Hypermotility in Clostridium perfringens strain SM101 is due to spontaneous mutations in genes linked to cell division.
Hypermotility in Clostridium perfringens strain SM101 is due to spontaneous mutations in genes linked to cell division.
复制标题
产气荚膜梭菌 SM101 菌株的过度运动是由于与细胞分裂相关的基因的自发突变所致。
DOI：
10.1128/jb.01614-14
复制
发表时间：
2014
影响因子：
3.2
通讯作者：
Melville,StephenB
中科院分区：
文献类型：
--
作者：
Liu,Hualan;McCord,KristinD;Howarth,Jonathon;Popham,DavidL;Jensen,RoderickV;Melville,StephenB
产气荚膜梭菌（Clostridium perfringens）是人和动物的革兰氏阳性厌氧病原体。虽然没有鞭毛，但C.产气荚膜杆菌细菌仍然可以利用一种滑动运动性迁移穿过表面，该滑动运动性涉及形成以端对端构象排列的细菌细丝。在菌株SM 101中，经常发现从琼脂平板上的菌落边缘产生的高运动变体。超运动细胞比野生型细胞更长，其滑动运动的视频显微镜表明它们形成长而细的细丝，快速远离菌落，类似于具有鞭毛的细菌中的群集细胞。为了确定运动过度表型的原因，测定并比较了正常菌株及其直接运动过度衍生物的基因组序列。菌株SM 124和SM 127分别是菌株SM 101和SM 102的高运动性衍生物，相对于其亲本菌株分别含有10个和6个单核苷酸多态性（SNP）。虽然SNPs在两组菌株中位于不同的基因中，但一个共同的特征是细胞分裂基因中的突变，菌株SM124（CPR_1831）中的anftsI同源物和菌株SM127（CPR_2104）中的aminE同源物。这些突变与每个基因的野生型拷贝互补恢复了正常的运动表型。一个模型解释的hypermotionality表型的原则。
Clostridium perfringens is a Gram-positive anaerobic pathogen of humans and animals. Although they lack flagella, C. perfringens bacteria can still migrate across surfaces using a type of gliding motility that involves the formation of filaments of bacteria lined up in an end-to-end conformation. In strain SM101, hypermotile variants are often found arising from the edges of colonies on agar plates. Hypermotile cells are longer than wild-type cells, and video microscopy of their gliding motility suggests that they form long, thin filaments that move rapidly away from a colony, analogously to swarmer cells in bacteria with flagella. To identify the cause(s) of the hypermotility phenotype, the genome sequences of normal strains and their direct hypermotile derivatives were determined and compared. Strains SM124 and SM127, hypermotile derivatives of strains SM101 and SM102, respectively, contained 10 and 6 single nucleotide polymorphisms (SNPs) relative to their parent strains. While SNPs were located in different genes in the two sets of strains, one feature in common was mutations in cell division genes, anftsIhomolog in strain SM124 (CPR_1831) and aminEhomolog in strain SM127 (CPR_2104). Complementation of these mutations with wild-type copies of each gene restored the normal motility phenotype. A model explaining the principles underlying the hypermotility phenotype is presented.