Pathogenic neisseriae can use hemoglobin, transferrin, and lactoferrin independently of the tonB locus.
Pathogenic neisseriae can use hemoglobin, transferrin, and lactoferrin independently of the tonB locus.
复制标题
致病性奈瑟菌可以独立于 tonB 基因座使用血红蛋白、转铁蛋白和乳铁蛋白。
DOI：
10.1128/jb.182.19.5586-5591.2000
复制
发表时间：
2000
影响因子：
3.2
通讯作者：
Genco,CA
中科院分区：
文献类型：
--
作者：
Desai,PJ;Garges,E;Genco,CA
最近在几种革兰氏阴性细菌中发现了冗余的TonB系统，它在TonB依赖的配体的铁运输中发挥作用。我们在这里证明，除了先前描述的BLOCUS之外，还有一种替代系统可用于在脑膜炎奈瑟菌和淋病奈瑟菌中利用来自血红蛋白、转铁蛋白或乳铁蛋白的铁。在含血红蛋白的培养液中孵育，脑膜炎奈瑟菌IR3436(TonB exbB exbD缺失突变体)和n.淋病PD3401(Ton插入突变体)产生的菌落可以与血红蛋白一起生长。将Hb+变异体(PD3437或PD3402)转移到以血红蛋白、转铁蛋白和/或乳铁蛋白为唯一铁源的培养基中，所产生的生长与观察到的野生型菌株相当。转变；转变；转变。脑膜炎IR3436或。带有来自Hb+变种的染色体DNA的淋病PD3401产生了能够与血红蛋白一起生长的转化子。当我们灭活NeisSeraHb+变异体中依赖TonB的外膜血红蛋白受体(HmbR或HpuB)时，这些菌株不能与血红蛋白一起生长；但可以观察到转铁蛋白和/或乳铁蛋白的生长。这些结果表明，致病性奈瑟氏菌中从血红蛋白、转铁蛋白和乳铁蛋白中积累的铁可以通过一个独立于先前描述的BLOCUS的系统发生。
Redundant TonB systems which function in iron transport from TonB-dependent ligands have recently been identified in several gram-negative bacteria. We demonstrate here that in addition to the previously describedtonBlocus, an alternative system exists for the utilization of iron from hemoglobin, transferrin, or lactoferrin inNeisseria meningitidisandNeisseria gonorrhoeae. Following incubation on media containing hemoglobin,N. meningitidisIR3436 (tonB exbB exbDdeletion mutant) andN. gonorrhoeaePD3401 (tonBinsertional mutant) give rise to colonies which can grow with hemoglobin. Transfer of Hb+variants (PD3437 or PD3402) to media containing hemoglobin, transferrin, and/or lactoferrin as sole iron sources resulted in growth comparable to that observed for the wild-type strains. Transformation ofN. meningitidisIR3436 orN. gonorrhoeaePD3401 with chromosomal DNA from the Hb+variants yielded transformants capable of growth with hemoglobin. When we inactivated the TonB-dependent outer membrane hemoglobin receptors (HmbR or HpuB) in theNeisseriaHb+variants, these strains could not grow with hemoglobin; however, growth was observed with transferrin and/or lactoferrin. These results demonstrate that accumulation of iron from hemoglobin, transferrin, and lactoferrin in the pathogenic neisseriae can occur via a system that is independent of the previously describedtonBlocus.