Intracellular Transposition of Mobile Genetic Elements Associated with the Colistin Resistance Gene mcr-1.
Intracellular Transposition of Mobile Genetic Elements Associated with the Colistin Resistance Gene mcr-1.
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DOI：
10.1128/spectrum.03278-22
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发表时间：
2023-02-14
影响因子：
3.7
通讯作者：
中科院分区：
文献类型：
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作者：
移动的粘菌素耐药（mcr）基因通常位于接合质粒上，在接合质粒上它们与插入序列的结合使得细菌复制子和群体中的细胞间和细胞内传播成为可能。在每一个可居住的大陆上，在许多细菌物种中，在质粒上都发现了多个mcr基因，并整合到染色体中。先前，我们显示了大肠杆菌菌株之间IncI 1质粒pMCR-E2899上mcr-1的细胞间转移。mcr-1转座和重组的细胞内动力学特征将进一步加深我们对这些重要基因如何在细菌群体中移动的理解，以及是否可以采取干预措施来阻止它们的传播。在这项研究中，我们的目的是表征转移事件的mcr-1-转座子Tn 7511（ISApl 1-mcr-1-pap 2-ISApl 1），位于质粒pMCR-E2899，使用pBACpAK截留载体。将pBACpAK转化到DH 5 α-Azir/pMCR-E2899接合子中，我们在pBACpAK中多次捕获ISAp 11，并首次观察到ISAp 11介导的mcr-1转座子（Tn 7511）转移到大肠杆菌染色体中。coli DH5α。全基因组测序使我们能够确定ISApl 1和Tn 7511在该菌株中的共有插入位点，这些位点的比较使我们能够解释观察到的转座事件。这些观察结果揭示了ISApl 1在同一细胞的多个复制子内和之间转座的结果，并显示mcr-1在细胞内转座是新型转座子Tn 7511的一部分。重要性通过分析临床相关转座子的细胞内转移，我们可以了解一旦质粒在接合后进入细胞，赋予移动的遗传元件（MGE）的耐药性的传播和演变。这些知识将有助于我们进一步了解这些重要基因如何在细菌种群中移动。利用pBACpAK包埋载体使我们能够确定新的mcr-1转座子Tn 7511的迁移率。
Mobile colistin resistance (mcr) genes are often located on conjugative plasmids, where their association with insertion sequences enables intercellular and intracellular dissemination throughout bacterial replicons and populations. Multiple mcr genes have been discovered in every habitable continent, in many bacterial species, on both plasmids and integrated into the chromosome. Previously, we showed the intercellular transfer of mcr-1 on an IncI1 plasmid, pMCR-E2899, between strains of Escherichia coli. Characterizing the intracellular dynamics of mcr-1 transposition and recombination would further our understanding of how these important genes move through bacterial populations and whether interventions can be put in place to stop their spread. In this study, we aimed to characterize transfer events from the mcr-1-containing transposon Tn7511 (ISApl1-mcr-1-pap2-ISApl1), located on plasmid pMCR-E2899, using the pBACpAK entrapment vector. Following the transformation of pBACpAK into our DH5α-Azir/pMCR-E2899 transconjugant, we captured ISApl1 in pBACpAK multiple times and, for the first time, observed the ISApl1-mediated transfer of the mcr-1 transposon (Tn7511) into the chromosome of E. coli DH5α. Whole-genome sequencing allowed us to determine consensus insertion sites of ISApl1 and Tn7511 in this strain, and comparison of these sites allowed us to explain the transposition events observed. These observations reveal the consequences of ISApl1 transposition within and between multiple replicons of the same cell and show mcr-1 transposition within the cell as part of the novel transposon Tn7511. IMPORTANCE By analyzing the intracellular transfer of clinically relevant transposons, we can understand the dissemination and evolution of drug resistance conferring mobile genetic elements (MGEs) once a plasmid enters a cell following conjugation. This knowledge will help further our understanding of how these important genes move through bacterial populations. Utilizing the pBACpAK entrapment vector has allowed us to determine the mobility of the novel mcr-1-containing transposon Tn7511.
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影响因子：
3.7
作者：
Dziewit L;Baj J;Szuplewska M;Maj A;Tabin M;Czyzkowska A;Skrzypczyk G;Adamczuk M;Sitarek T;Stawinski P;Tudek A;Wanasz K;Wardal E;Piechucka E;Bartosik D
通讯作者：
Bartosik D
影响因子：
6.4
作者：
Snesrud E;McGann P;Chandler M
通讯作者：
Chandler M
DOI：
10.1016/s0140-6736(21)02724-0
发表时间：
2022-02-12
期刊：
Lancet (London, England)
影响因子：
--
作者：
Antimicrobial Resistance Collaborators
通讯作者：
Antimicrobial Resistance Collaborators
DOI：
10.1093/jac/dkaa345
发表时间：
2020-12-01
期刊：
The Journal of antimicrobial chemotherapy
影响因子：
--
作者：
Bortolaia V;Kaas RS;Ruppe E;Roberts MC;Schwarz S;Cattoir V;Philippon A;Allesoe RL;Rebelo AR;Florensa AF;Fagelhauer L;Chakraborty T;Neumann B;Werner G;Bender JK;Stingl K;Nguyen M;Coppens J;Xavier BB;Malhotra-Kumar S;Westh H;Pinholt M;Anjum MF;Duggett NA;Kempf I;Nykäsenoja S;Olkkola S;Wieczorek K;Amaro A;Clemente L;Mossong J;Losch S;Ragimbeau C;Lund O;Aarestrup FM
通讯作者：
Aarestrup FM
影响因子：
46.9
作者：
Kolmogorov, Mikhail;Yuan, Jeffrey;Pevzner, Pavel A.
通讯作者：
Pevzner, Pavel A.