Lamont Richard J, Miller Daniel P
Department of Oral Immunology and Infectious Diseases, University of Louisville School of Dentistry, Louisville, KY, United States.
Department of Microbiology and Immunology, Virginia Commonwealth University Richmond, Richmond, VA, United States.
Front Oral Health. 2022 Feb 9;3:835586. doi: 10.3389/froh.2022.835586. eCollection 2022.
Tyrosine phosphorylation modifies the functionality of bacterial proteins and forms the basis of a versatile and tunable signal transduction system. The integrated action of tyrosine kinases and phosphatases controls bacterial processes important for metabolism and virulence. , a keystone pathogen in periodontal disease, possesses an extensive phosphotyrosine signaling network. The phosphorylation reaction is catalyzed by a bacterial tyrosine (BY) kinase, Ptk1, and a Ubiquitous bacterial Kinase UbK1. Dephosphorylation is mediated by a low-molecular-weight phosphatase, Ltp1 and a polymerase and histidinol phosphatase, Php1. Phosphotyrosine signaling controls exopolysaccharide production, gingipain activity, oxidative stress responses and synergistic community development with . Additionally, Ltp1 is secreted extracellularly and can be delivered inside gingival epithelial cells where it can override host cell signaling and readjust cellular physiology. The landscape of coordinated tyrosine kinase and phosphatase activity thus underlies the adaptive responses of to both the polymicrobial environment of bacterial communities and the intracellular environment of gingival epithelial cells.
酪氨酸磷酸化修饰细菌蛋白质的功能，并构成了一个通用且可调节的信号转导系统的基础。酪氨酸激酶和磷酸酶的综合作用控制着对细菌代谢和毒力至关重要的过程。牙龈卟啉单胞菌是牙周病中的关键病原体，拥有广泛的磷酸酪氨酸信号网络。磷酸化反应由细菌酪氨酸（BY）激酶Ptk1和普遍存在的细菌激酶UbK1催化。去磷酸化由低分子量磷酸酶Ltp1以及聚合酶和组氨醇磷酸酶Php1介导。磷酸酪氨酸信号控制胞外多糖的产生、牙龈蛋白酶活性、氧化应激反应以及与福赛坦氏菌的协同群落发展。此外，Ltp1分泌到细胞外，并可递送至牙龈上皮细胞内，在那里它可以超越宿主细胞信号传导并重新调整细胞生理状态。因此，酪氨酸激酶和磷酸酶活性的协同作用构成了牙龈卟啉单胞菌对细菌群落的多微生物环境和牙龈上皮细胞的细胞内环境的适应性反应的基础。
