单核细胞增生李斯特菌菌膜状态下的抗氧胁迫分子机制
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摘要
单核细胞增生李斯特菌（Listeria monocytogenes）是一种能引起人畜共患病的食源性致病菌。它在自然界中普遍存在，能通过各种途径进入食品及其加工环境，由它引起的李氏杆菌病致死率高达20～30%。在食品生产环境中，该菌能形成菌膜来阻止外界胁迫环境对自身产生伤害，从而增加食品在加工过程中受到污染的几率，为食品安全埋下隐患。
单核细胞增生李斯特菌菌膜的现有研究多集中于一些生理反应上，而在分子水平上，旨在揭示菌膜形成及其在胁迫环境中反应机理的研究还处于起步阶段。2004年，本实验室利用转座子Tn917随机插入一株单核细胞增生李斯特菌4b G（Listeria monocytogenes4b G）的基因组中，成功筛选到了一批菌膜形成能力发生变化的突变株。本论文在此基础上，首先对转座子Tn917在部分突变株基因组中的插入位点及其失活靶基因进行鉴定和分析，发现一株转座子插入失活突变株GB5表现出菌膜形成能力和抗氧胁迫能力同时减弱的表型；通过对该突变株失活靶基因gltB及其旁侧序列的功能分析，初步探索了影响单核细胞增生李斯特菌4b G中菌膜形成和抗氧胁迫的分子调控途径；同时通过观测多种单核细胞增生李斯特菌血清型菌株的菌膜形成能力及抗氧胁迫生理表型，并测定相关抗氧胁迫基因的表达水平，进一步研究该菌在菌膜状态下的抗氧胁迫机制。本论文的主要研究内容和结果如下：
1、转座子Tn917在菌膜形成能力变化突变株基因组中的插入位点及失活靶基因的鉴定。根据Tn917序列设计4对特异性引物进行反向PCR，对多株转座子插入突变株的反向PCR产物进行测序及BLASTN比对分析，发现其中3株的Tn917插入位点。3株突变株的基因序列与已测序菌株L. monocytogenes str.4b F2365对应基因高度同源，根据同源基因进行命名和注释，GB1中插入基因为lm.G_2324（1600bp），编码一个保守的假定蛋白（532aa）；GB5中插入基因为lm.G_1758，又称gltB（4.59kb），编码谷氨酸合成酶大片段（1530aa）；GB8中插入位点为基因lm.G_1497（438bp）的启动子区域，该基因编码一个MerR家族转录调控子（145aa）。经Southern杂交和回复突变实验验证，lm.G_2324、gltB和lm.G_1497基因的失活是引起GB1、GB5、GB8菌膜形成能力减弱的唯一原因。
2、菌膜形成能力减弱突变株GB1、GB5、GB8与野生亲本抗胁迫能力的比较分析。暴露于100mM的H2O2下，GB5的抑菌圈（直径约为2.18cm）显著大于野生亲本（直径约为1.48cm），即GB5中基因gltB的失活造成菌膜形成能力和抗氧胁迫能力的同时减弱。此外，3株菌膜形成突变株GB1、GB5、GB8与野生亲本在生长能力、细胞运动性、抗酸胁迫能力、耐高渗透压能力方面没有表现出显著性差异。
3、突变株GB5中相关基因缺失突变株的构建及其菌膜和抗氧胁迫表型的评价。利用温敏性质粒pAUL-A构建gltB及其上游调控基因gltC的缺失突变株△gltB和△gltC，用96孔平板法评价两者的菌膜表型，基因缺失突变株△gltB和转座子插入突变株GB5具有相同的菌膜形成表型，进一步证明了gltB基因同菌膜形成能力的相关性，而基因缺失突变株△gltC表现出同△gltB类似的菌膜表型，说明gltC同样能影响菌膜形成。收集对数生长期的细胞，用3种不同的氧化剂（过氧化氢、氢过氧化枯烯和过乙酸）处理△gltB和△gltC，与野生亲本相比，两者的抗氧胁迫能力都显著减弱，揭示了基因gltB和gltC两者都能正调控菌株的抗氧胁迫能力。
