The mobilizable resistance island Salmonella genomic island 1 (SGI1) is specifically mobilized by IncA and IncC conjugative plasmids. SGI1, its variants and IncC plasmids propagate multidrug resistance in pathogenic enterobacteria such as Salmonella enterica serovars and Proteus mirabilis. SGI1 modifies and uses the conjugation apparatus encoded by the helper IncC plasmid, thus enhancing its own propagation. Remarkably, although SGI1 needs a coresident IncC plasmid to excise from the chromosome and transfer to a new host, these elements have been reported to be incompatible. Here, the stability of SGI1 and its helper IncC plasmid, each expressing a different fluorescent reporter protein, was monitored using fluorescence-activated cell sorting (FACS). Without selective pressure, 95% of the cells segregated into two subpopulations containing either SGI1 or the helper plasmid. Furthermore, FACS analysis revealed a high level of SGI1-specific fluorescence in IncC⁺ cells, suggesting that SGI1 undergoes active replication in the presence of the helper plasmid. SGI1 replication was confirmed by quantitative PCR assays, and extraction and restriction of its plasmid form. Deletion of genes involved in SGI1 excision from the chromosome allowed a stable coexistence of SGI1 with its helper plasmid without selective pressure. In addition, deletion of S003 (rep) or of a downstream putative iteron-based origin of replication, while allowing SGI1 excision, abolished its replication, alleviated the incompatibility with the helper plasmid and enabled its cotransfer to a new host. Like SGI1 excision functions, rep expression was found to be controlled by AcaCD, the master activator of IncC plasmid transfer. Transient SGI1 replication seems to be a key feature of the life cycle of this family of genomic islands. Sequence database analysis revealed that SGI1 variants encode either a replication initiator protein with a RepA_C domain, or an alternative replication protein with N-terminal replicase and primase C terminal 1 domains.

可移动的抗性岛沙门氏菌基因组岛1（SGI1）是通过IncA和IncC结合质粒特异性动员的。SGI1，其变体和IncC质粒可在诸如肠沙门氏菌血清和奇异变形杆菌等病原性肠细菌中传播多重耐药性。SGI1修改并使用了由辅助IncC质粒编码的结合设备，从而增强了其自身的繁殖。值得注意的是，尽管SGI1需要一个共存的IncC质粒才能从染色体上切除并转移到新的宿主中，但据报道这些元件不兼容。在这里，使用荧光激活细胞分选术（FACS）来监测各自表达不同荧光报告蛋白的SGI1及其辅助IncC质粒的稳定性。在没有选择压力的情况下，95％的细胞会分成两个包含SGI1或辅助质粒的亚群。此外，FACS分析显示，IncC ⁺中存在高水平的SGI1特异性荧光提示SGI1在辅助质粒存在下会主动复制。SGI1复制已通过定量PCR分析以及其质粒形式的提取和限制得到证实。从染色体上删除与SGI1切除有关的基因可以使SGI1及其辅助质粒稳定地共存，而不会产生选择性压力。此外，删除S003（rep）或下游假定的基于Iteron的复制起点，同时允许SGI1切除，消除了其复制，减轻了与辅助质粒的不相容性，并使其共转移至新宿主。像SGI1切除功能一样，rep发现其表达受IncC质粒转移的主激活子AcaCD控制。瞬时SGI1复制似乎是该基因组岛族生命周期的关键特征。序列数据库分析表明，SGI1变体编码具有RepA_C结构域的复制起始蛋白或具有N末端复制酶和primase C末端1结构域的替代复制蛋白。