Professor Alistair Brown
Professor Alistair Brown The University of Aberdeen School of Medical Sciences 
Chair in Microbiology work +44 (0)1224 437482 work fax +44 (0)1224 437465 pref al.brown@abdn.ac.uk pref Aberdeen Fungal Group School of Medical Sciences University of Aberdeen Institute of Medical Sciences Foresterhill Aberdeen AB25 2ZD UK
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, FINSysB Marie Curie Initial Training Network
Deputy Chair and then Chair, BBSRC Research Committee D (Molecules, Cells and Industrial Biotechnology) 2009-2011
Currently:
Director, CRISP Systems Biology Consortium
European Research Council Advanced Grant Holder (STRIFE)
Chair, BBSRC Bioinformatics and Biological Resources Fund Panel 2013-
Chair, BBSRC Synthetic Biology Research Centres Panel 2013-
Candida albicans is the major systemic fungal pathogen of humans. Many people carry C. albicans as a relatively harmless commensal organism, but this yeast often causes irritating and recurrent infections of the mucosal epithelia (e.g. oral and vaginal thrush). Candida also causes life-threatening systemic infections in immunocompromised patients (e.g. transplant and chemotherapy patients).
A number of factors contribute to the pathogenicity of C. albicans. These include "Virulence Factors" such as the ability of C. albicans to undergo reversible morphological changes between yeast, pseudohyphal and hyphal growth forms (morphogenesis). How does this pathogenic fungus regulate its cell morphology in response to environmental stimuli? We are studying the molecular mechanisms and signalling pathways that control the yeast-hypha morphological transition.
The pathogenicity of C. albicans also depends upon its "Fitness Attributes". By this we mean the ability of Candida to tune its physiology to the changing microenvironments it encounters within its human host. The fitness of C. albicans is reliant upon robust stress responses (which help to counteract immune defences) and metabolic flexibility (which allow this yeast to thrive on available nutrients). How does this pathogen regulate its metabolism and stress responses in the multifarious microenvironments it occupies in its human host? How does C. albicans coordinate these responses with the control of Virulence Factors in these microenvironments? We are studying the molecular mechanisms and signalling pathways that coordinate morphogenetic, metabolic and stress responses in C. albicans.
We are combining several experimental approaches in our pursuit of these objectives. We are combining molecular and cell biology with biochemistry to study the structure and function of specific regulatory molecules. We are also using genomics (transcript profiling and proteomics) to define the global cellular roles of these regulators. We are using single cell profiling (GFP reporters) to examine the activation of these regulatory responses in specific microenvironments within the host. Furthermore we are using systems biology to mathematically model specific responses and predict the outcome of regulatory mutations upon these responses. In addition we are using bioinformatics to compare responses in pathogenic and model fungi.
I have benefited greatly from my collaborations with colleagues in the Aberdeen Fungal Group (Neil Gow, Frank Odds, Gordon Brown, Carol Munro, Alex Brand), with my partners in the European FINSysB Network and CRISP Consortium, and with other friends in the UK (Janet Quinn, Steve Oliver, Mick Tuite, ….), Europe and North America.
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 [http://www.galarfungail.org/data.htm]
C. albicans repressors: Nrg1, Tup1, Ssn6[http://www.galarfungail.org/data.htm]
C. albicans Msn4, Mnl1 and core stress responses [http://www.cbr.nrc.ca/genetics/stress/]
S. cerevisiae glucose responses [http://mips.gsf.de/proj/eurofan/eurofan_2/b2/]
S. cerevisiae pseudohyphal growth [http://mips.gsf.de/proj/eurofan/eurofan_2/b2/]
Proteomics:
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]
Models:
S. cerevisiae mRNA translation [EBI BioModels: MODEL8459127548]
Chair in Microbiology work +44 (0)1224 437482 work fax +44 (0)1224 437465 pref al.brown@abdn.ac.uk pref Aberdeen Fungal Group School of Medical Sciences University of Aberdeen Institute of Medical Sciences Foresterhill Aberdeen AB25 2ZD UK
Chair in Microbiology
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Biography
BSc (Hons) in Biochemistry, 1976PhD 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, FINSysB Marie Curie Initial Training Network
Deputy Chair and then Chair, BBSRC Research Committee D (Molecules, Cells and Industrial Biotechnology) 2009-2011
Currently:
Director, CRISP Systems Biology Consortium
European Research Council Advanced Grant Holder (STRIFE)
Chair, BBSRC Bioinformatics and Biological Resources Fund Panel 2013-
Chair, BBSRC Synthetic Biology Research Centres Panel 2013-
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Research Interests
Candida albicans Pathogenomics and Systems Biology
Candida albicans is the major systemic fungal pathogen of humans. Many people carry C. albicans as a relatively harmless commensal organism, but this yeast often causes irritating and recurrent infections of the mucosal epithelia (e.g. oral and vaginal thrush). Candida also causes life-threatening systemic infections in immunocompromised patients (e.g. transplant and chemotherapy patients).
A number of factors contribute to the pathogenicity of C. albicans. These include "Virulence Factors" such as the ability of C. albicans to undergo reversible morphological changes between yeast, pseudohyphal and hyphal growth forms (morphogenesis). How does this pathogenic fungus regulate its cell morphology in response to environmental stimuli? We are studying the molecular mechanisms and signalling pathways that control the yeast-hypha morphological transition.
The pathogenicity of C. albicans also depends upon its "Fitness Attributes". By this we mean the ability of Candida to tune its physiology to the changing microenvironments it encounters within its human host. The fitness of C. albicans is reliant upon robust stress responses (which help to counteract immune defences) and metabolic flexibility (which allow this yeast to thrive on available nutrients). How does this pathogen regulate its metabolism and stress responses in the multifarious microenvironments it occupies in its human host? How does C. albicans coordinate these responses with the control of Virulence Factors in these microenvironments? We are studying the molecular mechanisms and signalling pathways that coordinate morphogenetic, metabolic and stress responses in C. albicans.
We are combining several experimental approaches in our pursuit of these objectives. We are combining molecular and cell biology with biochemistry to study the structure and function of specific regulatory molecules. We are also using genomics (transcript profiling and proteomics) to define the global cellular roles of these regulators. We are using single cell profiling (GFP reporters) to examine the activation of these regulatory responses in specific microenvironments within the host. Furthermore we are using systems biology to mathematically model specific responses and predict the outcome of regulatory mutations upon these responses. In addition we are using bioinformatics to compare responses in pathogenic and model fungi.
I have benefited greatly from my collaborations with colleagues in the Aberdeen Fungal Group (Neil Gow, Frank Odds, Gordon Brown, Carol Munro, Alex Brand), with my partners in the European FINSysB Network and CRISP Consortium, and with other friends in the UK (Janet Quinn, Steve Oliver, Mick Tuite, ….), Europe and North America.
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Current Research
Recent Genomic Datasets and ModelsTranscript 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 [http://www.galarfungail.org/data.htm]
C. albicans repressors: Nrg1, Tup1, Ssn6[http://www.galarfungail.org/data.htm]
C. albicans Msn4, Mnl1 and core stress responses [http://www.cbr.nrc.ca/genetics/stress/]
S. cerevisiae glucose responses [http://mips.gsf.de/proj/eurofan/eurofan_2/b2/]
S. cerevisiae pseudohyphal growth [http://mips.gsf.de/proj/eurofan/eurofan_2/b2/]
Proteomics:
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]
Models:
S. cerevisiae mRNA translation [EBI BioModels: MODEL8459127548]
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