单核细胞增生李斯特菌超氧化物歧化酶在菌膜形成中的功能解析
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摘要
单核细胞增生李斯特菌是一种常见的食源性致病菌，可以引起人类的李氏杆菌病。它在自然界中分布广泛，并可在食品加工设备上形成菌膜。菌膜是微生物粘附在介质表面形成的大量细菌群居的一种生存状态。菌膜状态下的单核细胞增生李斯特菌对消毒剂等逆境的抗性明显增强，因此会增加食品反复被污染的几率，对公共卫生和人类健康带来严重危害。揭示单核细胞增生李斯特菌的菌膜形成机制对防止和控制它的危害具有重要意义。
本实验室前期构建了Tn917插入单核细胞增生李斯特菌（Listeriamonocytogenes4b G）基因组的突变子库，从中筛选到了菌膜形成能力增加的突变株LM-49，并确定了插入位点为lm.G_1771基因（编码一个假定的ABC转运子透性酶）。通过基因芯片和双向电泳技术，筛选野生型G和lm.G_1771基因缺失突变株（Δ1771）的差异表达基因和蛋白，发现超氧化物歧化酶（SOD）的表达量在Δ1771突变株中明显升高。本文在此基础上对单核细胞增生李斯特菌sod基因与lm.G_1771基因的相互关系及在菌膜形成中的作用进行了研究，并探究了抗氧胁迫相关基因与菌膜形成之间的关系，主要研究内容和结果如下：
1、同源重组载体的构建与突变株的筛选。（1）sod基因两端的同源臂连接于温敏型穿梭质粒pKSV7（含氯霉素抗性基因）中，成功构建了sod基因的同源重组载体pKSV7::sod14。（2）重组质粒分别电转化于感受态细胞G和Δ1771中，得到阳性转化子，经过双交换和抗性筛选得到sod基因单缺失突变株Δsod和lm.G_1771、sod双缺失突变株Δ1771Δsod，重组几率分别为0.46%（2/436）和0.38%（5/1300）。突变株的获得为深入研究SOD的功能以及与lm.G_1771的关系提供了必要的材料。
2、lm.G_1771基因与sod基因表达的相互影响。首先分别培养制备游离状态和菌膜状态的细胞，再利用RT-qPCR技术和酶谱分析技术测定野生型菌株G和Δ1771中的SOD表达量。结果显示，在游离状态下，Δ1771中的sod表达量与野生型相比没有发生明显变化；菌膜状态下，基因sod在Δ1771中的表达量提高了2.2倍，SOD的酶活增加了2.3倍。同时，菌膜状态下lm.G_1771基因在Δsod突变株与野生型菌株G中的表达量无明显差别。该结果表明，菌膜状态下lm.G_1771基因的缺失会使sod的表达量增加，但在游离状态下这种作用不明显；此外，菌膜状态下sod的缺失对lm.G_1771基因的表达无明显影响。
3、SOD在菌膜形成中的生理功能及其同lm.G_1771的关系。首先，利用96孔板结晶紫染色法和荧光显微镜对野生型菌株G和三株突变株（Δ1771，Δsod和Δ1771Δsod）的菌膜形成能力进行评定。其次，对这四株菌的生长能力、活性氧组分（ROS）产量和抗氧胁迫能力进行了比较。结果显示：（1）与Δ1771菌膜形成能力增强相反，Δsod和Δ1771Δsod的菌膜形成能力均明显下降，尤其是Δ1771Δsod减少地更明显；（2）Δ1771与野生型G的生长能力无明显区别，Δsod和Δ1771Δsod生长减慢并且培养相同时间形成的菌落明显偏小；（3）Δ1771与野生型G的ROS产量无明显差异，Δsod和Δ1771Δsod的ROS产量明显升高，尤其是在Δ1771Δsod中升高的更多；（4）Δ1771对氧化剂甲基紫晶（methyl viologen, MV）的敏感性与野生型G相似，Δsod和Δ1771Δsod对MV表现出高度敏感性，并且Δ1771Δsod比Δsod对甲基紫晶的敏感性还要强。上述结果表明，SOD作为重要的抗氧胁迫酶在维持细胞生长中起到重要作用，它可以抑制细胞过量ROS的产生，对菌膜形成起到正调控作用。并且，SOD可以与lm.G_1771一起调控菌膜的形成，两者在抵御氧胁迫中具有协同作用。
