Silva Anisia J, Parker William B, Allan Paula W, Ayala Julio C, Benitez Jorge A
Morehouse School of Medicine, Department of Microbiology, Biochemistry and Immunology, Atlanta, GA 30310, USA.
Southern Research Institute Drug Discovery Division, Birmingham, AL 35205, USA.
Biochem Biophys Res Commun. 2015 May 22;461(1):65-9. doi: 10.1016/j.bbrc.2015.03.170. Epub 2015 Apr 4.
In Vibrio cholerae, the genes required for biofilm development are repressed by quorum sensing at high cell density due to the accumulation in the medium of two signaling molecules, cholera autoinducer 1 (CAI-1) and autoinducer 2 (AI-2). A significant fraction of toxigenic V. cholerae isolates, however, exhibit dysfunctional quorum sensing pathways. It was reported that transition state analogs of the enzyme methylthioadenosine/S-adenosylhomocysteine nucleosidase (MtnN) required to make AI-2 inhibited biofilm formation in the prototype quorum sensing-deficient strain N16961. This finding prompted us to examine the role of both autoinducers and MtnN in biofilm development and virulence gene expression in a quorum sensing-deficient genetic background. Here we show that deletion of mtnN encoding methylthioadenosine/S-adenosylhomocysteine nucleosidase, cqsA (CAI-1), and/or luxS (AI-2) do not prevent biofilm development. However, two independent mtnN mutants exhibited diminished growth rate and motility in swarm agar plates suggesting that, under certain conditions, MtnN could influence biofilm formation indirectly. Nevertheless, MtnN is not required for the development of a mature biofilm.
在霍乱弧菌中，由于两种信号分子——霍乱自诱导物1（CAI-1）和自诱导物2（AI-2）在培养基中的积累，生物膜形成所需的基因在高细胞密度时会受到群体感应的抑制。然而，相当一部分产毒素的霍乱弧菌分离株表现出群体感应途径功能失调。据报道，生成AI-2所需的甲基硫代腺苷/S-腺苷高半胱氨酸核苷酶（MtnN）的过渡态类似物抑制了原型群体感应缺陷菌株N16961中的生物膜形成。这一发现促使我们研究在群体感应缺陷的遗传背景下，这两种自诱导物和MtnN在生物膜形成和毒力基因表达中的作用。在此我们表明，编码甲基硫代腺苷/S-腺苷高半胱氨酸核苷酶的mtnN、cqsA（CAI-1）和/或luxS（AI-2）的缺失并不能阻止生物膜的形成。然而，两个独立的mtnN突变体在群体琼脂平板上的生长速率和运动性降低，这表明在某些条件下，MtnN可能间接影响生物膜的形成。尽管如此，成熟生物膜的形成并不需要MtnN。
