RESUMO
Agarwood is derived from wounds in Aquilaria trees and is widely used in traditional medicine, incense, and perfume. Sesquiterpenes are one of the main active components in agarwood and are known to be induced by wounding or injury; However, the molecular mechanisms by which wounding leads to sesquiterpene formation remain largely unknown. Agarwood sesquiterpene synthase 1 (ASS1) is one of key enzymes responsible for the biosynthesis of sesquiterpenes and is a crucial jasmonate (JA)-responsive wound-inducible synthase. However, it is not known why ASS1 is not expressed in healthy trees and how its expression is induced as a result of wounding. Here, we report that ASS1 is a wound-induced gene with a promoter in which a 242-bp region (-973 to -731bp) is identified as the core sequence for responding to wound signals. AsWRKY44 binds directly to this region and represses ASS1 promoter activity. Down-regulation or disruption of AsWRKY44 can relieve the inhibition and activate ASS1 expression. In addition, AsWRKY44 is degraded and the expression of ASS1 is significantly up-regulated in response to exogenous application of methyl jasmonate. Thus, AsWRKY44 is a crucial negative regulator of wound-induced ASS1 transcription, and is central to the mechanism of sesquiterpene biosynthesis in agarwood.
Assuntos
Sesquiterpenos/metabolismo , Thymelaeaceae/metabolismo , Fatores de Transcrição/metabolismo , Regulação da Expressão Gênica de Plantas , Regiões Promotoras Genéticas , Thymelaeaceae/genéticaRESUMO
BACKGROUND: This study aimed to investigate the effect of electroacupuncture (EA) on behavior in a rat model of chronic unpredictable mild stress (CUMS) and to explore the underlying molecular mechanisms. METHODS: A total of 45 adult male Sprague-Dawley rats were randomly divided into three groups: the control, CUMS, and CUMS plus EA groups. Rats in the CUMS and EA groups were subjected to a 3-week CUMS condition, while rats in the EA group received EA at the Baihui (GV 20) acupoint (2 Hz, 0.6 mA) for 10 min once daily before being subjected to the CUMS condition. The sucrose preference test (SPT) was used as a measure to infer activation of the pleasure response to depression-like behaviour. After the behavioral test, 5-bromodeoxyuridine (BrdU) was intraperitoneally injected (100 mg/kg) and brain samples were collected 24 h later for the detection of hippocampal BrdU. Cell proliferation was determined according to the proportion of BrdU-positive cells. Brain-derived neurotrophic factor (BDNF) expression was detected. RESULTS: The severity of anhedonia, BDNF+ cells, and BrdU+ neurons in DG significantly decreased in CUMS rats, and was accompanied by a reduced BDNF and BrdU+ expression (P<0.05). After EA, the low levels of BDNF+ cells and BrdU+ expression and the depression-like behavior increased markedly (P<0.05). CONCLUSIONS: EA contributes to neuroprotection against CUMS by enhancing BDNF expression and improving hippocampal neurogenesis.