Camellia oleifera is an important economic woody oil plant in many Asian countries, and the anthracnose caused by Colletotrichum fructicola is prevalent in its cultivation regions, causing significant losses annually. We previously found that CfGcn5-mediated H3 acetylation governs virulence of C. fructicola. To further elucidate the regulatory mechanism of CfGcn5, we carried out mass spectrometry analysis for CfGcn5-interacting proteins and identified CfAda3 protein for functional analysis. We found that CfAda3 was mainly localized in nucleus and cooperated with CfGcn5 to acetylate H3K18 for global gene transcription. Targeted gene deletion revealed that CfAda3 is involved in growth and conidiation. Similar to ΔCfgcn5 mutant, the ΔCfada3 mutant is defective in conidial germination, appressorial formation, autophagy, and in the response to environmental stresses. These combined effects result in its non-virulence on C. oleifera. In addition, we provided evidence showing that both NLS region and ADA3 domain are required for the localization and function of CfAda3. Moreover, we indicated that the interaction with CfGcn5 is essential but not sufficient for the normal localization and full function of CfAda3. Taken together, our studies not only illustrate the prominent roles of CfAda3 in growth, development, and virulence but also highlight how CfAda3 functions together with CfGcn5 in C. fructicola.
Chen et al. (Tue,) studied this question.