4、氧化剂MV（ROS产生诱导剂）对菌膜形成的影响。选取5种血清型共10株单核细胞增生李斯特菌野生型菌株，分别对它们在TSB培养基和TSB+MV培养基中的菌膜形成能力进行比较。结果显示，1mM MV可以明显抑制菌膜的形成，并影响该菌在玻片上的聚集，表明ROS不利于菌膜的形成。该结果为SOD通过抑制ROS的产生来调控菌膜形成的这一假说提供了辅证。
5、双向电泳（2-DE）及质谱联用鉴定SOD调控的蛋白。运用PDQuest8.0软件对野生型和Δsod突变株的双向电泳结果进行分析，共找到差异表达2倍以上的蛋白14个，其中10个在Δsod中下调，4个在Δsod中上调。下调的蛋白涉及细胞调节子、代谢、生长和压力反应相关的酶类；上调的蛋白涉及代谢和细胞壁合成相关的酶类；并且部分差异蛋白在菌膜形成中起到重要作用。这些结果暗示了SOD在生长和抗性方面可能的作用方式，推测了SOD正调控菌膜形成的途径。
6、利用RT-qPCR技术分析抗氧胁迫相关基因在不同状态及不同突变株中的表达。研究涉及的抗氧胁迫相关基因共分为三类：直接参与抗氧胁迫的基因（kat和fri）；抗氧胁迫基因表达的反应调节子（perR和sigB）；氧化损伤DNA修复基因（recA）。结果显示：（1）游离状态下，Δ1771和Δsod中抗氧胁迫基因和反应调节子的表达均比野生型要低，表明lm.G_1771和sod对这些基因均有正调控作用，并且这两个基因不影响recA的表达；但在双突变株Δ1771Δsod中，recA基因的表达量明显升高，由于recA具有启动SOS来维持生存的功能，表明了sod基因和lm.G_1771基因在共同维持细胞的正常生长中起到重要作用。（2）菌膜的形成会导致部分抗氧胁迫基因的上调，尤其在sod缺失突变株中，表明了菌膜的形成有利于抗氧胁迫缺陷菌株抗氧能力的修复。（3）MV可以刺激机体产生过量的内源性ROS，在MV的作用下，所研究的目的基因在野生型G中均被诱导上调，表明菌膜中形成的氧胁迫适应机制比起单纯的氧化剂刺激引起的适应机制复杂得多。
综上所述，ROS可以抑制菌膜的形成，菌膜的形成需要氧胁迫相关基因的参与。SOD可以消除机体代谢产生的过量ROS，抵御氧胁迫的损伤，影响抗性、代谢和生长相关酶类的表达，维持细胞的正常生长和菌膜的形成。并且，在菌膜形成中SOD的表达会受到lm.G_1771的影响，在抗氧胁迫中两者表现出协同效应。总之，SOD可与lm.G_1771基因编码的ABC转运子透性酶一起调控菌膜的形成，在菌膜形成中起到重要作用。
Listeria monocytogenes is a foodborne pathogen capable of causinglisteriosis in human. It is widely distributed in the environment and formsbiofilms on food processing equipments, which are communities ofmicroorganisms adhering to a surface. The resistance of L.monocytogenes in biofilm to adversity such as disinfectant is significantlyincreased, thus the pathogen can contaminate food repeatedly andthreaten public hygiene and human health. The mechanism of biofilmformation is not yet clear in L. monocytogenes, therefore, the mechanisticstudy has significant importance for food safety.
