Project description:Trichomonas vaginalis, a common sexually transmitted parasite that colonizes the human urogenital tract, secretes extracellular vesicles (TvEVs) that are taken up by human cells and are speculated to be taken up by parasites as well. While the crosstalk between TvEVs and human cells has led to insight into host:parasite interactions, the role of TvEVs in infection have largely been one-sided, with little known about the effect of TvEV uptake by T. vaginalis. Approximately 11% of infections are found to be co-infections of multiple T. vaginalis strains. Clinical isolates often differ in their adherence to and cytolysis of host cells, underscoring the importance of understanding the effects of TvEV uptake within the parasite population. To address this question our lab observed the effects of EV uptake by T. vaginalis on parasite gene expression. Using RNA-seq, we showed that TvEVs upregulate expression of predicted parasite membrane proteins and identified a novel adherence factor, heteropolysaccharide binding protein (HPB2).
Project description:We aimed to delineate mechanisms of T. vaginalis resistance using transcriptome profiling of metronidazole (MTZ)-resistant and sensitive T. vaginalis clinical isolates.
Project description:The flagellated protozoan parasite Trichomonas vaginalis is the etiologic agent of trichomoniasis, the most common non-viral sexually transmitted infection worldwide. As an obligate extracellular pathogen, adherence to epithelial cells is critical for parasite survival within the human host and a better understanding of this process is a prerequisite for the development of therapies to combat infection. In this sense, recent work has shown S-acylation as a key modification that regulates pathogenesis in different protozoan parasites. However, there are no reports indicating whether this post-translational modification is a mechanism operating in T. vaginalis In order to study the extent and function of S-acylation in T. vaginalis biology, we undertook a proteomic study to profile the full scope of S-acylated proteins in this parasite and reported the identification of 363 proteins involved in a variety of biological processes such as protein transport, pathogenesis related and signaling, among others. Importantly, treatment of parasites with the palmitoylation inhibitor 2-bromopalmitate causes a significant decrease in parasite: parasite aggregation as well as adherence to host cells suggesting that palmitoylation could be modifying proteins that are key regulators of Trichomonas vaginalis pathogenesis.
Project description:Trichomonas vaginalis is an extracellular flagellated protozoan responsible for trichomoniasis, one of the most prevalent non-viral sexually transmitted infections. To persist in the host, T. vaginalis employs sophisticated gene regulation mechanisms to adapt to hostile environmental conditions. Although transcriptional regulation is crucial for this adaptation, the specific molecular mechanisms remain poorly understood. Epigenetic regulation, particularly through histone modifications, has emerged as a key modulator of gene expression. Our previous study demonstrated the role of histone modifications H3K4me3 and H3K27Ac in promoting active transcription. However, the full extent of epigenetic regulation in T. vaginalis remained unclear. In this study, we extend these findings by exploring the repressive role of two additional histone H3 modifications, H3K9me3 and H3K27me3. Genome-wide analysis reveals that these modifications are negatively correlated with gene expression, impacting not only protein-coding genes but also repeat genes and transposable elements. These findings offer new insights into the dual role of histone modifications in both activating and repressing gene expression, providing a more comprehensive understanding of epigenetic regulation in T. vaginalis. This expanded knowledge could inform the development of novel therapeutic strategies targeting the epigenetic machinery of this parasite.
Project description:Trichomonas vaginalis is an extracellular flagellated protozoan responsible for trichomoniasis, one of the most prevalent non-viral sexually transmitted infections. To persist in the host, T. vaginalis employs sophisticated gene regulation mechanisms to adapt to hostile environmental conditions. Although transcriptional regulation is crucial for this adaptation, the specific molecular mechanisms remain poorly understood. Epigenetic regulation, particularly through histone modifications, has emerged as a key modulator of gene expression. Our previous study demonstrated the role of histone modifications H3K4me3 and H3K27Ac in promoting active transcription. However, the full extent of epigenetic regulation in T. vaginalis remained unclear. In this study, we extend these findings by exploring the repressive role of two additional histone H3 modifications, H3K9me3 and H3K27me3. Genome-wide analysis reveals that these modifications are negatively correlated with gene expression, impacting not only protein-coding genes but also repeat genes and transposable elements. These findings offer new insights into the dual role of histone modifications in both activating and repressing gene expression, providing a more comprehensive understanding of epigenetic regulation in T. vaginalis. This expanded knowledge could inform the development of novel therapeutic strategies targeting the epigenetic machinery of this parasite.
Project description:The sexually transmitted parasite Trichomonas vaginalis secretes extracellular vesicles (TvEVs) that are internalized by human host cells. The goal of this experiment was to identify the effects of TvEV uptake on host cell gene expression.