kdsA mutations affect FtsZ-ring formation in Escherichia coli K-12
kdsA mutations affect FtsZ-ring formation in Escherichia coli K-12
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DOI：
10.1099/00221287-148-1-103
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发表时间：
2002-01-01
期刊：
影响因子：
2.8
通讯作者：
Nagai, K
中科院分区：
文献类型：
--
作者：
Fujishima, H;Nishimura, A;Nagai, K
到目前为止，还没有人研究外膜的性质和细胞分裂之间的关系。kdsA编码3-脱氧-d -甘露糖醛酸（KDO） 8-磷酸合成酶，该合成酶催化KDO合成的第一步，是脂质A与脂多糖（LIPS）的低聚糖之间的连接物。7个含有kdsA错义突变的温度敏感突变体在KDO的产生中受到影响，所有突变体在41°c时停止分裂，形成带有一个或没有FtsZ环的细丝。所有观察到的缺陷都被质粒携带的野生型kdsA基因逆转。然而，Western blotting分析表明，FtsZ蛋白的数量不受突变的影响。突变体对各种疏水材料如新生物素、伊红Y和SDS在36℃时更敏感。然而，亚甲基蓝恢复了kdsA突变体的生长。质粒携带的野生型msbA编码ABC家族的脂质a转运蛋白，部分抑制kdsA突变。IpxA突变在脂质A生物合成的第一阶段起作用，抑制细胞分裂和生长，产生短丝。这些结果表明，由KDO生物合成缺陷引起的外膜不稳定性影响了ftsz环的形成。
No one has, as yet, addressed the relationship between the nature of the outer membrane and cell division. kdsA encodes 3-deoxy-D-manno-octulosonic acid (KDO) 8-phosphate synthetase which catalyses the first step in the synthesis of KDO, the linker between lipid A and oligosaccharide of lipopolysaccharide (LIPS). Seven temperature-sensitive mutants containing missense mutations in kdsA were affected in the production of KDO and all mutants stopped dividing at 41 degreesC and formed filaments with either one or no FtsZ ring. All observed defects were reversed by the plasmid-borne wild-type kdsA gene. Western blotting analysis, however, demonstrated that the amount of FtsZ protein was not affected by the mutation. The mutants were more susceptible to various hydrophobic materials, such as novobiocin, eosin Y and SDS at 36 degreesC. Methylene blue, however, restored kdsA mutant growth. Plasmid-borne wildtype msbA, encoding a lipid A transporter in the ABC family, partially suppressed kdsA mutation. A mutation of IpxA, functioning at the first stage in lipid A biosynthesis, inhibited both cell division and growth, producing short filaments. These results indicate that the instability of the outer membrane, caused by the defect in KDO biosynthesis, affects FtsZ-ring formation.