麻豆传媒

Dr Emma Briggs is a molecular parasitologist working with eukaryotic unicellular parasites that cause both human and animal diseases. She has primarily conducted research into Trypanosoma brucei and other trypanosomatida species using state-of-the art "omics" and genetic editing methods to uncover aspects of these parasites biology. This has included studying the impact R-loop nucleic acid structures in the Trypanosoma brucei genome and antigenic variation, and most recently using single cell transcriptomics to resolve dynamic gene expression changes during the parasite life cycle and cell cycle.

Her research is now focused on uncovering the molecular machinery that drive parasite proliferation or lead to cell cycle arrest, as well as the impact these proliferative and arrested parasite forms have on disease progression and transmission between hosts. This work uses genetically edited fluorescent parasite lines and paralleled genetic screening with the high-throughput robotics.

• MRC Career Development Award Fellowship, 麻豆传媒, 2024-present
• Sir Henry Wellcome Fellowship, Wellcome Trust, University of Edinburgh and University of Glasgow - 2020-2024
• Research Assistant, University of Glasgow, 2019
• PhD in Molecular Parasitology, University of Glasgow 2014-2018

Other roles

• British Society of Parasitology Council

Trypanosoma brucei, Trypanosoma cruzi and Lieshmania spp. parasites cause three Neglected Tropical Diseases; Human African Trypanosomiasis, Chagas Disease and Leishmaniasis. These unicellular parasites are transmitted between humans and animals by biting insect vectors. In each species, the parasites must adapt to their changing environments as they move between the mammal and insect, as well as between the various tissues and organs in each. To do this, they show remarkable flexibility by undergoing cellular differentiation to alter many aspects of their biology. This includes a complete remodel of the protein surface coat, altered energy metabolism, changes in morphology and movement patterns. Additionally these parasites switch between proliferating and non-proliferating arrested forms to pre-adapt for transmission from the insect to the mammal and, in the case of T. brucei, from the mammal back to the tsetse fly vector.

We're interested in:

• How these parasites switch between actively proliferating forms and cell cycle arrested forms
• The molecular machinery and protein interactions that drive these switches
• Where the parasites are proliferating and where they are arresting in the mammal and insect tissues
• The impact arrested forms have on transmission and infection dynamics

To study these questions we use both molecular and bioinformatic methods including CRISPR/cas9 gene editing, combined microscopy and flow cytometry, single cell transcriptomics, and genetic screening.

• Articles

  • Larcombe SD, Briggs EM, Savill N, Szoor B, Matthews KR. . Proceedings of the National Academy of Sciences of the United States of America 2023, 120(42), e2306848120.
  • Girasol MJ, Krasilnikova M, Marques CA, Damasceno JD, Lapsley C, Lemgruber L, Burchmore R, Beraldi D, Carruthers R, Briggs EM, McCulloch R. . Proceedings of the National Academy of Sciences 2023, 120(48), e2309306120.
  • Briggs EM, Marques CA, Oldrieve GR, Hu J, Otto TD, Matthews KR. . eLife 2023, 12, e86325.
  • Girasol MJ, Briggs EM, Marques CA, Batista JM, Beraldi D, Burchmore R, Lemgruber L, McCulloch R. . Nucleic Acids Research 2023, 51(20), 11123-11141.
  • Quintana JF, Chandrasegaran P, Sinton MC, Briggs EM, Otto TD, Heslop R, Bentley-Abbot C, Loney C, de Lecea L, Mabbott NA, MacLeod A. . Nature Communications 2022, 13(1), 5752.
  • Kent RS, Briggs EM, Colon BL, Alvarez C, Silva Pereira S, De Niz M. . Frontiers in Cellular and Infection Microbiology 2022, 12, 900878.
  • Faria J, Briggs EM, Black JA, McCulloch R. . Current Opinion in Microbiology 2022, 70, 102209.
  • Briggs EM, Rojas F, McCulloch R, Matthews KR, Otto TD. . Nature Communications 2021, 12, 5268.
  • Damasceno JD, Marques CA, Black J, Briggs E, McCulloch R. . Trends in Genetics 2021, 37(1), 21-34.
  • Briggs EM, Warren FSL, Matthews KR, McCulloch R, Otto TD. . Parasitology 2021, 148(10), 1223-1236.
  • Leal AZ, Schwebs M, Briggs E, Weisert N, Reis H, Lemgruber L, Luko K, Wilkes J, Butter F, McCulloch R, Janzen CJ. Genome maintenance functions of a putative Trypanosoma brucei translesion DNA polymerase include telomere association and a role in antigenic variation. Nucleic Acids Res 2020, 48(17), 9660-9680.
  • Briggs E, Crouch K, Lemgruber L, Hamilton G, Lapsley C, McCulloch R. Trypanosoma brucei ribonuclease H2A is an essential R-loop processing enzyme whose loss causes DNA damage during transcription initiation and antigenic variation. Nucleic Acids Research 2019, 47(17), 9180-9197.
  • Briggs E, Crouch K, Lemgruber L, Lapsley C, McCulloch R. Ribonuclease H1-targeted R-loops in surface antigen gene expression sites can direct trypanosome immune evasion. PLoS Genet 2018, 14(12), e1007729.
  • Briggs E, Hamilton G, Crouch K, Lapsley C, McCulloch R. Genome-wide mapping reveals conserved and diverged R-loop activities in the unusual genetic landscape of the African trypanosome genome. Nucleic Acids Res 2018, 46(22), 11789-11805.
  • da Silva MS, Hovel-Miner GA, Briggs EM, Elias MC, McCulloch R. Evaluation of mechanisms that may generate DNA lesions triggering antigenic variation in African trypanosomes. PLoS Pathog 2018, 14(11), e1007321.
  • Stortz JA, Serafim TD, Alsford S, Wilkes J, Fernandez-Cortes F, Hamilton G, Briggs E, Lemgruber L, Horn D, Mottram JC, McCulloch R. Genome-wide and protein kinase-focused RNAi screens reveal conserved and novel damage response pathways in Trypanosoma brucei. PLoS Pathog 2017, 13(7), e1006477.

• Book Chapter

  • Briggs EM, Marques CA, Reis-Cunha J, Black J, Campbell S, Damasceno J, Bartholomeu D, Crouch K, McCulloch R. Next-Generation Analysis of Trypanosomatid Genome Stability and Instability. In: Paul A. M. Michels, Michael L. Ginger, Dan Zilberstein, ed. Trypanosomatids Methods and Protocols. Methods Mol Biol, 2020, pp.225–262.