4、基因gltB和gltC对菌膜形成及抗氧胁迫能力的调控途径分析。初步粘附实验结果显示，与野生型相比，△gltB和△gltC在玻璃表面的粘附能力显著降低，暗示了gltB或gltC基因的缺失可能是改变细胞表面粘附性的重要原因，这可能是引起菌膜形成能力减弱的原因。荧光定量PCR结果显示，氧胁迫环境导致野生亲本中的gltB基因表达量上调了8倍左右，gltC基因表达量上调了14倍左右，进一步证明了gltB和gltC都参与了细菌的抗氧胁迫反应。在氧胁迫环境下，基因缺失突变株△gltC中的gltB基因比野生亲本中的表达量下调了5倍左右，而△gltB中的gltC基因比野生亲本中的表达量下调了3倍左右，说明gltB和gltC基因在氧胁迫环境下能进行正向互调控，解释了△gltB和△gltC具有相同抗氧胁迫能力表型的原因。基因gltC能编码一个LysR家族转录调控子，参照同一家族成员的功能并结合上述实验结果，推测gltC基因编码的调控子能影响一些氧胁迫相关基因和细胞表面物质合成基因的表达，进而改变菌株抗性和菌膜形成，而gltB则是通过与gltC的互调控来实现影响菌株抗性和菌膜形成。
5、单核细胞增生李斯特菌中与菌膜形成及抗氧胁迫相关基因的进一步筛选。除了野生亲本4b G菌株，选取血清型为4b和1/2a的单核细胞增生李斯特菌各6株，进一步评价其菌膜形成和抗氧胁迫能力。发现在所测条件下，1/2a血清型菌株的平均菌膜形成能力（OD590约为1.17）显著高于4b血清型的（OD590约为0.66），而在对数生长期和长期存活期（20天）内，4b血清型菌株的平均抗氧胁迫能力成倍（＞2倍）高于1/2a血清型。利用Pearson相关性分析，发现在长期存活状态下（20天）的4b血清型，其菌膜形成能力和抗氧胁迫能力呈现正相关性，而1/2a血清型的两种能力间则没有明显关联。荧光定量PCR结果显示，氧胁迫相关基因sod，fri和perR在4b血清型菌株中的转录水平显著高于血清型1/2a，暗示这3个基因可能与4b血清型的强抗氧胁迫能力相关，而DNA损伤修复基因recA在菌膜状态下能够高表达，说明它在菌膜形成中可能具有重要地位。
综上所述，在单核细胞增生李斯特菌4b G中，鉴定出3个与菌膜相关的新基因lm.G_2324、gltB和lm.G_1497，其中gltB能协同其上游调控基因gltC共同影响抗氧胁迫能力和菌膜形成能力，推测其调控途径是通过gltC所编码的调控子对一些细胞表面蛋白合成基因和抗氧胁迫基因的调控来实现的；除了gltB和gltC外，在常见血清型4b和1/2a血清型菌株中，发现另外4个氧胁迫基因sod，fri，perR和recA，可能在菌膜形成及抗氧胁迫过程中具有重要作用；此外，发现只有在长期存活状态下（20天）的4b血清型菌株中，能观察到菌膜形成能力与抗氧胁迫能力的正相关性。
The foodborne pathogen Listeria monocytogenes has capability topersist on surfaces in food-processing environments, which makes it moreresistant to environmental stresses. Once L. monocytogenes persists on foodcontact surfaces and forms biofilm, it is difficult to remove by conventionalcleaning methods or inactivate by disinfection. Subsequently, food productsmay become contaminated during processing, which may introduce newchallenges to food safety in the food industry.
