Analysis of Volatile Organic Compounds Emitted by Plant Growth-inhibiting bacteria Enterobacter aerogenes for growth inhibition effects on tobacco

• Main Authors: Fang-WeiHwu, 胡芳瑋
• Other Authors: Hao-Jen Huang
• Format: Others
• Language: zh-TW
• Published: 2016
• Online Access: http://ndltd.ncl.edu.tw/handle/ncus34

碩士 === 國立成功大學 === 生命科學系 === 104 === Microbes affect plant growth through several mechanisms. One of the mechanisms affected by microbial volatile organic compounds (mVOCs) are gaseous molecules released by microbes. There are lots of reports that focus on the influence by mixing mVOCs. Just a few researches have analyzed the compositions of mVOCs. Here I analyzed two volatile organic compounds, which are released by Enterobacter aerogenes, a plant growth-inhibiting bacteria. I found the major inhibiting compound, C2, the second large compound in E. aerogenes mVOCs. Using next generation sequencing technique, I found that the key genes of autophagy, exocyst and asparagines synthesis were up regulated when tobacco was exposed to mVOCs of E. aerogenes or C2 compound. To further confirm how vesicle trafficking results in tobacco defense mechanism, virus-induced gene silence (VIGS) was performed to silence Exo70, an important gene participates in autophagy process. NbExo70 silenced tobacco was sensitive to mVOCs of E. aerogenes and C2 compound. H2O2 was not accumulated in leaves when NbExo70 silenced tobacco exposed to mVOCs of E. aerogenes and C2 compound. According to the results I can conclude that Exo70 induces the accumulation of H2O2. The accumulation of H2O2 would induce hypersensitive response programmed cell death(HR-PCD). When the level of H2O2 was abnormal accumulation, it would disturbe the HR-PCD of plant. Thus, Exo70 would help the autophagosomal degradation of H2O2 signaling related protein. NbExo70 silenced tobacco has less deposition in callose, but when it is exposed to mVOCs of E. aerogenes and C2 compound the deposition in callose will be higher than wild-type. It seems that Exo70 is involved in callose deposition, but when under the stress tobacco will turn on another mechanism.