Professor Alistair Brown

Professor Alistair Brown

Chair in Microbiology

Professor Alistair Brown
Professor Alistair Brown

Contact Details

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The University of Aberdeen Aberdeen Fungal Group, MRC Centre for Medical Mycology, University of Aberdeen, Institute of Medical Sciences, Rm 4:18, Foresterhill, Aberdeen AB25 2ZD, UK

 Aberdeen Fungal Group  

 MRC Centre for Medical Mycology


 Aberdeen Proteomics

 Core Facilities



BSc (Hons) in Biochemistry, 1976

PhD in Molecular Biology, 1979

DSc in Fungal Gene Regulation, 2003


SGM Kathleen Barton-Wright Memorial Prize, 2002

Fellow, Institute of Biology (now Society of Biology), 2004

Fellow, Royal Society of Edinburgh, 2005

Fellow, American Academy of Microbiology, 2008


Coordinator, Galar Fungail 1 Consortium, 2000-2003

Assistant Coordinator, Galar Fungail 2 Marie Curie Research Training Network, 2004-2007

Coordinator, FINSysB Marie Curie Initial Training Network, 2008-2012

Director, SABR Systems Biology Consortium (CRISP) 2008-2014

European Research Council Advanced Grant Holder (STRIFE), 2010-2015

Co-director, Wellcome Trust Strategic Award in Medical Mycology & Fungal Immunology, 2012-2017


Deputy Chair, then Chair, BBSRC Research Committee D (Molecules, Cells and Industrial

Biotechnology), 2009-2011

Chair, BBSRC Bioinformatics and Biological Resources Fund Panel, 2013-2014

Chair, BBSRC Synthetic Biology Research Centres Panel, 2013-2014


Publications at


E-prints for Nature Microbiology paper on ß-glucan masking HERE



Research Interests



Fungal adaptation to host niches during infection


Candida albicans is the major systemic fungal pathogen of humans.  Depending upon the immune status of the individual, C. albicans can colonise diverse niches in humans such as the mouth, gastrointestinal tract, urogenital tract, blood and internal organs.  The ability of this fungus to colonise these niches depends upon effective adaptation to the local microenvironments in these niches.  This requires the activation of robust stress responses that help to protect the fungus against local environmental challenges that include host immune defences.  It also requires metabolic adaptation to promote the efficient assimilation of available nutrients, and hence growth.   We integrate genomics, proteomics, molecular and cellular biology, biochemistry, systems biology and infection biology to define how C. albicans integrates stress adaptation with nutrient assimilation during infection. 


In collaboration with our friends and colleagues in the Aberdeen Fungal Group, the UK and worldwide, we have examined the molecular and cellular responses of C. albicans to specific environmental signals such as oxidative, osmotic and nitrosative stresses, heat shock, changes in carbon source, and amino acid starvation, and defined the contributions of these individual adaptive response to infection.  However, host niches are both complex and dynamic, and therefore C. albicans cells are exposed to multiple environmental inputs in these microenvironments.  Therefore, we are also examining the responses of C. albicans cells to combinations of environmental inputs that they experience in host niches.  Interestingly, the fungus displays non-additive responses to certain carbon sources and combinations of stress. These responses were not predicted based on the responses of cells to the corresponding individual stimuli.  We also find that metabolic adaptation turns C. albicans into a moving target for the immune system, affects their pathogenicity, and strongly influences their resistance to antifungal drug therapies. 


Publications at



Current Research

Recent Genomic Datasets and Models

Transcript Profiling:

C. albicans transcriptome during kidney infection

C. albicans glucose responses [EBI ArrayExpress Accession: E-MEXP-1151]

C. albicans Hsf1 and heat shock [EBI ArrayExpress Accession: E-MEXP-2044, E-MEXP-1369]

C. albicans Hog1 and osmotic, oxidative and heavy metal stress responses [EBI ArrayExpress Accession: E-MEXP-1134]

C. albicans Hac1 and unfolded protein response [EBI ArrayExpress Accession: E-MEXP-1307]

C. albicans and C. dubliniensis acute osmotic, oxidative and heat stress responses [EBI ArrayExpress Accession: E-MEXP-1650]

C. albicans Mnl1 and weak acid stress response [EBI ArrayExpress Accession: EMEXP-1633, E-MEXP-1641, and E-MEXP-1645]

Transcript Profiling pre-2006:

C. albicans Gcn4, Gcn2 and amino acid starvation []

C. albicans repressors: Nrg1, Tup1, Ssn6[]

C. albicans Msn4, Mnl1 and core stress responses []

S. cerevisiae glucose responses []

S. cerevisiae pseudohyphal growth []


C. albicans glucose responses and comparisons with growth on lactate, amino acids and oleic acid [EBI Pride Accession: 3186-3192]

C. albicans Hog1 and osmotic, oxidative and heavy metal stress responses [EBI Pride Accession: 3218–3225]

C. glabrata Ace2 secretome [EBI Pride Accession: 3212-3213]

C. glabrata pH reponse [EBI Pride Accession: 10960-10962]

C. albicans Gcn4 and amino acid starvation [EBI Pride Accession: 1874-1875]

C. glabrata Ace2 intracellular proteome [EBI Pride Accession: 1876-1877]

S. cerevisiae Gcn4 and amino acid starvation [EBI Pride Accession: 1872-1873]


S. cerevisiae mRNA translation [EBI BioModels: MODEL8459127548]


Further Info


AFG, December 2014


Publications at


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