The increased attention has been paid to biofilm formation by L.monocytogenes since the high mortality rate associated with listeriosis(20-30%). Most researches focused on physiological responses of L.monocytogenes in biofilm, while the molecular mechanism of biofilmformation is still unclear. Recently, some mutants with the decreasedcapability of forming biofilm have been identified by screening a libraryconstructed via transposon Tn917mutagenesis of L. monocytogenes4b G(serotype4b) in our lab. In order to better understand the mechanismunderlying biofilm formation and stress-responses in L. monocytogenes, theinactivated genes of the mutants were identified first in the present study.GB5showing reduced biofilm formation and sensitivity to oxidative stress was further characterized. In addition, six serotype4b strains and six serotype1/2a strains were selected to observe biofilm formation and oxidative stresstolerance from physiological and genetic response. The main results are asfollows:
Firstly, the inactivated genes caused by transposon Tn917insertion wereidentified by inverse PCR (IPCR), and the revertants were constructed toverify their functions on biofilm formation. Four pair sets of specific primerswere designed according to the sequence of Tn917for inverse PCR, and thesuspected PCR products were sequenced. BLASTN analyses indicated thatthe inactivated gene in mutant GB1was identical to gene LMOf2365_2324(encoding a conserved hypothetical protein), that in GB5was identical toLMOf2365_1758(gltB, encoding the large subunit of glutamate synthase)and that in mutant GB8was identical to LMOf2365_1497(encoding a MerRfamily transcriptional regulator). Thus these genes were named as lm.G_2324,lm.G_1758(gltB) and lm.G_1497. The results of southern blot assay andbiofilm recovery of revertants showed that lm.G_2324, gltB and lm.G_1497were solely responsible for the positive regulation of biofilm formation intheir corresponding mutants.
Secondly, stress tolerance of biofilm formation mutants GB1, GB5, GB8and the wild-type was compared. Only mutant GB5yielded reducedoxidative stress tolerance compared with the wild-type strain, demonstratingthe involvement of the inactivated gene in GB5(gltB) in both biofilmformation and oxidative stress tolerance. Other environmental stress factorssuch as osmotic pressure (1%-10%NaCl), low and high pH (2.5-7.5),different growth temperature (4C,10C,37C,42C), and induction ofautolysis (induced by0.05%Triton X-100) did not result in significant differences between the wild-type and mutant strains.
Thirdly, mutants with deletions in gltB and its upstream gene gltC wereconstructed, and their phenotypes were observed. The temperature-sensitiveplasmid pAUL-A was usded to construct the deletion mutants△gltB and△gltC. Both△gltB and△gltC showed reduced biofilm formation andincreased sensitivity to three oxidant agents (H2O2, CHP, PAA) relative to thewild-type, implying their role in the regulation of biofilm formation as wellas oxidative stress tolerance.
Fourthly, functional analysis was carried out on△gltB and△gltC withqRT-PCR and initial adhesion assay. In the wild-type strain, gltB and gltCexpression was induced approximately8-fold and14-fold, respectively, withexposure to H2O2, providing further evidence that their gene products may beinvolved in the response to oxidative stress. The results of qRT-PCR revealedthat the gltB or gltC was most likely affected through mutual regulation underoxidative stress. Initial adhesion under liquid flow was tested in an adhesionassay, and the mutants△gltB and△gltC exhibited decreased adherence toglass surface, indicating that cell surface characteristics may be altered in themutants. It is hypothesized that a LysR-type transcriptional regulator encodedby gltC plays a critical role in controlling expression of genes involved inoxidative stress tolerance, surface attachment and biofilm formation.
Fifthly, the genes except for gltB and gltC related with biofilm formationas well as oxidative stress tolerance in L. monocytogenes were analyzed, andthe molecular mechanism was explored. Twelve strains from two commonserotypes (1/2a and4b) of L. monocytogenes were selected for furthercharacterization on biofilm formation and oxidative stress tolerance. Most1/2a strains exhibited a relatively hyper-biofilm than the4b strains in test conditions, while the later demonstrated a stronger tolerance than the former.Interestingly, in L. monocytogenes4b strains, it seems that there was apositive correlation between biofilm-formation and oxidative-stress-response,while no connection in1/2a strains. In a qRT-PCR assay, threeoxidative-stress-related genes (sod, fri and perR) displayed their importanceof serotype variation in stress resistance and the recA gene appeared to becritical for survival of L. monocytogenes in biofilm.
Overall, three novel genes were identified to be involved in positiveregulation of the biofilm formation by L. monocytogenes in this study, whichare named lm.G_2324, gltB and lm.G_1497. Among them, the gltB gene(encoding the large glutamate synthase), mutually regulating its upstreamgene gltC,(encoding a LysR-family transcriptional regulator of the gltBDoperon), was responsible for oxidation resistance and biofilm formation in L.monocytogenes4b G. The gltC gene might play a critical role in controllingexpression of genes involved in oxidative stress tolerance, surface attachmentand biofilm formation. Except for gltB and gltC, other four genes sod, fri,perR, recA showed the importance for the oxidative stress tolerance andbiofilm formation in L. monocytogenes serotypes4b and1/2a strains. Inaddition, there was a positive correlation between biofilm formation andoxidative stress response in L. monocytogenes4b strains.
