Rebecca joined the University of Kent in April 2020 as a lecturer in Microbial Adaptation. Rebecca is an alumnus of the University of Kent having completed her PhD under the supervision of Dr Peter Klappa and Prof Fritz Muhlschlegel in 2007, which investigated how the nematode C. elegans adapts to environmental pH. Rebecca then remained at the University for a postdoctoral position, focusing on how the fungal pathogen Candida albicans adapts to carbon dioxide, a key environmental signal that triggers fungal pathogenesis. Rebecca then moved the University of Aberdeen, to work with Prof Neil Gow on fungal cell wall biosynthesis and innate immunity to fungal infections, before joining the University of Birmingham in 2014 as an independent research fellow funded by a Medical Research Council Career Development Award. Rebecca’s team now forms part of the Kent Fungal Group (KFG) and is focused on understanding how pathogenic fungi (Candida, Cryptococcus and Rhizopus) adapt to life within the human host and how, in turn, this adaptation affects the host-pathogen interaction.
The Hall lab is interested in understanding the biology and pathogenicity of fungi. Our research largely focuses on the opportunistic fungal pathogen Candida albicans, which causes a range of infections from superficial mucosal infections (i.e. thrush) to life-threatening systemic disease (i.e. candidiasis). We also work on with Mucoromycetes that are filamentous fungi responsible for food spoilage and the life-threatening infection mucormycosis.
The group is interested in understanding the following:
Previous work from the group include:
Alam F. et al. 2019 Candida albicans enhances meropenem tolerance of Pseudomonas aeruginosa in a dual-species biofilm. J. Antimicrob Chemother. dkz514
Cottier F. et al. 2019 Remasking of Candida albicans β-Glucan in Response to Environmental pH Is Regulated by Quorum Sensing. mBio 10 e02347-19
Kousser C. et al. 2019 Pseudomonas aeruginosa inhibits Rhizopus microsporus germination through sequestration of free environmental iron. Sci. Rep. 9 5714
Sherrington S. et al. 2017 Adaptation of Candida albicans to environmental pH induces cell wall remodelling and enhances innate immune recognition. Plos Path. 13 e1006403.
If you are interested in doing a PhD in fungal biology please contact Rebecca (firstname.lastname@example.org) to discuss projects and opportunities.
MSc-R projects available for 2021
Elucidating the role of the host environment in controlling the fungal-host pathogen interaction
Candida albicans is an opportunistic fungal pathogen that forms part of the natural flora of the oral, genital and gastrointestinal tracts of healthy individuals. However, changes in the host’s environment, activate adaptation responses in the fungus that enable the fungus to switch from commensal growth to a more pathogenic state. One of these adaptation events is the structural remodelling of the fungal cell wall. As the cell wall is the first point of contact between the invading pathogen and innate immune system, modification of its structure affects the host-pathogen interaction, enabling the fungus to either evade the immune system, or to hyperactivate pro-inflammatory immune responses and induce host damage. However, the host environmental signals and fungal signalling cascades that control cell wall adaptation are largely unknown. The aim of this project is to determine which host environmental signals drive fungal pathogenicity through modulation of the fungal cell wall and to elucidate the novel fungal signalling pathways that mediate this adaptation.
Investigating the role of polymicrobial interactions in antimicrobial resistance
Polymicrobial interactions play an essential role in life and are important for agriculture, food production, and disease. Polymicrobial communities normally form biofilms, which are complex communities of microorganisms encased in a self-produced extracellular matrix. Biofilms provide a unique habitat for microbial growth and as a result, gene expression profiles of cells isolated from biofilms are significantly different compared to planktonic growing cells. Biofilms readily form on indwelling medical devices, and are one of the leading causes of nosocomial infections due to their increased resistance to antimicrobial therapy. Currently our understanding of the interactions that occur in polymicrobial biofilms, and the impact these interactions have on antimicrobial drug resistance is poorly understood. The aim of this project is to investigate the impact of polymicrobial interactions on antimicrobial resistance.
Exploring the potential use of bacteria to kill fungal pathogens
In their natural environment fungi and bacteria compete with each other for space and nutrients. This natural competition has led the evolution of chemical weapons to give one species the advantage over another. For example, penicillin is produced by the fungus Penicillium chrysogenum to kill bacteria giving the fungus the upper hand. However, there are very limited examples of bacterial products that have significant antifungal activity, with clinical potential. Therefore, there is large potential for the discovery of natural, bacterial secreted antifungal compounds. We have identified that the bacterium Pseudomonas aeruginosa is able to kill fungi through an unknown mechanism. The aim of this project is to identify how the bacterium kills fungi. To achieve these objectives, you will employ molecular biology, together with advanced microscopy techniques (super resolution, scanning electron and transmission electron microscopy). This project has the potential to not only improve the efficacy of our current antifungal drugs, but to also identify a novel antifungal agent which will be of considerable clinical importance.