In our previous work, a mutant library was constructed by insertingTn917into the genome of L. monocytogenes4b G. One mutant strain(LM-49) with increased biofilm formation capacity was obtained throughscreening in the library, and the insertion site of Tn917located inlm.G_1771gene encoding a putative ABC transporter permease wasidentified. Two-dimensional gel electrophoresis (2-DE) and microarrayanalyses revealed that superoxide dismutase (SOD) was also up-regulatedby about2-fold in the Δ1771mutant in comparison to the wild-type4b G. In this dissertation, we analyzed the function of the sod gene in biofilmformation and its relationship with the lm.G_1771gene, and explored therelationship between antioxidative genes and biofilm formation based onthe previous studies. The main contents and conclusions are shown as thefollowing:
1. Vector construction for homologous recombination and screeningsod-deleted mutants.5’ and3’ flanking sequences of the sod gene werelinked into the temperature-sensitive shuttle vector pKSV7containing thechloromycetin resistant gene, and vector pKSV7::sod14of the sod genefor homologous recombination was constructed successfully. Therecombinant plasmid was transformed into the competent cells of thewild-type G and Δ1771respectively, positive transformants were obtained,and then the sod gene deletion mutant Δsod and double deletion mutantΔ1771Δsod were screened by double exchange and resistance selection.Recombination probability was0.46%(2/436) and0.38%(5/1300),respectively. The successful mutant construction provided the necessaryexperimental materials for the function analysis of SOD anddetermination of its relationship with lm.G_1771.
2. Determination of the relationship between the lm.G_1771geneand the sod gene. First, planktonic and biofilm cells of the wild-type Gand the mutant strain Δ1771were cultured respectively. Second,RT-qPCR and zymographic analysis were performed to determine the expression level of SOD in the wild type G and Δ1771. Research resultsshowed that there was no distinct change in the expression level of SODbetween the wild-type G and Δ1771in planktonic cells, but thetranscriptional level and activity of SOD were separately increased by2.2-fold and2.3-fold in Δ1771compared to the wild type G in biofilmcells. In addition, the expression level of lm.G_1771in Δsod mutant wasnearly consistent with in the wild type G. These results showed that theexpression level of the sod was increased due to the deletion of thelm.G_1771gene in biofilm cells but not obvious in planktonic cells, andthe sod gene had no distinct impact on the expression of lm.G_1771inbiofilm cells.
3. Physiological function of SOD in biofilm formation and itsrelationship with lm.G_1771. First, the abilities of biofilm formation inthe wild type G and three mutants (Δ1771, Δsod and Δ1771Δsod) wereassessed using crystal violet staining with96-well plates and afluorescence microscope. Second, the growth ability, ROS output and theantioxidative capacity were determined and compared among these fourstrains. The main results are as follows:(1) In contrast to the increasedability of biofilm formation in Δ1771, the biofilm formation abilities werereduced in both sod and Δ1771, especially in Δ1771Δsod.(2) There wasno obvious difference in growth rate between Δ1771and the wild-type G,but the growth rates of Δsod and Δ1771Δsod were slower than the wild-type G and their colony sizes were also smaller than the wild type Gunder the same culture conditions.(3) There was no significant differencein ROS output between Δ1771and the wild type G, and the ROSproduction of Δsod and Δ1771Δsod was enhanced distinctly compared tothe wild type G, especially in Δ1771Δsod.(4) The sensitivity of Δ1771tomethyl viologen (MV) was similar to the wild type G. Both Δsod andΔ1771Δsod were more sensitive to MV than wild type G, and thesensitivity of Δ1771Δsod was higher than that of Δsod. These resultsindicated that SOD served as an important antioxidase playing animportant role in maintaining the normal cell growth of L. monocytogenesand restraining excess ROS output, and positively regulated biofilmformation together with the lm.G_1771gene. There was a synergisticeffect in oxidative stress resistance between SOD and lm.G_1771.
4. Influence of methyl violet (MV) inducing ROS production onbiofilm formation. The biofilm formation capabilities of five serotypes often wild-type L. monocytogenes strains in TSB were compared with inTSB+MV. Results showed that1mM MV obviously inhibited biofilmformation and cell clustering on the sheet glasses, showing that ROS wentagainst biofilm formation, which provided an evidence for the hypothesisthat SOD regulated biofilm formation by suppressing ROS.
