The HmERF1-HmbZIP1 module increases powdery mildew resistance by inhibiting HmSWEET1 sugars transporting in Heracleum moellendorffii Hance.

Abstract

Powdery mildew (PM) caused by Eeysiphe heraclei is a serious concern in Heracleum moellendorffii Hance. E. heraclei is a biotrophic fungus that absorbs glucose as the major carbon energy source, using haustoria after infection. However, the mechanisms of sugar efflux from host cells to the fungus remain undetermined. Our previous study revealed that E. heraclei infection altered sugar transfer and distribution in H. moellendorffii, and that increased sugar concentrated in the infected regions. Here, RNA-sequencing was used to identify a key sugar transporter, HmSWEET1, which transported hexose sugars. Overexpression or silencing of the HmSWEET1 gene in H. moellendorffii enhanced or reduced resistance to PM by regulating sugar concentrations in infection sites. Further analysis identified two key transcription factors, HmERF1 and HmbZIP1, which are bound to the HmSWEET1 promoter, inhibit the gene expression. Furthermore, overexpression of HmERF1 and HmbZIP1 in H. moellendorffii enhanced plant resistance to PM by interfering with the ability of HmSWEET1 to transport sugars, thereby decreasing the sugar concentrations in infected leaf areas. Moreover, HmERF1 interaction with HmbZIP1 in H. moellendorffii further enhanced plant resistance. The results identified a novel HmERF1-HmbZIP1-HmSWEET1 module, which strengthened PM' resistance by reducing sugar supplies in H. moellendorffii through suppression of sugar transport by HmSWEET1.