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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Amano, Atsuo Sakanaka, Akito Kuboniwa, Masae Takeuchi, Hiroki Hashino, Ei |
| Description | Author Affiliation: Sakanaka A ( From the Department of Preventive Dentistry, Osaka University Graduate School of Dentistry, Suita, Osaka 565-0871 and.); Kuboniwa M ( From the Department of Preventive Dentistry, Osaka University Graduate School of Dentistry, Suita, Osaka 565-0871 and CREST, Japan Science and Technology Agency, Saitama 332-0012, Japan kuboniwa@dent.osaka-u.ac.jp.); Takeuchi H ( From the Department of Preventive Dentistry, Osaka University Graduate School of Dentistry, Suita, Osaka 565-0871 and.); Hashino E ( From the Department of Preventive Dentistry, Osaka University Graduate School of Dentistry, Suita, Osaka 565-0871 and.); Amano A ( From the Department of Preventive Dentistry, Osaka University Graduate School of Dentistry, Suita, Osaka 565-0871 and.) |
| Abstract | Arginine is utilized by the oral inhabitant Streptococcus gordonii as a substrate of the arginine deiminase system (ADS), eventually producing ATP and $NH_{3},$ the latter of which is responsible for microbial resistance to pH stress. S. gordonii expresses a putative arginine-ornithine antiporter (ArcD) whose function has not been investigated despite relevance to the ADS and potential influence on inter-bacterial communication with periodontal pathogens that utilize amino acids as a main energy source. Here, we generated an S. gordonii ΔarcD mutant to explore the role of ArcD in physiological homeostasis and bacterial cross-feeding. First, we confirmed that S. gordonii ArcD plays crucial roles for mediating arginine uptake and promoting bacterial growth, particularly under arginine-limited conditions. Next, metabolomic profiling and transcriptional analysis of the ΔarcD mutant revealed that deletion of this gene caused intracellular accumulation of ornithine leading to malfunction of the ADS and suppression of de novo arginine biosynthesis. The mutant strain also showed increased susceptibility to low pH stress due to reduced production of ammonia. Finally, accumulation of Fusobacterium nucleatum was found to be significantly decreased in biofilm formed by the ΔarcD mutant as compared with the wild-type strain, although ornithine supplementation restored fusobacterium biovolume in dual-species biofilms with the ΔarcD mutant and also enhanced single species biofilm development by F. nucleatum. Our results are the first direct evidence showing that S. gordonii ArcD modulates not only alkali and energy production but also interspecies interaction with F. nucleatum, thus initiating a middle stage of periodontopathic biofilm formation, by metabolic cross-feeding. |
| ISSN | 00219258 |
| e-ISSN | 1083351X |
| Journal | Journal of Biological Chemistry |
| Issue Number | 35 |
| Volume Number | 290 |
| Language | English |
| Publisher | American Society for Biochemistry and Molecular Biology (United States) |
| Publisher Date | 2015-08-28 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | Amino Acid Transport Systems Metabolism Antiporters Arginine Bacterial Proteins Biofilms Streptococcal Infections Microbiology Streptococcus Gordonii Physiology Genetics Growth & Development Fusobacterium Nucleatum Gene Deletion Microbial Interactions Ornithine Research Support, Non-U.S. Gov't Biochemistry Molecular Biology |
| Content Type | Text |
| Resource Type | Article |
| Subject | Cell Biology Biochemistry Molecular Biology |
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