5. Two-dimensional electrophoresis (2-DE) and mass spectrometrywere conducted to identify proteins regulated by SOD.2-DE protein gel images were analysed by PDQuest8.0software to identify differentialprotein spots. As a result,14differentially spots with at least2-foldchange in intensity were identified, of which10were down-regulated and4up-regulated in Δsod. The down-regulated proteins were some enzymesinvolved in cell regulator, metabolism, growth and stress response. Theup-regulated proteins were enzymes related to metabolism and cell wallsynthesis. Part of these differential proteins played important roles inbiofilm formation. These results indicate the action mechanism of sod ingrowth and resistance and the action pathway of SOD positivelyregulating biofilm formation.
6. RT-qPCR was conducted to analyze the expression of theanti-oxidative related genes in the deletion mutants both in biofilm andplanktonic cells. The anti-oxidative related genes studied in this thesiswere divided into three classes: direct participants for antioxidation suchas kat and fri, regulators (perR and sigB) for stress response regulatingthe expression of anti-oxidative genes, and genes involved in repairingDNA damage caused by oxidization such as recA. The following resultswere obtained in this section.(1) In planktonic cells, the expression levelsof antioxidative genes and regulators were lower in Δ1771and Δsod thanin the wild-type G, showing that both lm.G_1771and sod genespositively regulated these antioxidative genes and did not influence theexpression of recA. The expression level of recA was obviously increased in Δ1771Δsod. Because recA could activate SOS, it was suggested thatsod and lm.G_1771played important roles together in maintaining cellnormal growth.(2) Biofilm formation caused the up-regulation of partialantioxidative genes, especially in Δsod, showing that biofilm formationcontributed to repairing antioxdative capacity in antioxidation deficientstrains.(3) MV could stimulate L. monocytogenes cells to generate excessendogenous ROS. Under MV treatment, the expressions of allabove-mentioned genes were up-regulated in the wild type G, indicatingthat the adaptive mechanism to oxidative stress generated in biofilmformation was more complicated than that caused by the stimulation ofonly oxidant.
In conclusion, biofilm formation can be restrained by ROS, and someanti-oxidative stress related genes were involved in biofilm formation.SOD participates in cellular detoxification and protects microorganismsagainst ROS by organism metabolism. The expression of some enzymesrelated to resistance, metabolism and growth was influenced by SOD. Inaddition, the expression of SOD was influenced by lm.G_1771, and thetwo genes showed synergistic effects on oxidative stress resistance. Theseresults indicate that SOD together with an ABC transporter coded bylm.G_1771influences biofilm formation, and they play important roles inbiofilm formation.
