Publications by authors named "Emma M Briggs"
Article Synopsis
- * In African trypanosomes, a specific process called targeted recombination helps them evade host immunity by activating one out of many silent variant genes, with unclear mechanisms behind it.
- * The enzyme RAD51 interacts with RNA-DNA hybrids and is crucial for repairing DNA breaks, with mutations in RAD51 affecting the abundance of these hybrids and disrupting the repair related to immune evasion strategies.
Article Synopsis
- * Research on the African trypanosome, a unique single-cell eukaryotic parasite, identified 602 potential proteins that interact with RNA-DNA hybrids, revealing both shared and unique functions compared to mammals.
- * Certain factors, like helicases and RAD51 paralogues, are crucial for maintaining RNA-DNA hybrid levels and DNA damage repair in T. brucei, influencing its ability to evade the host's immune response.
Article Synopsis
- The transition of mammalian parasites from "slender" to "stumpy" forms occurs through a process regulated by quorum-sensing, marking a key morphological change during infection.
- Research shows that once parasites enter the "stumpy" phase, they undergo an irreversible developmental arrest, impacting their ability to replicate in both acute and chronic infections in mice.
- Analysis reveals that while stumpy forms dominate, replicating parasites are rare in the bloodstream once the infection is established, suggesting these parasites have adapted more for transmission rather than proliferation or evading the immune system.
Article Synopsis
- - African trypanosomes exist in two main forms: bloodstream forms (BSFs) in mammals and procyclic forms in the tsetse fly, which are essential for their life cycle and host colonization.
- - Researchers used single-cell transcriptomics to analyze the gene expression during the cell cycle of these forms without needing to sort or synchronize the cells first.
- - The study established a core set of genes that are consistently expressed across both forms and found differences in transcript dynamics, including delays between gene expression and protein levels, leading to new insights that can be explored through an interactive web tool.
Survival of the African trypanosome within its mammalian hosts, and hence transmission between hosts, relies upon antigenic variation, where stochastic changes in the composition of their protective variant-surface glycoprotein (VSG) coat thwart effective removal of the pathogen by adaptive immunity. Antigenic variation has evolved remarkable mechanistic complexity in Trypanosoma brucei, with switching of the VSG coat executed by either transcriptional or recombination reactions. In the former, a single T.
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- Human African trypanosomiasis, also known as sleeping sickness, is caused by the Trypanosoma brucei parasite and leads to significant neuroinflammation and glial cell activation in the brain.
- Researchers used advanced techniques like single cell and spatial transcriptomics to study these brain responses, focusing on areas around the circumventricular organs where the parasite is found.
- The study revealed a new interaction between microglia and plasma cells influenced by IL-10 and BAFF signaling, providing valuable insights into how the brain reacts to this chronic infection.
Paving the Way: Contributions of Big Data to Apicomplexan and Kinetoplastid Research.
Front Cell Infect Microbiol
June 2022
Article Synopsis
- The review explores methods in research on Apicomplexan and Kinetoplastid organisms, focusing on how to optimize the use of generated big datasets.
- It evaluates the advantages and drawbacks of existing technologies in this field while suggesting potential improvements for future research.
- The review also addresses challenges in effectively utilizing the vast amount of biological data that has been and will be collected.
Article Synopsis
- - The study explores the life-cycle of *Trypanosoma brucei*, focusing on the transition between its replicative 'slender' and transmissible 'stumpy' forms which are crucial for survival and transmission between hosts.
- - Researchers utilized single-cell transcriptomics to capture gene expression profiles of 8,599 parasites, allowing them to map biological events and gene expression dynamics during the differentiation process.
- - The findings also include the identification of a key regulatory protein, ZC3H20, whose mutation highlights its role in the developmental transitions of the parasites, suggesting a new approach to understanding similar processes in other pathogens.
Kinetoplastid parasites are responsible for both human and animal diseases across the globe where they have a great impact on health and economic well-being. Many species and life cycle stages are difficult to study due to limitations in isolation and culture, as well as to their existence as heterogeneous populations in hosts and vectors. Single-cell transcriptomics (scRNA-seq) has the capacity to overcome many of these difficulties, and can be leveraged to disentangle heterogeneous populations, highlight genes crucial for propagation through the life cycle, and enable detailed analysis of host–parasite interactions.
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- Advances in DNA sequencing now allow for whole-genome analysis, making it easier to study genome variation patterns compared to older localized methods.
- Whole-genome analyses can use both short- and long-read sequencing technologies.
- The study focuses on using these sequencing methods in trypanosomatids to investigate DNA replication dynamics, the effects of genome damage on modified histone H2A, and changes in genome variation related to ploidy.
Article Synopsis
- Antigenic variation through VSG coat switching is a complex immune evasion technique used by African trypanosomes to escape host defenses, primarily mediated by changes in transcription of VSG genes.
- The process of VSG switching mainly involves DNA recombination at the bloodstream VSG expression site, which is influenced by mechanisms like homologous recombination triggered by DNA breaks.
- Research is ongoing to identify the sources of these DNA breaks, including factors like nucleases, repetitive DNA, and transcriptional activity, indicating that understanding these mechanisms could lead to new treatments against trypanosomiasis.