Transcriptome analysis provides insights into the bases of salicylic acid-induced resistance to anthracnose in sorghum

Key Message Transcriptome analysis of SA sensitive and tolerant lines indicates that SA enhances anthracnose resistance in sorghum by upregulating the expression of some immune-related genes and pathways. Abstract Anthracnose caused by the hemibiotrophic pathogen Colletotrichum sublineolum is one of the most destructive diseases of sorghum, the fifth most important cereal crop in the world. Salicylic acid (SA) is a phytohormone essential for plant immunity; however, the role of SA in sorghum resistance to anthracnose has not been well explored. In this study, we found that Colletotrichum sublineolum infection induced the expression of SA-responsive genes and that exogenous SA enhanced resistance to anthracnose in the sorghum line BTx623. To rule out the possibility that SA triggers anthracnose resistance in sorghum by its direct toxic function on pathogen, an SA-tolerant line, WHEATLAND, was identified, and we found that SA treatment could not induce anthracnose resistance in WHEATLAND. Then, SA-induced transcriptome changes during Colletotrichum sublineolum infection in BTx623 and WHEATLAND were analyzed to explore the molecular mechanism of SA-triggered resistance. SA pretreatment regulated the expression of 2125 genes in BTx623 but only 524 genes in WHEATLAND during Colletotrichum sublineolum infection. The cutin, suberine and wax biosynthesis pathway involved in the plant immune response and the flavonoid biosynthesis pathway involved in anthracnose resistance were enriched in BTx623-specifically upregulated genes. Additionally, some immune-related genes, including multiple resistance genes, were differentially expressed in BTx623 and WHEATLAND. Taken together, our results revealed the mechanisms of SA-induced anthracnose resistance in sorghum at the transcriptional level and shed light on the possibility of enhancing sorghum resistance to anthracnose by activating the SA signaling pathway by molecular breeding.