核糖開關(guān)（Riboswitches）是結(jié)構(gòu)性RNA元素，它們與特定配體結(jié)合,，來控制它們所結(jié)合的基因的表達(dá),。核黃素和相關(guān)化合物的輸送及合成中所涉及的幾個(gè)細(xì)菌基因由一個(gè)與黃素單核苷酸（FMN）結(jié)合的核糖開關(guān)調(diào)控。
Serganov等人報(bào)告了與FMN,、核黃素和一個(gè)抗生素相結(jié)合的代謝物傳感區(qū)域的異乎尋常的結(jié)構(gòu),。這一相對來說比較開放的袋狀配體結(jié)合區(qū)域表明,，我們有可能設(shè)計(jì)基于FMN的抗菌素。（生物谷Bioon.com）
生物谷推薦原始出處：
Nature 458, 233-237 (12 March 2009) | doi:10.1038/nature07642
Coenzyme recognition and gene regulation by a flavin mononucleotide riboswitch
Alexander Serganov1,2, Lili Huang1,2 & Dinshaw J. Patel1
1 Structural Biology Program, Memorial Sloan-Kettering Cancer Center, New York, New York 10065, USA
2 These authors contributed equally to this work.
The biosynthesis of several protein cofactors is subject to feedback regulation by riboswitches1, 2, 3. Flavin mononucleotide (FMN)-specific riboswitches4, 5, also known as RFN elements6, direct expression of bacterial genes involved in the biosynthesis and transport of riboflavin (vitamin B2) and related compounds. Here we present the crystal structures of the Fusobacterium nucleatum riboswitch bound to FMN, riboflavin and antibiotic roseoflavin7. The FMN riboswitch structure, centred on an FMN-bound six-stem junction, does not fold by collinear stacking of adjacent helices, typical for folding of large RNAs. Rather, it adopts a butterfly-like scaffold, stapled together by opposingly directed but nearly identically folded peripheral domains. FMN is positioned asymmetrically within the junctional site and is specifically bound to RNA through interactions with the isoalloxazine ring chromophore and direct and Mg2+-mediated contacts with the phosphate moiety. Our structural data, complemented by binding and footprinting experiments, imply a largely pre-folded tertiary RNA architecture and FMN recognition mediated by conformational transitions within the junctional binding pocket. The inherent plasticity of the FMN-binding pocket and the availability of large openings make the riboswitch an attractive target for structure-based design of FMN-like antimicrobial compounds. Our studies also explain the effects of spontaneous and antibiotic-induced deregulatory mutations and provided molecular insights into FMN-based control of gene expression in normal and riboflavin-overproducing bacterial strains.