本实验室前期构建了Tn917插入单核细胞增生李斯特菌（Listeriamonocytogenes4b G）基因组的突变子库，从中筛选到了菌膜形成能力增加的突变株LM-49，并确定了插入位点为lm.G_1771基因（编码一个假定的ABC转运子透性酶）。通过基因芯片和双向电泳技术，筛选野生型G和lm.G_1771基因缺失突变株（Δ1771）的差异表达基因和蛋白，发现超氧化物歧化酶（SOD）的表达量在Δ1771突变株中明显升高。本文在此基础上对单核细胞增生李斯特菌sod基因与lm.G_1771基因的相互关系及在菌膜形成中的作用进行了研究，并探究了抗氧胁迫相关基因与菌膜形成之间的关系，主要研究内容和结果如下：
1、同源重组载体的构建与突变株的筛选。（1）sod基因两端的同源臂连接于温敏型穿梭质粒pKSV7（含氯霉素抗性基因）中，成功构建了sod基因的同源重组载体pKSV7::sod14。（2）重组质粒分别电转化于感受态细胞G和Δ1771中，得到阳性转化子，经过双交换和抗性筛选得到sod基因单缺失突变株Δsod和lm.G_1771、sod双缺失突变株Δ1771Δsod，重组几率分别为0.46%（2/436）和0.38%（5/1300）。突变株的获得为深入研究SOD的功能以及与lm.G_1771的关系提供了必要的材料。
2、lm.G_1771基因与sod基因表达的相互影响。首先分别培养制备游离状态和菌膜状态的细胞，再利用RT-qPCR技术和酶谱分析技术测定野生型菌株G和Δ1771中的SOD表达量。结果显示，在游离状态下，Δ1771中的sod表达量与野生型相比没有发生明显变化；菌膜状态下，基因sod在Δ1771中的表达量提高了2.2倍，SOD的酶活增加了2.3倍。同时，菌膜状态下lm.G_1771基因在Δsod突变株与野生型菌株G中的表达量无明显差别。该结果表明，菌膜状态下lm.G_1771基因的缺失会使sod的表达量增加，但在游离状态下这种作用不明显；此外，菌膜状态下sod的缺失对lm.G_1771基因的表达无明显影响。
3、SOD在菌膜形成中的生理功能及其同lm.G_1771的关系。首先，利用96孔板结晶紫染色法和荧光显微镜对野生型菌株G和三株突变株（Δ1771，Δsod和Δ1771Δsod）的菌膜形成能力进行评定。其次，对这四株菌的生长能力、活性氧组分（ROS）产量和抗氧胁迫能力进行了比较。结果显示：（1）与Δ1771菌膜形成能力增强相反，Δsod和Δ1771Δsod的菌膜形成能力均明显下降，尤其是Δ1771Δsod减少地更明显；（2）Δ1771与野生型G的生长能力无明显区别，Δsod和Δ1771Δsod生长减慢并且培养相同时间形成的菌落明显偏小；（3）Δ1771与野生型G的ROS产量无明显差异，Δsod和Δ1771Δsod的ROS产量明显升高，尤其是在Δ1771Δsod中升高的更多；（4）Δ1771对氧化剂甲基紫晶（methyl viologen, MV）的敏感性与野生型G相似，Δsod和Δ1771Δsod对MV表现出高度敏感性，并且Δ1771Δsod比Δsod对甲基紫晶的敏感性还要强。上述结果表明，SOD作为重要的抗氧胁迫酶在维持细胞生长中起到重要作用，它可以抑制细胞过量ROS的产生，对菌膜形成起到正调控作用。并且，SOD可以与lm.G_1771一起调控菌膜的形成，两者在抵御氧胁迫中具有协同作用。
4、氧化剂MV（ROS产生诱导剂）对菌膜形成的影响。选取5种血清型共10株单核细胞增生李斯特菌野生型菌株，分别对它们在TSB培养基和TSB+MV培养基中的菌膜形成能力进行比较。结果显示，1mM MV可以明显抑制菌膜的形成，并影响该菌在玻片上的聚集，表明ROS不利于菌膜的形成。该结果为SOD通过抑制ROS的产生来调控菌膜形成的这一假说提供了辅证。
5、双向电泳（2-DE）及质谱联用鉴定SOD调控的蛋白。运用PDQuest8.0软件对野生型和Δsod突变株的双向电泳结果进行分析，共找到差异表达2倍以上的蛋白14个，其中10个在Δsod中下调，4个在Δsod中上调。下调的蛋白涉及细胞调节子、代谢、生长和压力反应相关的酶类；上调的蛋白涉及代谢和细胞壁合成相关的酶类；并且部分差异蛋白在菌膜形成中起到重要作用。这些结果暗示了SOD在生长和抗性方面可能的作用方式，推测了SOD正调控菌膜形成的途径。
6、利用RT-qPCR技术分析抗氧胁迫相关基因在不同状态及不同突变株中的表达。研究涉及的抗氧胁迫相关基因共分为三类：直接参与抗氧胁迫的基因（kat和fri）；抗氧胁迫基因表达的反应调节子（perR和sigB）；氧化损伤DNA修复基因（recA）。结果显示：（1）游离状态下，Δ1771和Δsod中抗氧胁迫基因和反应调节子的表达均比野生型要低，表明lm.G_1771和sod对这些基因均有正调控作用，并且这两个基因不影响recA的表达；但在双突变株Δ1771Δsod中，recA基因的表达量明显升高，由于recA具有启动SOS来维持生存的功能，表明了sod基因和lm.G_1771基因在共同维持细胞的正常生长中起到重要作用。（2）菌膜的形成会导致部分抗氧胁迫基因的上调，尤其在sod缺失突变株中，表明了菌膜的形成有利于抗氧胁迫缺陷菌株抗氧能力的修复。（3）MV可以刺激机体产生过量的内源性ROS，在MV的作用下，所研究的目的基因在野生型G中均被诱导上调，表明菌膜中形成的氧胁迫适应机制比起单纯的氧化剂刺激引起的适应机制复杂得多。
综上所述，ROS可以抑制菌膜的形成，菌膜的形成需要氧胁迫相关基因的参与。SOD可以消除机体代谢产生的过量ROS，抵御氧胁迫的损伤，影响抗性、代谢和生长相关酶类的表达，维持细胞的正常生长和菌膜的形成。并且，在菌膜形成中SOD的表达会受到lm.G_1771的影响，在抗氧胁迫中两者表现出协同效应。总之，SOD可与lm.G_1771基因编码的ABC转运子透性酶一起调控菌膜的形成，在菌膜形成中起到重要作用。
Listeria monocytogenes is a foodborne pathogen capable of causinglisteriosis in human. It is widely distributed in the environment and formsbiofilms on food processing equipments, which are communities ofmicroorganisms adhering to a surface. The resistance of L.monocytogenes in biofilm to adversity such as disinfectant is significantlyincreased, thus the pathogen can contaminate food repeatedly andthreaten public hygiene and human health. The mechanism of biofilmformation is not yet clear in L. monocytogenes, therefore, the mechanisticstudy has significant importance for food safety.
