The BHLH Transcriptional Factor PIF4 Competes with the R2R3-MYB Transcriptional Factor MYB75 to Fine-Tune Seeds Germination under High Glucose Stress

Abstract

It is known that the high level of sugar including glucose suppresses seed germination through ABA signal. ABI5 is an essential component to mediate ABA-dependent seed germination inhibition, but underlying mechanism needs more investigation. Previous study demonstrated the PIF4 activated the expression of ABI5 to suppress seed germination in darkness. Here we reported that PIF4 also mediated the seed germination inhibition through ABI5 under high concentration of glucose treatment. Furthermore, we found that PIF4 interacted with PAP1, the central factor to control anthocyanin biosynthesis. Such interaction was confirmed in vitro and in planta. Biochemical and physiological analysis revealed that PAP1 bond the promoter of ABI5 to suppress its expression, thus enhanced seed germination under high concentration of glucose treatment. Specially, PAP1 competed with PIF4 to antagonize the activation of PIF4 on ABI5 expression, thus promoted seed germination under high glucose treatment. Given these, we uncover a novel role for PIF4 and PAP1 in controlling seed germination under high glucose treatment, and reveal their antagonistic mechanism by which coordinates ABI5 expression to control seed germination in response to the glucose signal.