Cenci Ugo, Ducatez Mathieu, Kadouche Derifa, Colleoni Christophe, Ball Steven G
Unité de Glycobiologie Structurale et Fonctionnelle, UMR8576 Centre National de la Recherche Scientifique, Université des Sciences et Technologies de Lille, Villeneuve d'Ascq France.
Front Cell Infect Microbiol. 2016 Jun 22;6:67. doi: 10.3389/fcimb.2016.00067. eCollection 2016.
Chlamydiales were recently proposed to have sheltered the future cyanobacterial ancestor of plastids in a common inclusion. The intracellular pathogens are thought to have donated those critical transporters that triggered the efflux of photosynthetic carbon and the consequent onset of symbiosis. Chlamydiales are also suspected to have encoded glycogen metabolism TTS (Type Three Secretion) effectors responsible for photosynthetic carbon assimilation in the eukaryotic cytosol. We now review the reasons underlying other chlamydial lateral gene transfers evidenced in the descendants of plastid endosymbiosis. In particular we show that half of the genes encoding enzymes of tryptophan synthesis in Archaeplastida are of chlamydial origin. Tryptophan concentration is an essential cue triggering two alternative modes of replication in Chlamydiales. In addition, sophisticated tryptophan starvation mechanisms are known to act as antibacterial defenses in animal hosts. We propose that Chlamydiales have donated their tryptophan operon to the emerging plastid to ensure increased synthesis of tryptophan by the plastid ancestor. This would have allowed massive expression of the tryptophan rich chlamydial transporters responsible for symbiosis. It would also have allowed possible export of this valuable amino-acid in the inclusion of the tryptophan hungry pathogens. Free-living single cell cyanobacteria are devoid of proteins able to transport this amino-acid. We therefore investigated the phylogeny of the Tyr/Trp transporters homologous to E. coli TyrP/Mre and found yet another LGT from Chlamydiales to Archaeplastida thereby considerably strengthening our proposal.
衣原体最近被提出,它曾在一个共同的包涵体中庇护了质体未来的蓝藻祖先。这些细胞内病原体被认为提供了那些关键的转运蛋白,这些转运蛋白引发了光合碳的外流以及随后共生关系的开始。衣原体还被怀疑编码了负责真核细胞质中光合碳同化的糖原代谢三型分泌(TTS)效应器。我们现在回顾质体内共生后代中其他衣原体横向基因转移背后的原因。特别是,我们发现古质体中编码色氨酸合成酶的基因有一半来自衣原体。色氨酸浓度是触发衣原体两种替代复制模式的关键线索。此外,复杂的色氨酸饥饿机制已知在动物宿主中作为抗菌防御起作用。我们提出,衣原体已将其色氨酸操纵子捐赠给新兴的质体,以确保质体祖先增加色氨酸的合成。这将使得负责共生的富含色氨酸的衣原体转运蛋白大量表达。这也将使得这种有价值的氨基酸有可能输出到缺乏色氨酸的病原体的包涵体中。自由生活的单细胞蓝藻缺乏能够转运这种氨基酸的蛋白质。因此,我们研究了与大肠杆菌TyrP/Mre同源的酪氨酸/色氨酸转运蛋白的系统发育,发现了衣原体向古质体的又一次横向基因转移,从而大大加强了我们的提议。