Anaerobic utilization of Fe(III)-xenosiderophores among Bacteroides species and the distinct assimilation of Fe(III)-ferrichrome by Bacteroides fragilis within the genus.
Anaerobic utilization of Fe(III)-xenosiderophores among Bacteroides species and the distinct assimilation of Fe(III)-ferrichrome by Bacteroides fragilis within the genus.
复制标题
拟杆菌属物种中 Fe(III)-异铁载体的厌氧利用以及该属内脆弱拟杆菌对 Fe(III)-铁铬的明显同化。
DOI：
10.1002/mbo3.479
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发表时间：
2017
期刊：
影响因子：
3.4
通讯作者：
Krykunivsky,AnnaS
中科院分区：
文献类型：
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作者：
Rocha,EdsonR;Krykunivsky,AnnaS
在本研究中，我们表明拟杆菌属物种利用 Fe(III)-异铁载体作为外源铁的唯一来源，以支持体外缺氧条件下铁限制条件下的生长。脆弱拟杆菌是唯一能够利用 Fe(III)-铁铬的物种，而普通拟杆菌 ATCC 8482 和 Bacteroides thetaiotaomicronVPI 5482 能够同时利用这两种物质Fe(III)-肠杆菌素和 Fe(III)-沙莫螯素 S4 是唯一的铁来源，且呈剂量依赖性。我们研究了方法B. fragilis同化 Fe(III)-铁铬作为初始模型来了解异铁载体在厌氧菌中的利用。 fragilis 含有两个外膜 TonB 依赖性转运蛋白 (TBDT)：FchA1 和 FchA2，它们是大肠杆菌色素转运蛋白 FhuA 的同源物。与亲本菌株相比，破坏的offchA1基因在Fe(III)-铁铬上仅存在部分生长缺陷，而fchA2突变体没有生长缺陷。 chA1基因的遗传互补使生长恢复到亲本菌株水平，表明它在Fe(III)-铁红同化中发挥作用，尽管我们不能排除asB运输系统中的一些功能重叠。 fragilis 含有丰富的 TBDT，但其功能尚不清楚。然而，B的增长。 fragilison Fe(III)-铁铬在afeoAB突变体中被消除，表明在通过FeoAB运输系统运输之前，运输到周质空间的Fe(III)-铁铬在释放亚铁的周质中被减少。此外，铁色素中铁的释放可能与硫醇氧化还原系统有关，因为 trxB 缺失突变体在 Fe(III)-铁色素存在下也无法生长。基因互补的offeoABandtrxB突变体完全恢复了Fe(III)-铁铬的生长。总之，这些发现表明，拟杆菌属物种已发展出在厌氧生长条件下利用与异铁载体结合的三价铁的机制，尽管拟杆菌属在厌氧肠道环境中的生物学调节和作用仍有待了解。
In this study, we show thatBacteroidesspecies utilize Fe(III)‐xenosiderophores as the only source of exogenous iron to support growth under iron‐limiting conditions in vitro anaerobically.Bacteroides fragiliswas the only species able to utilize Fe(III)‐ferrichrome whileBacteroides vulgatusATCC 8482 andBacteroides thetaiotaomicronVPI 5482 were able to utilize both Fe(III)‐enterobactin and Fe(III)‐salmochelin S4 as the only source of iron in a dose‐dependent manner. We have investigated the wayB. fragilisassimilates Fe(III)‐ferrichrome as initial model to understand the utilization of xenosiderophores in anaerobes.B. fragiliscontains two outer membrane TonB‐dependent transporters (TBDTs), FchA1 and FchA2, which are homologues toEscherichia coliferrichrome transporter FhuA. The disruption offchA1gene had only partial growth defect on Fe(III)‐ferrichrome while thefchA2mutant had no growth defect compared to the parent strain. The genetic complementation offchA1gene restored growth to parent strain levels indicating that it plays a role in Fe(III)‐ferrichrome assimilation though we cannot rule out some functional overlap in transport systems asB. fragiliscontains abundant TBDTs whose functions are yet not understood. However, the growth ofB. fragilison Fe(III)‐ferrichrome was abolished in afeoABmutant indicating that Fe(III)‐ferrichrome transported into the periplasmic space was reduced in the periplasm releasing ferrous iron prior to transport through the FeoAB transport system. Moreover, the release of iron from the ferrichrome may be linked to the thiol redox system as thetrxBdeletion mutant was also unable to grow in the presence of Fe(III)‐ferrichrome. The genetic complementation offeoABandtrxBmutants completely restored growth on Fe(III)‐ferrichrome. Taken together, these findings show thatBacteroidesspecies have developed mechanisms to utilize ferric iron bound to xenosiderophores under anaerobic growth conditions though the regulation and role in the biology ofBacteroidesin the anaerobic intestinal environment remain to be understood.