IbNAC1 is known to activate the defense system by reprogramming a genetic network against herbivory in sweet potato.This regulatory activity elevates plant defense potential but relatively weakens plants by IbNAC1-mediated JA response.The mechanism controlling IbNAC1 expression to balance plant vitality and Eye Care survival remains unclear.In this study, a wound-responsive G-box cis-element in the IbNAC1 promoter from -1484 to -1479 bp was identified.From a screen of wound-activated transcriptomic data, one transcriptional activator, IbbHLH3, and one repressor, IbbHLH4, were selected that bind to and activate or repress, respectively, the G-box motif in the IbNAC1 promoter to modulate the IbNAC1-mediated response.
In the early wound response, the IbbHLH3-IbbHLH3 protein complex binds to the G-box motif to activate IbNAC1 expression.Thus, an elegant defense network is activated against wounding stress.Until the late stages of wounding, IbbHLH4 interacts with IbbHLH3, and the IbbHLH3-IbbHLH4 heterodimer competes with the IbbHLH3-IbbHLH3 complex to bind the G-box and suppress IbNAC1 expression and timely terminates the defense network.Moreover, the JAZs and IbEIL1 proteins interact with IbbHLH3 to repress Leather Trousers the transactivation function of IbbHLH3 in non-wounded condition, but their transcription is immediately inhibited upon early wounding.Our work provides a genetic model that accurately switches the regulatory mechanism of IbNAC1 expression to adjust wounding physiology and represents a delicate defense regulatory network in plants.