| Gram-negative bacterias secrete signaling molecules for coordinating activities,that are N-acyl homoserine lactone(AHLs).Previous studies in recent years proved that AHLs not only be recognized by bacterias,it can also be perceived by plants,which causes a series of physiological changes in plant activity.N-3-oxo-octanoyl-homoserine lactone(3OC8-HSL),which is one of signal molecule produced by the plant pathogens Erwinia Carotovora Subsp.Carotovora,Ecc.Previous studies have shown that 3OC8-HSL can promote plant root growth.The purpose of this study is to explore whether 3OC8-HSL can regulate plant disease resistance,and its mechanism.Resistance analysis showed that pretreatment with 3OC8-HSL of Arabidopsis and subseguent inoculation with Ecc,significantly reduced the proliferation bacterial of pathogens in plants compared with those without pretreatment of 3OC8-HSL.The strongest induction of disease resistance was obtained by pretreatment with 3OC8-HSL for 48 h.The results showed that 3OC8-HSL pretreatment can activate plant defense systems.Jasmonate(Jasmonic,JA)is endogenous growth regulators in higher plants,with a wide range of physiological functions,and plays an important role in the plant defense mechanisms.The study found that 10 μM 3OC8-HSL can significantly increase the content of JA in plants.Further with analysis revealed that the 3OC8-HSL-induced resistance in wild-type Arabidopsis was abolished in JA-signaling mutant coi1 and jar1.Gene expression analysis showed that the key gene AOS,AOC,LOX2 expression was significantly upregulated in response to AHL,suggesting that JA signaling pathway involved in 3OC8-HSL induced resistance.qRT-PCR results showed that 3OC8-HSL pretreatment significantly increased the expression of JA signal pathway resistance marker gene PDF1.2,VSP1,MYC2 in wild-type Arabidopsis,while the expression of PDF1.2,VSP1 and MYC2 are not subjected to 3OC8-HSL induction in coi1 and jar1 mutant.These results indicated that JA mediated pathway might participate 3OC8-HSL regulation of plant disease resistance. |