effects result in its non-pathogenicity on C. oleifera. Furthermore, we found that the ZnF_ZZ and SANT domains of CfAda2 are essential for its interaction with CfGcn5 and that both of the domains are important for normal CfAda2 functions. Taken together, our study presents the multiple functions of CfAda2 in regulating fungal growth, development, and pathogenicity of C. fructicola.