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Research teams utilising the Birmingham Fly Facility

Research teams at the University of Birmingham use the fruit-fly Drosophila as a model organism as it is the most powerful model organism for in vivo genetic analysis of biological processes.

Drosophila has enabled fundamental discoveries on how life works, and its underlying and universal principles. Six Nobel Prizes have been awarded for discoveries made using fruit-flies. Fundamental Drosophila research contributes to the understanding of human health and disease.

Using Birmingham Fly Facility, we are addressing questions into how RNA is regulated to generate cell type diversity and neuronal function; what are the molecular mechanisms that control RNA splicing, processing translation and decay; how chromatin modifying complexes regulate gene expression to control developmental innate immunity and other pathways.

At the cell biology level, we investigate how cells ‘know’ how to achieve normal organ and organismal integrity, how they regulate each other to maintain tissue homeostasis, prevent cancer and enable regeneration. We investigate the brain, here linking genes, molecules, neural circuits and behaviour. We want to understand how the brain changes throughout life, how behaviour relates to brain structure; whether we can use genetics to promote central nervous system regeneration after injury; how RNA splicing impacts in behaviour; how we make decisions upon conflicting possibilities; and how disruptions on molecular events result in brain disease.

Research teams

Brain plasticity and regeneration

Our research investigates structural plasticity and degeneration, regeneration and repair in the central nervous system (CNS). Using the robust genetic toolkit and invivo neurobiological studies offered by the fruit-fly Drosophila, we span the breadth from genes and cells to neural circuits and behavior. Through our work, we unravel networks of genes and fundamental principles, alongside in vivo processes that shed light on brain function, all contributing to insights relevant to human neurological health and disorders.

Our lab aims to understand structural plasticity of the nervous system: in development, regeneration and repair. That is, what is the link between structure and function in the brain? How does the brain change as we grow, learn and age? What happens in nervous system injury and disease, and how can we promote regeneration and repair?

Principal Investigator

Find out more from our website

Tissue homeostasis, cancer and regeneration

In multicellular organisms, tissue homeostasis requires coordinated cell death, cell proliferation and cell differentiation. Disruption of this balance can lead to many human diseases including degenerative disorders and cancer. Dr Fan’s group investigates the molecular control of cell death and how dying cells communicate with their neighbours to maintain tissue homeostasis, as well as the implications of these findings for understanding human diseases.

Principal Investigator 

Dr Yun Fan, Associate Professor in Cell and Developmental Genetics 

Dr Fan’s research interest centres on understanding how cell death, cell proliferation and cell differentiation are coordinated to maintain tissue homeostasis. This has important implications for cancer development and tissue regeneration.

Genetics of behavioural choices

Animals must make crucial behavioural choices on a minute by minute basis to survive in a changing environment. A long-standing enigma is, how are alternative options evaluated in the brain and specific actions prioritised. We know that cues conveying external information (e.g., access to food, potential dangers) and internal state (e.g., fear, hunger) guide behavioural choices. However, how the brain prioritises specific actions remains unknown.

Our lab addresses this fascinating question using the fruit fly model, Drosophila. Fruit flies exhibit complex behaviours that are controlled by a relatively small brain. Thanks to sophisticated tools available in the fruit fly, we can interrupt specific genes, as well as visualise and manipulate individual neurons with great resolution. With these tools, we can study how the fly brain responds when there are conflicting options available, and how it chooses amongst them. By studying how the brain makes decisions at a genetic, cellular and circuit level, in an accessible experimental system, we aim to reveal fundamental principles underlying behavioural choices that might be present across species.

Principal Investigator

Mitochondrial DNA transmission and maintenance

In addition to the nuclear genome, all animals have another genome packed inside the mitochondrion called mtDNA. This maternally inherited genome encodes important proteins for energy production. During development and ageing as mtDNA continues to replicate and turnover, mutations can occur to some of the copies. The subsequent prevalence of these mutants, which determines the progression and inheritance of the clinical abnormalities of mitochondrial disorders, depends on how they compete with the co-existing wild-type genomes for transmission. To date, over 50 mtDNA-linked disorders have been described in humans.

We are interested in understanding the molecular mechanisms that govern mtDNA heteroplasmy transmission during development and ageing. In particular, we want to know why a mutant mitochondrial genome increases in abundance to cause diseases in some cases while in others, it is eliminated. By creating fruit flies carrying both functional and pathogenic mitochondrial genomes, we perform systematic and detailed studies to identify nuclear factors and mtDNA sequence polymorphisms that bias the transmission of one genome over the other to impact the progression and inheritance of mtDNA-linked disorders.

We are also interested in understanding how repair mechanisms maintain mtDNA integrity during development, how maternal inheritance of mtDNA is guaranteed and how complex mito-nuclear interactions modulate the pathogenic expression of mtDNA mutations. These studies provide insights into genome evolution, ageing and human diseases.

Principal Investigator

Professor Hansong Ma, Professor in Genetics

Hansong is a leading expert in mitochondrial genetics. Her group developed tools and systems in Drosophila to study mitochondrial DNA transmission and maintenance.

Find out more on her website

RNA biology

Saverio group’s research is interested in understanding what ribosomes do in the cell nucleus. Yes, there are functional ribosomes in the nucleus. We and others have found direct evidence of this in Drosophila cells (see our publications). We now want to understand what these ribosomes do. We suspect that they play a role in gene expression and nuclear mRNA processing in particular, including playing a role in nonsense-mediated mRNA decay (NMD): a conserved eukaryotic phenomenon without a satisfactory mechanism yet. We research these topics in yeast, mostly S. pombe, as well as Drosophila.

Principal Investigator

Dr Saverio Brogna, Reader in RNA Biology and Group Leader

Dr Brogna is a Reader in RNA biology. His group's research focuses on understanding the mechanisms that connect pre-mRNA processing with translation and Nonsense Mediated mRNA Decay (NMD). A second interest of the laboratory is understanding the functions of ribosomes and ribosomal proteins within the nucleus.

Lab website 

Gene regulation and splicing

The Soller lab is interested in how genes are regulated at the RNA level including mRNA methylation, alternative splicing and 3’end processing, and how RNA regulation contributes to sexual differentiation, neuronal development and function.

Principal Investigator 

Dr Matthias Soller, Associate Professor 

His prime research interest is how the information encoded in chromosomes instructs building of the most complex organ, the brain, and allows an organism to perform elaborate tasks.

DNA damage in neurological disease

Richard’s group is interested in the biology of neurodegenerative disorders. We have a particular focus on understanding how the nervous system responds to the DNA damage that accumulates in neurological disorders. Damage accumulates in both long-term, chronic disorders such as neurodegeneration and after acute trauma affecting the nervous system, such as stroke. We are focussed on understanding why activating the DNA damage responses can be toxic to neurons with the aim of developing therapies to support the nervous system in patients with neurological disorders.

We use a range of Drosophila models of neurological disease to help address these questions. These include models of common late-onset neurodegenerative diseases, including Alzheimer’s disease and amyotrophic lateral sclerosis (motor neurone disease), and also inherited early-onset disorders such as ataxia-telangiectasia and neuronal ceroid lipofuscinosis (Batten disease). With partners, we also use models of acute trauma to the nervous system to identify features that are common to all neurological disease that may be good targets for therapy.

Principal Investigator 

Dr Richard Tuxworth, Associate Professor and Head of Education 

Richard is a cell biologist with a particular interest in understanding DNA damage in neurological disease.