Callose and Salicylic Acid Are Key Determinants of Strigolactone-Mediated Disease Resistance in Arabidopsis

Research has demonstrated that strigolactones (SLs) mediate plant disease resistance; however, the basal mechanism is unclear. Here, we provide key genetic evidence supporting how SLs mediate plant disease resistance. Exogenous application of the SL analog, <i>rac</i>-GR24, increased <i>Arabidopsis thaliana</i> resistance to virulent <i>Pseudomonas syringae</i>. SL-biosynthetic mutants and overexpression lines of more axillary growth 1 (<i>MAX1</i>, an SL-biosynthetic gene) enhanced and reduced bacterial susceptibility, respectively. In addition, <i>rac</i>-GR24 promoted bacterial pattern flg22-induced callose deposition and hydrogen peroxide production. SL-biosynthetic mutants displayed reduced callose deposition but not hydrogen peroxide production under flg22 treatment. Moreover, <i>rac</i>-GR24 did not affect avirulent effector-induced cell death between Col-0 and SL-biosynthetic mutants. Furthermore, <i>rac</i>-GR24 increased the free salicylic acid (SA) content and significantly promoted the expression of pathogenesis-related gene 1 related to SA signaling. Importantly, <i>rac</i>-GR24- and <i>MAX1</i>-induced bacterial resistance disappeared completely in Arabidopsis plants lacking both callose synthase and SA. Taken together, our data revealed that callose and SA are two important determinants in SL-mediated plant disease resistance, at least in Arabidopsis.