In our previous work, a mutant library was constructed by insertingTn917into the genome of L. monocytogenes4b G. One mutant strain(LM-49) with increased biofilm formation capacity was obtained throughscreening in the library, and the insertion site of Tn917located inlm.G_1771gene encoding a putative ABC transporter permease wasidentified. Two-dimensional gel electrophoresis (2-DE) and microarrayanalyses revealed that superoxide dismutase (SOD) was also up-regulatedby about2-fold in the Δ1771mutant in comparison to the wild-type4b G. In this dissertation, we analyzed the function of the sod gene in biofilmformation and its relationship with the lm.G_1771gene, and explored therelationship between antioxidative genes and biofilm formation based onthe previous studies. The main contents and conclusions are shown as thefollowing:
1. Vector construction for homologous recombination and screeningsod-deleted mutants.5’ and3’ flanking sequences of the sod gene werelinked into the temperature-sensitive shuttle vector pKSV7containing thechloromycetin resistant gene, and vector pKSV7::sod14of the sod genefor homologous recombination was constructed successfully. Therecombinant plasmid was transformed into the competent cells of thewild-type G and Δ1771respectively, positive transformants were obtained,and then the sod gene deletion mutant Δsod and double deletion mutantΔ1771Δsod were screened by double exchange and resistance selection.Recombination probability was0.46%(2/436) and0.38%(5/1300),respectively. The successful mutant construction provided the necessaryexperimental materials for the function analysis of SOD anddetermination of its relationship with lm.G_1771.
2. Determination of the relationship between the lm.G_1771geneand the sod gene. First, planktonic and biofilm cells of the wild-type Gand the mutant strain Δ1771were cultured respectively. Second,RT-qPCR and zymographic analysis were performed to determine the expression level of SOD in the wild type G and Δ1771. Research resultsshowed that there was no distinct change in the expression level of SODbetween the wild-type G and Δ1771in planktonic cells, but thetranscriptional level and activity of SOD were separately increased by2.2-fold and2.3-fold in Δ1771compared to the wild type G in biofilmcells. In addition, the expression level of lm.G_1771in Δsod mutant wasnearly consistent with in the wild type G. These results showed that theexpression level of the sod was increased due to the deletion of thelm.G_1771gene in biofilm cells but not obvious in planktonic cells, andthe sod gene had no distinct impact on the expression of lm.G_1771inbiofilm cells.
