subsp commonly colonizes the human gut and is capable of metabolizing fucose, which is abundant in the gut. Multiple studies have focused on the mechanisms of -fucose utilization by subsp, but the regulatory pathways governing the expression of these catabolic processes are still unclear. In this study, we have conducted a structural and functional analysis of fucose metabolism transcription factor FucR derived from subsp Bi-26. Our results indicated that FucR is a fucose-sensitive repressor with more α-helices, fewer β-sheets, and β-turns. Transcriptional analysis revealed that FucR displays weak negative self-regulation, which is counteracted in the presence of -fucose. Isothermal titration calorimetry indicated that FucR has a 2:1 stoichiometry with fucose. The key amino acid residues for FucR binding fucose are Asp280 and Arg331, with mutation of Asp280 to Ala resulting in a decrease in the affinity between FucR and fucose with the value from 2.58 to 11.68 μM, and mutation of Arg331 to Ala abolishes the binding ability of FucR towards fucose. FucR specifically recognized and bound to a 20-bp incomplete palindrome sequence (5’-ACCCCAATTACGAAAATTTTT-3’), and the affinity of the fucose-loaded FucR for the DNA fragment was lower than apo-FucR. The results provided new insights into the regulating -fucose metabolism by subsp

中文翻译：

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对 FucR 转录因子控制长双歧杆菌亚种 L-岩藻糖代谢的分子见解。婴儿

亚种通常定植于人类肠道，并且能够代谢肠道中丰富的岩藻糖。多项研究都集中在亚种利用β-岩藻糖的机制上，但控制这些分解代谢过程表达的调控途径仍不清楚。在本研究中，我们对 Bi-26 亚种衍生的岩藻糖代谢转录因子 FucR 进行了结构和功能分析。我们的结果表明，FucR 是一种岩藻糖敏感阻遏蛋白，具有更多的 α 螺旋、更少的 β 折叠和 β 转角。转录分析表明，FucR 显示出较弱的负向自我调节，而这种负向自我调节在 β-岩藻糖的存在下会被抵消。等温滴定量热法表明FucR与岩藻糖的化学计量比为2:1。 FucR结合岩藻糖的关键氨基酸残基是Asp280和Arg331，Asp280突变为Ala导致FucR与岩藻糖的亲和力降低，值为2.58~11.68 μM，Arg331突变为Ala则丧失了结合能力FucR 朝向岩藻糖。 FucR特异性识别并结合20 bp不完整回文序列（5'-ACCCCAATTACGAAAATTTTT-3'），并且负载岩藻糖的FucR对该DNA片段的亲和力低于apo-FucR。该结果为亚种调节岩藻糖代谢提供了新的见解。