Streptococcus mutans utilizes numerous metabolite transporters to obtain essential nutrients in the “feast or famine” environment of the human mouth. S. mutans and most other streptococci are considered auxotrophic for several essential vitamins including riboflavin (vitamin B₂), which is used to generate key cofactors and to perform numerous cellular redox reactions. Despite the well-known contributions of this vitamin to central metabolism, little is known about how S. mutans obtains and metabolizes B₂. The uncharacterized protein SMU.1703c displays high sequence homology to the riboflavin transporter RibU. Deletion of SMU.1703c hindered S. mutans growth in complex and defined medium in the absence of saturating levels of exogenous riboflavin, whereas deletion of cotranscribed SMU.1702c alone had no apparent effect on growth. Expression of SMU.1703c in a Bacillus subtilis riboflavin auxotroph functionally complemented growth in nonsaturating riboflavin conditions. S. mutans was also able to grow on flavin adenine dinucleotide (FAD) or flavin mononucleotide (FMN) in an SMU.1703c-dependent manner. Deletion of SMU.1703c and/or SMU.1702c impacted S. mutans acid stress tolerance, as all mutants showed improved growth at pH 5.5 compared to that of the wild type when medium was supplemented with saturating riboflavin. Cooccurrence of SMU.1703c and SMU.1702c, a hypothetical PAP2 family acid phosphatase gene, appears unique to the streptococci and may suggest a connection of SMU.1702c to the acquisition or metabolism of flavins within this genus. Identification of SMU.1703c as a RibU-like riboflavin transporter furthers our understanding of how S. mutans acquires essential micronutrients within the oral cavity and how this pathogen successfully competes within nutrient-starved oral biofilms.

中文翻译：

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变形链球菌SMU.1703c-SMU.1702c操纵子的表征揭示了其在核黄素输入和对酸胁迫的响应中的作用

变形链球菌利用多种代谢物转运蛋白在人口的“盛宴或饥荒”环境中获取必需的营养素。变形链球菌和大多数其他链球菌被认为对包括核黄素（维生素B ₂）在内的几种必需维生素是营养缺陷的，而核黄素可用于产生关键辅因子并进行许多细胞氧化还原反应。尽管这种维生素对中枢代谢的贡献众所周知，但对变形链球菌如何获得和代谢B ₂知之甚少。未表征的蛋白质SMU.1703c与核黄素转运蛋白RibU表现出高序列同源性。SMU.1703c的删除阻碍了变形链球菌在没有饱和水平的外源核黄素的情况下，在复杂且确定的培养基中生长，而单独删除共转录的SMU.1702c对生长没有明显影响。SMU.1703c在枯草芽孢杆菌核黄素营养缺陷型中的表达在非饱和核黄素条件下功能性地补充了生长。变形链球菌还能够以SMU.1703c依赖性方式在黄素腺嘌呤二核苷酸（FAD）或黄素单核苷酸（FMN）上生长。SMU.1703c和/或SMU.1702c的删除影响变形链球菌耐酸胁迫，因为当培养基中添加了饱和核黄素时，与野生型相比，所有突变体在pH 5.5下均显示出改善的生长。共现SMU.1703c和SMU.1702c，一个假设PAP2家族酸性磷酸酶基因，将出现独特的链球菌可以建议SMU.1702c到黄素收购或代谢这个属中的连接。将SMU.1703c鉴定为RibU样核黄素转运蛋白，使我们对变形链球菌如何在口腔中获得必需的微量营养素以及该病原体如何在营养缺乏的口腔生物膜中成功竞争的理解更加深入。