单核细胞增生李斯特菌菌膜的现有研究多集中于一些生理反应上，而在分子水平上，旨在揭示菌膜形成及其在胁迫环境中反应机理的研究还处于起步阶段。2004年，本实验室利用转座子Tn917随机插入一株单核细胞增生李斯特菌4b G（Listeria monocytogenes4b G）的基因组中，成功筛选到了一批菌膜形成能力发生变化的突变株。本论文在此基础上，首先对转座子Tn917在部分突变株基因组中的插入位点及其失活靶基因进行鉴定和分析，发现一株转座子插入失活突变株GB5表现出菌膜形成能力和抗氧胁迫能力同时减弱的表型；通过对该突变株失活靶基因gltB及其旁侧序列的功能分析，初步探索了影响单核细胞增生李斯特菌4b G中菌膜形成和抗氧胁迫的分子调控途径；同时通过观测多种单核细胞增生李斯特菌血清型菌株的菌膜形成能力及抗氧胁迫生理表型，并测定相关抗氧胁迫基因的表达水平，进一步研究该菌在菌膜状态下的抗氧胁迫机制。本论文的主要研究内容和结果如下：
1、转座子Tn917在菌膜形成能力变化突变株基因组中的插入位点及失活靶基因的鉴定。根据Tn917序列设计4对特异性引物进行反向PCR，对多株转座子插入突变株的反向PCR产物进行测序及BLASTN比对分析，发现其中3株的Tn917插入位点。3株突变株的基因序列与已测序菌株L. monocytogenes str.4b F2365对应基因高度同源，根据同源基因进行命名和注释，GB1中插入基因为lm.G_2324（1600bp），编码一个保守的假定蛋白（532aa）；GB5中插入基因为lm.G_1758，又称gltB（4.59kb），编码谷氨酸合成酶大片段（1530aa）；GB8中插入位点为基因lm.G_1497（438bp）的启动子区域，该基因编码一个MerR家族转录调控子（145aa）。经Southern杂交和回复突变实验验证，lm.G_2324、gltB和lm.G_1497基因的失活是引起GB1、GB5、GB8菌膜形成能力减弱的唯一原因。
2、菌膜形成能力减弱突变株GB1、GB5、GB8与野生亲本抗胁迫能力的比较分析。暴露于100mM的H2O2下，GB5的抑菌圈（直径约为2.18cm）显著大于野生亲本（直径约为1.48cm），即GB5中基因gltB的失活造成菌膜形成能力和抗氧胁迫能力的同时减弱。此外，3株菌膜形成突变株GB1、GB5、GB8与野生亲本在生长能力、细胞运动性、抗酸胁迫能力、耐高渗透压能力方面没有表现出显著性差异。
3、突变株GB5中相关基因缺失突变株的构建及其菌膜和抗氧胁迫表型的评价。利用温敏性质粒pAUL-A构建gltB及其上游调控基因gltC的缺失突变株△gltB和△gltC，用96孔平板法评价两者的菌膜表型，基因缺失突变株△gltB和转座子插入突变株GB5具有相同的菌膜形成表型，进一步证明了gltB基因同菌膜形成能力的相关性，而基因缺失突变株△gltC表现出同△gltB类似的菌膜表型，说明gltC同样能影响菌膜形成。收集对数生长期的细胞，用3种不同的氧化剂（过氧化氢、氢过氧化枯烯和过乙酸）处理△gltB和△gltC，与野生亲本相比，两者的抗氧胁迫能力都显著减弱，揭示了基因gltB和gltC两者都能正调控菌株的抗氧胁迫能力。
4、基因gltB和gltC对菌膜形成及抗氧胁迫能力的调控途径分析。初步粘附实验结果显示，与野生型相比，△gltB和△gltC在玻璃表面的粘附能力显著降低，暗示了gltB或gltC基因的缺失可能是改变细胞表面粘附性的重要原因，这可能是引起菌膜形成能力减弱的原因。荧光定量PCR结果显示，氧胁迫环境导致野生亲本中的gltB基因表达量上调了8倍左右，gltC基因表达量上调了14倍左右，进一步证明了gltB和gltC都参与了细菌的抗氧胁迫反应。在氧胁迫环境下，基因缺失突变株△gltC中的gltB基因比野生亲本中的表达量下调了5倍左右，而△gltB中的gltC基因比野生亲本中的表达量下调了3倍左右，说明gltB和gltC基因在氧胁迫环境下能进行正向互调控，解释了△gltB和△gltC具有相同抗氧胁迫能力表型的原因。基因gltC能编码一个LysR家族转录调控子，参照同一家族成员的功能并结合上述实验结果，推测gltC基因编码的调控子能影响一些氧胁迫相关基因和细胞表面物质合成基因的表达，进而改变菌株抗性和菌膜形成，而gltB则是通过与gltC的互调控来实现影响菌株抗性和菌膜形成。
5、单核细胞增生李斯特菌中与菌膜形成及抗氧胁迫相关基因的进一步筛选。除了野生亲本4b G菌株，选取血清型为4b和1/2a的单核细胞增生李斯特菌各6株，进一步评价其菌膜形成和抗氧胁迫能力。发现在所测条件下，1/2a血清型菌株的平均菌膜形成能力（OD590约为1.17）显著高于4b血清型的（OD590约为0.66），而在对数生长期和长期存活期（20天）内，4b血清型菌株的平均抗氧胁迫能力成倍（＞2倍）高于1/2a血清型。利用Pearson相关性分析，发现在长期存活状态下（20天）的4b血清型，其菌膜形成能力和抗氧胁迫能力呈现正相关性，而1/2a血清型的两种能力间则没有明显关联。荧光定量PCR结果显示，氧胁迫相关基因sod，fri和perR在4b血清型菌株中的转录水平显著高于血清型1/2a，暗示这3个基因可能与4b血清型的强抗氧胁迫能力相关，而DNA损伤修复基因recA在菌膜状态下能够高表达，说明它在菌膜形成中可能具有重要地位。
综上所述，在单核细胞增生李斯特菌4b G中，鉴定出3个与菌膜相关的新基因lm.G_2324、gltB和lm.G_1497，其中gltB能协同其上游调控基因gltC共同影响抗氧胁迫能力和菌膜形成能力，推测其调控途径是通过gltC所编码的调控子对一些细胞表面蛋白合成基因和抗氧胁迫基因的调控来实现的；除了gltB和gltC外，在常见血清型4b和1/2a血清型菌株中，发现另外4个氧胁迫基因sod，fri，perR和recA，可能在菌膜形成及抗氧胁迫过程中具有重要作用；此外，发现只有在长期存活状态下（20天）的4b血清型菌株中，能观察到菌膜形成能力与抗氧胁迫能力的正相关性。
