Wang Yanlong, Hu Bin, Du Shipeng, Gao Shan, Chen Xiwen, Chen Defu
Department of Genetics and Cell Biology, College of Life Sciences, Nankai University, Tianjin, 300071, China.
Department of Zoology and Developmental Biology, College of Life Sciences, Nankai University, Tianjin, 300071, China.
PLoS One. 2016 May 2;11(5):e0153640. doi: 10.1371/journal.pone.0153640. eCollection 2016.
We previously screened the novel gene Ds-26-16 from a 4 M salt-stressed Dunaliella salina cDNA library and discovered that this gene conferred salt tolerance to broad-spectrum organisms, including E. coli (Escherichia coli), Haematococcus pluvialis and tobacco. To determine the mechanism of this gene conferring salt tolerance, we studied the proteome of E. coli overexpressing the full-length cDNA of Ds-26-16 using the iTRAQ (isobaric tags for relative and absolute quantification) approach. A total of 1,610 proteins were identified, which comprised 39.4% of the whole proteome. Of the 559 differential proteins, 259 were up-regulated and 300 were down-regulated. GO (gene ontology) and KEGG (Kyoto encyclopedia of genes and genomes) enrichment analyses identified 202 major proteins, including those involved in amino acid and organic acid metabolism, energy metabolism, carbon metabolism, ROS (reactive oxygen species) scavenging, membrane proteins and ABC (ATP binding cassette) transporters, and peptidoglycan synthesis, as well as 5 up-regulated transcription factors. Our iTRAQ data suggest that Ds-26-16 up-regulates the transcription factors in E. coli to enhance salt resistance through osmotic balance, energy metabolism, and oxidative stress protection. Changes in the proteome were also observed in E. coli overexpressing the ORF (open reading frame) of Ds-26-16. Furthermore, pH, nitric oxide and glycerol content analyses indicated that Ds-26-16 overexpression increases nitric oxide content but has no effect on glycerol content, thus confirming that enhanced nitric oxide synthesis via lower intercellular pH was one of the mechanisms by which Ds-26-16 confers salt tolerance to E. coli.
我们之前从一个4M盐胁迫的杜氏盐藻cDNA文库中筛选出了新基因Ds-26-16,并发现该基因赋予了包括大肠杆菌、雨生红球藻和烟草在内的广谱生物耐盐性。为了确定该基因赋予耐盐性的机制,我们使用iTRAQ(相对和绝对定量的等压标签)方法研究了过表达Ds-26-16全长cDNA的大肠杆菌的蛋白质组。共鉴定出1610种蛋白质,占整个蛋白质组的39.4%。在559种差异蛋白质中,259种上调,300种下调。GO(基因本体论)和KEGG(京都基因与基因组百科全书)富集分析确定了202种主要蛋白质,包括参与氨基酸和有机酸代谢、能量代谢、碳代谢、ROS(活性氧)清除、膜蛋白和ABC(ATP结合盒)转运体以及肽聚糖合成的蛋白质,以及5种上调的转录因子。我们的iTRAQ数据表明,Ds-26-16上调大肠杆菌中的转录因子,通过渗透平衡、能量代谢和氧化应激保护来增强耐盐性。在过表达Ds-26-16的开放阅读框(ORF)的大肠杆菌中也观察到了蛋白质组的变化。此外,pH、一氧化氮和甘油含量分析表明,Ds-26-16的过表达增加了一氧化氮含量,但对甘油含量没有影响,从而证实通过降低细胞内pH增强一氧化氮合成是Ds-26-16赋予大肠杆菌耐盐性的机制之一。