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In this study, we used virus‐mediated gene silencing technology and found that the  HSP17.4  gene‐silenced cultivar Sweet Charlie plants were more susceptible to  Colletotrichum gloeosporioides  than the wild‐type Sweet Charlie, and the level of infection was even higher than that of the susceptible cultivar Benihopp. The results of differential quantitative proteomics showed that after infection with the pathogen, the expression of the downstream response genes  NPR1 ,  TGA , and  PR‐1  of the salicylic acid (SA) signalling pathway was fully up‐regulated in the wild‐type Sweet Charlie, and the expression of the core transcription factor MYC2 of the jasmonic acid (JA) pathway was significantly down‐regulated. The expression of the proteins encoded by these genes did not change significantly in the  HSP17.4 ‐silenced Sweet Charlie, indicating that the expression of HSP17.4 activated the up‐regulation of downstream signals of SA and inhibited the JA signal pathway. The experiments that used SA, methyl jasmonate, and their inhibitors to treat plants provide additional evidence that the antagonism between SA and JA regulates the resistance of strawberry plants to  C .  gloeosporioides .

HSP17.4 mediates salicylic acid and jasmonic acid pathways in the regulation of resistance to Colletotrichum gloeosporioides in strawberry