Hannauer Mélissa, Sheldon Jessica R, Heinrichs David E
Department of Microbiology and Immunology, University of Western Ontario, London, Ontario N6A 5C1, Canada.
Department of Microbiology and Immunology, University of Western Ontario, London, Ontario N6A 5C1, Canada; Centre for Human Immunology, University of Western Ontario, London, Ontario N6A 5C1 Canada.
FEBS Lett. 2015 Mar 12;589(6):730-7. doi: 10.1016/j.febslet.2015.02.002. Epub 2015 Feb 11.
A paucity of information exists concerning the mechanism(s) by which bacteria secrete siderophores into the extracellular compartment. We investigated the role of SfaA and SbnD, two major facilitator superfamily (MFS)-type efflux proteins, in the secretion of the Staphylococcus aureus siderophores staphyloferrin A (SA) and staphyloferrin B (SB), respectively. Deletion of sfaA resulted in a drastic reduction of SA secreted into the supernatant with a corresponding accumulation of SA in the cytoplasm and a significant growth defect in cells devoid of SB synthesis. In contrast, sbnD mutants showed transiently lowered levels of secreted SB, suggesting the involvement of additional efflux mechanisms.
关于细菌将铁载体分泌到细胞外区室的机制，目前信息匮乏。我们分别研究了两种主要易化子超家族（MFS）型外排蛋白SfaA和SbnD在金黄色葡萄球菌铁载体A（SA）和铁载体B（SB）分泌中的作用。缺失sfaA导致分泌到上清液中的SA大幅减少，相应地SA在细胞质中积累，并且在缺乏SB合成的细胞中出现明显的生长缺陷。相比之下，sbnD突变体显示分泌的SB水平暂时降低，这表明还存在其他外排机制。
