A Positive Regulator CsPR10‐9 Confers Resistance to Anthracnose (Colletotrichum gloeosporioides) Is Negatively Regulated by CsMYB72 in Tea Plants

ABSTRACT Anthracnose is a devastating fungal disease in tea plants caused by the pathogen Colletotrichum species. It severely affects tea yield and quality. Pathogenesis‐related (PR) genes play indispensable roles in plant resistance to fungal pathogens. Our transcriptome data showed that PR10 family genes are involved in the immune response to anthracnose infection in tea plants; however, the underlying regulatory mechanisms remain unclear. Here, we identified a PR10 family gene, CsPR10‐9 , which was highly induced by Colletotrichum gloeosporioides infection and salicylic acid (SA)/methyl jasmonate (MeJA) treatments. Transient silencing of CsPR10‐9 substantially compromised the disease resistance of tea plants, and this was accompanied by reduced activities of the antioxidant enzymes, peroxidase (POD) and superoxide dismutase (SOD), resulting in elevated reactive oxygen species (ROS) levels, decreased SA content, and increased jasmonic acid (JA) content. Transient overexpression of CsPR10‐9 in tobacco leaves showed that the lesion area on CsPR10‐9‐overexpressing leaves was significantly smaller than the control leaves, accompanied by decreased H 2 O 2 level and increased POD and SOD activities. CsPR10‐9 was negatively regulated by an R2R3‐type MYB transcription factor, CsMYB72, which directly bound to MYB transcription factor binding site cis ‐acting elements in its promoter to inhibit the expression of CsPR10‐9 . CsMYB72 is localised in the nucleus and participate in the response to anthracnose infection and SA/MeJA treatment. Moreover, silencing of CsMYB72 significantly enhanced disease resistance, increased POD and SOD activities, reduced ROS levels, increased SA content, and decreased JA content. Taken together, our results revealed that the CsMYB72‐CsPR10‐9 module regulates the SA/JA‐mediated defence response of tea plants to anthracnose. This study provides new molecular targets and a theoretical foundation for breeding of disease‐resistant tea germplasms.