IADR Abstract Archives
Quorum sensing modulates the epiparasitic relationship between XH001 and TM7x
Objectives: Meta-transcriptomic profiling revealed a set of differentially regulated genes in the XH001 background when associated with TM7x versus XH001 as mono-species, including the most highly expressed gene, an lsrB homologue, encoding a putative periplasmic binding protein for the auto inducer (AI) 2 signaling molecule. The primary focus of this study was to establish a genetic system for XH001 to elucidate the role of AI-2 quorum sensing in the facilitation of the epibiotic parasitic relationship between XH001 and TM7x.
Methods: We established a genetic system in XH001, which enabled the successful construction of an XH001lsrB defective mutant. This mutant was subjected to phenotypic analyses, including growth kinetics and biofilm formation. Meanwhile, the impact of the lsrB mutation on the establishment and maintenance of the epibiotic parasitic interaction between XH001 and TM7x was further investigated. Utilizing a developed TM7x re-attachment method, we monitored this relationship using phase contrast microscopy and Fluorescence in situ Hybridization (FISH). In addition, SDS-PAGE was applied for comparison of the surface protein profiles among XH001 and XH001lsrB, both as mono-species, as well as while serving as a host for TM7x. Furthermore, the biofilm formation capability of TM7x-associated XH001 and the XH001lsrB mutant was investigated.
Results: We determined that the lsrB mutation in XH001 resulted in no phenotypic variation when cultured as mono-species compared to XH001 wild type. Strikingly, however, phase contrast microscopy and FISH analysis revealed significantly reduced micro-aggregates in the XH001lsrB background when associated with TM7x compared to wild type. SDS-PAGE analysis of the surface membrane protein composition in the TM7x-associated XH001lsrB background displayed a drastically different profile compared to wild type. Additionally, after establishing the epibiotic parasitic relationship with TM7x, XH001lsrB displayed reduced biofilm formation ability compared to TM7x-associated wildtype XH001.
Conclusions: AI-2 quorum sensing likely plays a significant role in modulating epibiotic parasitic relationship between XH001 and TM7x.
Methods: We established a genetic system in XH001, which enabled the successful construction of an XH001lsrB defective mutant. This mutant was subjected to phenotypic analyses, including growth kinetics and biofilm formation. Meanwhile, the impact of the lsrB mutation on the establishment and maintenance of the epibiotic parasitic interaction between XH001 and TM7x was further investigated. Utilizing a developed TM7x re-attachment method, we monitored this relationship using phase contrast microscopy and Fluorescence in situ Hybridization (FISH). In addition, SDS-PAGE was applied for comparison of the surface protein profiles among XH001 and XH001lsrB, both as mono-species, as well as while serving as a host for TM7x. Furthermore, the biofilm formation capability of TM7x-associated XH001 and the XH001lsrB mutant was investigated.
Results: We determined that the lsrB mutation in XH001 resulted in no phenotypic variation when cultured as mono-species compared to XH001 wild type. Strikingly, however, phase contrast microscopy and FISH analysis revealed significantly reduced micro-aggregates in the XH001lsrB background when associated with TM7x compared to wild type. SDS-PAGE analysis of the surface membrane protein composition in the TM7x-associated XH001lsrB background displayed a drastically different profile compared to wild type. Additionally, after establishing the epibiotic parasitic relationship with TM7x, XH001lsrB displayed reduced biofilm formation ability compared to TM7x-associated wildtype XH001.
Conclusions: AI-2 quorum sensing likely plays a significant role in modulating epibiotic parasitic relationship between XH001 and TM7x.