The foodborne pathogen Listeria monocytogenes has capability topersist on surfaces in food-processing environments, which makes it moreresistant to environmental stresses. Once L. monocytogenes persists on foodcontact surfaces and forms biofilm, it is difficult to remove by conventionalcleaning methods or inactivate by disinfection. Subsequently, food productsmay become contaminated during processing, which may introduce newchallenges to food safety in the food industry.
The increased attention has been paid to biofilm formation by L.monocytogenes since the high mortality rate associated with listeriosis(20-30%). Most researches focused on physiological responses of L.monocytogenes in biofilm, while the molecular mechanism of biofilmformation is still unclear. Recently, some mutants with the decreasedcapability of forming biofilm have been identified by screening a libraryconstructed via transposon Tn917mutagenesis of L. monocytogenes4b G(serotype4b) in our lab. In order to better understand the mechanismunderlying biofilm formation and stress-responses in L. monocytogenes, theinactivated genes of the mutants were identified first in the present study.GB5showing reduced biofilm formation and sensitivity to oxidative stress was further characterized. In addition, six serotype4b strains and six serotype1/2a strains were selected to observe biofilm formation and oxidative stresstolerance from physiological and genetic response. The main results are asfollows:
Firstly, the inactivated genes caused by transposon Tn917insertion wereidentified by inverse PCR (IPCR), and the revertants were constructed toverify their functions on biofilm formation. Four pair sets of specific primerswere designed according to the sequence of Tn917for inverse PCR, and thesuspected PCR products were sequenced. BLASTN analyses indicated thatthe inactivated gene in mutant GB1was identical to gene LMOf2365_2324(encoding a conserved hypothetical protein), that in GB5was identical toLMOf2365_1758(gltB, encoding the large subunit of glutamate synthase)and that in mutant GB8was identical to LMOf2365_1497(encoding a MerRfamily transcriptional regulator). Thus these genes were named as lm.G_2324,lm.G_1758(gltB) and lm.G_1497. The results of southern blot assay andbiofilm recovery of revertants showed that lm.G_2324, gltB and lm.G_1497were solely responsible for the positive regulation of biofilm formation intheir corresponding mutants.
