UCLA Department of Microbiology, Immunology and Molecular Genetics, Los Angeles, CA, 90095, USA.
Microb Ecol. 2014 Aug;68(2):379-87. doi: 10.1007/s00248-014-0400-y. Epub 2014 Mar 20.
The oral opportunistic pathogen Fusobacterium nucleatum is known to interact with a large number of different bacterial species residing in the oral cavity. It adheres to a variety of Gram-positive bacteria, including oral streptococci via the arginine-inhibitable adhesin RadD. In this study, we describe a novel protein encoded by the predicted open reading frame FN1253 that appears to play a role in interspecies interactions of F. nucleatum, particularly with oral streptococci and related Gram-positive species. We designated FN1253 as aid1 (Adherence Inducing Determinant 1). Expression analyses demonstrated that this gene was induced in F. nucleatum single species biofilms, while the presence of representative members of the oral microbiota known to adhere to F. nucleatum triggered its suppression. Inactivation as well as overexpression of aid1 affected the ability of F. nucleatum to coaggregate with oral streptococci and the closely related Enterococcus faecalis, but not other Gram-positive oral species tested. Furthermore, overexpression of aid1 led to a drastic change in the structure of dual species biofilms of F. nucleatum with oral streptococci. Aid1 function was abolished in the presence of arginine and found to be dependent on RadD. Interestingly, differential expression of aid1 did not affect messenger RNA and protein levels of RadD. These findings indicate that RadD-mediated adhesion to oral streptococci involves more complex cellular processes than the simple interaction of adhesins on the surface of partner strains. Aid1 could potentially play an important role in facilitating RadD-mediated interaction with oral streptococci by increasing binding specificity of F. nucleatum to other microbial species.
口腔机会性病原体具核梭杆菌已知与大量存在于口腔中的不同细菌物种相互作用。它通过精氨酸抑制性粘附素 RadD 粘附于多种革兰氏阳性细菌,包括口腔链球菌。在这项研究中,我们描述了由预测的开放阅读框 FN1253 编码的一种新型蛋白,该蛋白似乎在具核梭杆菌的种间相互作用中发挥作用,特别是与口腔链球菌和相关的革兰氏阳性物种。我们将 FN1253 命名为 aid1(粘附诱导决定簇 1)。表达分析表明,该基因在具核梭杆菌单种生物膜中被诱导,而已知粘附具核梭杆菌的口腔微生物群代表成员的存在则触发其抑制。aid1 的失活和过表达会影响具核梭杆菌与口腔链球菌和密切相关的粪肠球菌共聚集的能力,但不会影响其他测试的革兰氏阳性口腔物种。此外,aid1 的过表达导致具核梭杆菌与口腔链球菌的双种生物膜结构发生剧烈变化。在精氨酸存在下,aid1 功能被废除,并且发现其依赖于 RadD。有趣的是,aid1 的差异表达不会影响 RadD 的信使 RNA 和蛋白质水平。这些发现表明,RadD 介导的与口腔链球菌的粘附涉及比粘附素在菌株表面简单相互作用更复杂的细胞过程。Aid1 可以通过增加具核梭杆菌与其他微生物物种的结合特异性,在促进 RadD 介导的与口腔链球菌相互作用中发挥重要作用。