Abstract
AbstractRice bacterial blight, caused byXanthomonas oryzaepv.Oryzae(Xoo), threatens plant growth and yield. However, the molecular mechanisms underlying rice immunity againstXooremain elusive. Here, we demonstrated down-regulation of a NAC (NAM-ATAF-CUC) transcription factorOsNAC2enhanced resistance to bacterial blight disease in rice. Consistently, salicylic acid (SA) biosynthesis was greatly attenuated when OsNAC2 overexpressed. Furthermore, study demonstrated that OsNAC2 can down-regulated the expression of SA synthesis genes, thus mediating SA signal transmission. Simultaneously, OsNAC2 interacted with OsEREBP1 (AP2/ERF family) in the nucleus, may be bloking the inhibition of OsNAC2 toOsICS1,OsPAL3and so on. Furthermore, OsEREBP1 interacted with OsXb22a in the cytoplasm to exert its positive regulatory effects to bacterial blight. However,OsNAC2-overexpression kept OsEREBP1 in the nucleus and be rapidly degraded in pathogen infection, which adversely affects the interaction of OsEREBP1-OsXb22a. Our results determined that OsNAC2 inhibits the SA signaling and stably interacts with OsEREBP1 to maintain disease resistance. This OsNAC2-OsEREBP1-based homeostatic mechanism provides new insights into rice disease resistance, and it may be useful for improving the disease resistance of important crops through breeding.
Publisher
Cold Spring Harbor Laboratory
Cited by
1 articles.
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