3. Physiological function of SOD in biofilm formation and itsrelationship with lm.G_1771. First, the abilities of biofilm formation inthe wild type G and three mutants (Δ1771, Δsod and Δ1771Δsod) wereassessed using crystal violet staining with96-well plates and afluorescence microscope. Second, the growth ability, ROS output and theantioxidative capacity were determined and compared among these fourstrains. The main results are as follows:(1) In contrast to the increasedability of biofilm formation in Δ1771, the biofilm formation abilities werereduced in both sod and Δ1771, especially in Δ1771Δsod.(2) There wasno obvious difference in growth rate between Δ1771and the wild-type G,but the growth rates of Δsod and Δ1771Δsod were slower than the wild-type G and their colony sizes were also smaller than the wild type Gunder the same culture conditions.(3) There was no significant differencein ROS output between Δ1771and the wild type G, and the ROSproduction of Δsod and Δ1771Δsod was enhanced distinctly compared tothe wild type G, especially in Δ1771Δsod.(4) The sensitivity of Δ1771tomethyl viologen (MV) was similar to the wild type G. Both Δsod andΔ1771Δsod were more sensitive to MV than wild type G, and thesensitivity of Δ1771Δsod was higher than that of Δsod. These resultsindicated that SOD served as an important antioxidase playing animportant role in maintaining the normal cell growth of L. monocytogenesand restraining excess ROS output, and positively regulated biofilmformation together with the lm.G_1771gene. There was a synergisticeffect in oxidative stress resistance between SOD and lm.G_1771.
4. Influence of methyl violet (MV) inducing ROS production onbiofilm formation. The biofilm formation capabilities of five serotypes often wild-type L. monocytogenes strains in TSB were compared with inTSB+MV. Results showed that1mM MV obviously inhibited biofilmformation and cell clustering on the sheet glasses, showing that ROS wentagainst biofilm formation, which provided an evidence for the hypothesisthat SOD regulated biofilm formation by suppressing ROS.
5. Two-dimensional electrophoresis (2-DE) and mass spectrometrywere conducted to identify proteins regulated by SOD.2-DE protein gel images were analysed by PDQuest8.0software to identify differentialprotein spots. As a result,14differentially spots with at least2-foldchange in intensity were identified, of which10were down-regulated and4up-regulated in Δsod. The down-regulated proteins were some enzymesinvolved in cell regulator, metabolism, growth and stress response. Theup-regulated proteins were enzymes related to metabolism and cell wallsynthesis. Part of these differential proteins played important roles inbiofilm formation. These results indicate the action mechanism of sod ingrowth and resistance and the action pathway of SOD positivelyregulating biofilm formation.
6. RT-qPCR was conducted to analyze the expression of theanti-oxidative related genes in the deletion mutants both in biofilm andplanktonic cells. The anti-oxidative related genes studied in this thesiswere divided into three classes: direct participants for antioxidation suchas kat and fri, regulators (perR and sigB) for stress response regulatingthe expression of anti-oxidative genes, and genes involved in repairingDNA damage caused by oxidization such as recA. The following resultswere obtained in this section.(1) In planktonic cells, the expression levelsof antioxidative genes and regulators were lower in Δ1771and Δsod thanin the wild-type G, showing that both lm.G_1771and sod genespositively regulated these antioxidative genes and did not influence theexpression of recA. The expression level of recA was obviously increased in Δ1771Δsod. Because recA could activate SOS, it was suggested thatsod and lm.G_1771played important roles together in maintaining cellnormal growth.(2) Biofilm formation caused the up-regulation of partialantioxidative genes, especially in Δsod, showing that biofilm formationcontributed to repairing antioxdative capacity in antioxidation deficientstrains.(3) MV could stimulate L. monocytogenes cells to generate excessendogenous ROS. Under MV treatment, the expressions of allabove-mentioned genes were up-regulated in the wild type G, indicatingthat the adaptive mechanism to oxidative stress generated in biofilmformation was more complicated than that caused by the stimulation ofonly oxidant.
In conclusion, biofilm formation can be restrained by ROS, and someanti-oxidative stress related genes were involved in biofilm formation.SOD participates in cellular detoxification and protects microorganismsagainst ROS by organism metabolism. The expression of some enzymesrelated to resistance, metabolism and growth was influenced by SOD. Inaddition, the expression of SOD was influenced by lm.G_1771, and thetwo genes showed synergistic effects on oxidative stress resistance. Theseresults indicate that SOD together with an ABC transporter coded bylm.G_1771influences biofilm formation, and they play important roles inbiofilm formation.
引文
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