Secondly, stress tolerance of biofilm formation mutants GB1, GB5, GB8and the wild-type was compared. Only mutant GB5yielded reducedoxidative stress tolerance compared with the wild-type strain, demonstratingthe involvement of the inactivated gene in GB5(gltB) in both biofilmformation and oxidative stress tolerance. Other environmental stress factorssuch as osmotic pressure (1%-10%NaCl), low and high pH (2.5-7.5),different growth temperature (4C,10C,37C,42C), and induction ofautolysis (induced by0.05%Triton X-100) did not result in significant differences between the wild-type and mutant strains.
Thirdly, mutants with deletions in gltB and its upstream gene gltC wereconstructed, and their phenotypes were observed. The temperature-sensitiveplasmid pAUL-A was usded to construct the deletion mutants△gltB and△gltC. Both△gltB and△gltC showed reduced biofilm formation andincreased sensitivity to three oxidant agents (H2O2, CHP, PAA) relative to thewild-type, implying their role in the regulation of biofilm formation as wellas oxidative stress tolerance.
Fourthly, functional analysis was carried out on△gltB and△gltC withqRT-PCR and initial adhesion assay. In the wild-type strain, gltB and gltCexpression was induced approximately8-fold and14-fold, respectively, withexposure to H2O2, providing further evidence that their gene products may beinvolved in the response to oxidative stress. The results of qRT-PCR revealedthat the gltB or gltC was most likely affected through mutual regulation underoxidative stress. Initial adhesion under liquid flow was tested in an adhesionassay, and the mutants△gltB and△gltC exhibited decreased adherence toglass surface, indicating that cell surface characteristics may be altered in themutants. It is hypothesized that a LysR-type transcriptional regulator encodedby gltC plays a critical role in controlling expression of genes involved inoxidative stress tolerance, surface attachment and biofilm formation.
Fifthly, the genes except for gltB and gltC related with biofilm formationas well as oxidative stress tolerance in L. monocytogenes were analyzed, andthe molecular mechanism was explored. Twelve strains from two commonserotypes (1/2a and4b) of L. monocytogenes were selected for furthercharacterization on biofilm formation and oxidative stress tolerance. Most1/2a strains exhibited a relatively hyper-biofilm than the4b strains in test conditions, while the later demonstrated a stronger tolerance than the former.Interestingly, in L. monocytogenes4b strains, it seems that there was apositive correlation between biofilm-formation and oxidative-stress-response,while no connection in1/2a strains. In a qRT-PCR assay, threeoxidative-stress-related genes (sod, fri and perR) displayed their importanceof serotype variation in stress resistance and the recA gene appeared to becritical for survival of L. monocytogenes in biofilm.
Overall, three novel genes were identified to be involved in positiveregulation of the biofilm formation by L. monocytogenes in this study, whichare named lm.G_2324, gltB and lm.G_1497. Among them, the gltB gene(encoding the large glutamate synthase), mutually regulating its upstreamgene gltC,(encoding a LysR-family transcriptional regulator of the gltBDoperon), was responsible for oxidation resistance and biofilm formation in L.monocytogenes4b G. The gltC gene might play a critical role in controllingexpression of genes involved in oxidative stress tolerance, surface attachmentand biofilm formation. Except for gltB and gltC, other four genes sod, fri,perR, recA showed the importance for the oxidative stress tolerance andbiofilm formation in L. monocytogenes serotypes4b and1/2a strains. Inaddition, there was a positive correlation between biofilm formation andoxidative stress response in L. monocytogenes4b strains.
引文
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