Dr. Gabriela Bodea received her PhD in 2014 with highest honours (Summa cum laude) from the University of Bonn, Germany. Subsequently, Dr Bodea joined the Genome Plasticity and Disease group at the Mater Research Institute in Australia. Here, Dr. Bodea began investigating the role of LINE-1 retrotransposons, a class of mobile DNA elements colloquially referred to as "jumping genes", in creating genetic variability within neurons. In 2017, Dr. Bodea joined the Queensland Brain Institute, University of Queensland, where she is currently a Research Fellow in the Computational and Molecular Biology lab. Dr. Bodea's research aims to understand how the dynamic regulation of retrotransposons shapes neuronal identity in the mammalian brain and why certain neuronal subtypes are more susceptible to neurodegenerative and neuropsychiatric disorders. Dr Bodea's work has been supported by prestigious fellowships awarded by the German Research Foundation (DFG) and the NHMRC-ARC Dementia Research Development. Dr. Bodea has published in top journals such as Nature Neuroscience, Cell Reports, Genome Research, and Development. Dr Bodea has also been involved in the training and mentorship of MSc and PhD students and participated in course coordination and lecturing activities.
Research in the Bredy laboratory is aimed at elucidating how the genome is connected to the environment through epigenetic modifications, and how this relationship shapes brain and behaviour throughout life. The group is particularly interested in how epigenetic mechanisms, including DNA methylation, histone modifications. the activity of non-coding RNAs, and RNA modification regulate the formation and maintenance of associative fear-related memory.
We are using the genetic model organism, C. elegans, do investigate the genetic basis of both normal and disordered behaviour. Our current interests are identifying the genes responsible for anxiety and depression as well as the genes for eating disoders and addiction. Using C. elegans as a model organism will also allow us to study gene function as it relates to behaviour.
Molecular mechanisms of phosphine resistance (other research)
Genetic mapping of oxidative stress resistance genes. The fumigant phosphine disrupts oxidative metabolism, resulting in the production of reactive oxygen intermediates. This causes the premature ageing and death of targeted pests. Insect pests of stored grain in Australia now exhibit resistance to phosphine at levels more than 200 times the normal lethal dose.
We have genetically mappedf and identified the genes responsible for phosphine resistance in tall major insect pests of stored grain. We are using a systems biology approach in the model organism C. elegans to understand the molecular basis of phosphine action. Our genetic studies have recently shown that resistance to phosphine is associated with an extension of lifespan
Australian Institute for Bioengineering and Nanotechnology
Availability:
Available for supervision
Media expert
Professor Wolvetang is an international leader in the area of pluripotent stem cell biology and human functional genomics. he initiated and leads Cell Reprogramming Australia, a collaborative framework that facilitates induced pluripotent stem cell research in Australa and is co-director of the UQ Centre in Stem Cell Ageing and Regenerative Engineering (StemCARE). He has extensive expertise in reprogramming somatic cells, differentiation and tissue engineering with adult, embryonic and induced pluripotent stem cells, genome manipulation with CRISPR, molecular biology, transcriptome analysis, high content image analysis, development and use of microfluidic devices for cell analysis, nanoparticle and scaffold design and delivery, and stem cell and cell-free regenerative medicine approaches.Professor Wolvetang has been instrumental in establishing and enabling the technology for derivation of induced pluripotent stem cells across Australia. Professor Wolvetang made the strategic decision to focus on the generation of induced pluripotent stem from patients with neurological and cardiac disorders because live human cells from such patients can usually not be obtained whereas induced pluripotent stem cells have the ability to generate every cell type of the human brain in unlimited amounts and can recapitulate the disease in the dish. Induced pluripotent stem cells combined with emerging technologies such as CRISPR-based genome editing offers a unique opportunity to study the role of individual genes and combinatorial gene regulatory pathways in the eatiology of monogenic and complex brain disorders. Indeed, combined with RNA-seq and organoid generation we are now for the first time able to gain insight into gene regulatory pathways operational in individual brain cell types of healthy and diseased individuals, investigate the connectivity and function of cells, as well as pinpoint where and when during early development such deregulated pathways lead to pathological changes. Induced pluripotent stem cells further not only provide insight into the underlying pathogenesis of neurological disorders but also constitute a valuable drugscreening platform and, following CRISPR-based gene correction, can form the basis of patient specific cellular therapies for currently incurable diseases.
Professor Wolvetang received his PhD in 1992 from the Department of Biochemistry, University of Amsterdam for his original work on peroxisomal disease (6 papers). He undertook postdoctoral studies at the Department of Biochemistry and the Institute for Reproduction and Development of Monash University, investigating apoptosis, Down syndrome and Ets transcription factors, respectively, obtaining the first evidence for an intra-chromosomal regulatory loop on chromosome 21 involving Ets2 (3 papers), and revealing the role of p53 in immune-suppression in Down syndrome (Hum Mol. Genetics). He then joined Prof Martin Pera in the Australian Stem Cell Centre in 2003 to pioneer human embryonic stem cell research in Australia, resulting in a first author Nature Biotechnology paper in 2006 identifying CD30 as a marker for genetically abnormal hESC (72 cites). He was appointed group leader of the Basic human stem cell biology laboratory in the ASCC research laboratory and senior lecturer in the Department of Anatomy and Cell biology until he accepted his current position as an independent group leader at the AIBN and Professor in stem cell biology at the University of Queensland in 2008. There he started to generate integration-free induced pluripotent stem cells from human neurological diseases such as ataxia-telangiectasia (Stem cells translational medicine). In recognition of his leadership role in this area of research he was appointed leader of the “Reprogramming and Induction of pluripotency” Collaborative Stream of the Australian Stem Cell Centre until the end of that initiative in 2011, coordinating collaborative research between eight stem cell laboratories across Australia. He subsequently initiated and is now the president of Cell Reprogramming Australia, a collaborative framework aiming to facilitate and accelerate iPS cell research in Australia and the Asia pacific region and inform the general public about reprogramming technology. His research continues to combine cell reprogramming technology, genome editing/analysis tools and microfluidic/nanoparticle based detection/ delivery technologies with the aim of creating human in vitro models of disease, unravel the underlying gene regulatory networks and enable novel cell- and delivery-based therapeutics, respectively. He further co-direct the UQ-Centre for stem cell ageing and regenerative engineering (UQ-StemCARE).
