Professor in Developmental Biology, School of Biomedical Sciences, The University of QLD
Senior Group Leader Stem Cell Engineering Group & Director Australian Organoid Facility (AOF) at The University of Queensland
Assistant Professor
University of California Davis,
Department of Neurology
Dr. Fink’s lab is focused on the therapeutic development of gene modifying modalities such as Zinc Fingers, Transcription Activator-like Effectors, and CRISPR/Cas9 to treat genetically-linked neurological disorders. Dr. Fink’s unique academic training and research experience have provided me with an excellent background in multiple biological disciplines including neuroscience, molecular biology, microbiology, chemistry, and genetics. As a graduate student with Dr. Gary Dunbar and Dr. Laurent Lescaudron, my research focused on therapeutic potential of genetically-engineered stem cells in animal models of Huntington’s disease. This work was performed under an international fellowship provided by the French Embassy of Science and Technology to work with a neuroimmunology group at an INSERM lab in France. During his undergraduate and graduate careers, he received several research awards, including the being named the top neuroscience predoctoral student in the state of Michigan. During my postdoctoral training, Dr. Fink was awarded a Ruth L. Kirschstein National Research Service Award from the NIH to develop novel gene therapies for Huntington’s Disease, with Dr. Jan Nolta, a world’s leader in regenerative medicine. Dr. Fink has also played an integral role in obtaining grant funding from NIH, CIRM, UPenn Orphan Disease Center, the Loulou Foundation and Rett Syndrome Trust to develop gene modifying therapies. His lab is focused on translating novel gene modifying therapeutics using patient-derived human iPSC, transgenic rodents, and large animals for translation.
Dr. Fink’s group focuses on assessments of cellular phenotypes in human models of disease, such as induced pluripotent stem cells, indictors of molecular efficacy in transgenic rodent models, and optimization of delivery modalities, such as viral vectors, liponanoparticles and hemapoetic blood and mesenchymal stem cells
Professor
The overarching Silverman laboratory goal is to apply her 20 years of experience with rodent model systems to design and implement effective translational science for neurodevelopmental disorders (NDDs) in four thematic areas. Her research uses multi-faceted approaches in order to: 1) define clinically relevant outcome measures and identify biological markers using next generation genetic models of intellectual disability (ID), autism spectrum disorders (ASD) and paediatric epilepsy with known genetic origins; 2) develop rigorous methods for phenotypic detection in rat models of NDDs and neurodegenerative disorders; 3) continue to evaluate the most prominent environmental contributors to risk of NDDs and neurodegenerative disorders; and 4) utilize innovative, non-behaviorally based phenotypes, such as ex and in vivo neuroimaging, and neurophysiology including EEG, sleep/circadian analysis and sleep spindle modulation, which are biomarkers and translationally relevant to the symptoms of multiple brain disorders.
A major goal of the Department of Psychiatry is fostering distinguished basic neuroscience research. Dr. Silverman’s translational research on the causes of, and development of treatments for, severe genetically based neurodevelopmental disorders (NDDs), is a timely and crucial component to the department. During this evaluation period, from 2017-2020, Dr. Silverman expanded her independent research program that uses novel preclinical rodent models and innovative assays for translational research to include several new techniques and to narrow down therapeutic discovery angles from the wide array of repurposed existing compounds to the development, validation, safety and efficacy testing of gene and stem cell based “curative, precision strategies,” for single gene caused NDDs, IDs and pediatric epilepsy. This shift from treatment screening to focused development of innovative cures occurred organically as the Silverman lab shifted from non-known causal or idiopathic ASDs to known genetic syndromic NDDs.
Professor
Research Interests
Zinc finger, TALE, CRISPR/Cas genome engineering and targeted gene regulation for applications in research and therapeutics, especially neurologic disorders.
Research Synopsis
Addressing the challenges for gene editing in the clinic.
As part of the NIH Somatic Cell Genome Engineering consortium, we continue to develop new methodologies for genome editing and delivery in small and large animal models. Our work involves testing new viral vectors and a detailed analysis of on- and off-target editing in live animals. The SCGE consortium is composed of 40+ labs around the country. Through the Innovative Genomics Institute at UC Berkeley, we are creating new molecular tools for manipulating and studying the genome. We have recently developed molecular probes that can detect unique DNA sequences (such as a gene edit) in individual living cells. And that’s just the beginning.
Postdoctoral Scholar
As a postdoctoral scholar under the mentorship of Dr. Kyle Fink, Julian’s research focusses on epigenome editing strategies to specifically target epi-alleles of genes that are causative for disease utilizing the DNA binding platform CRISPR/dCas9 fused to transcriptional activators and epigenetic editors.
These DNA modifying modalities are engineered to alter gene-expression with the ultimate goal to permanently change aberrantly transcribed genes as a novel therapeutic approach.Julian’s work is focused on adapting CRISPR in a translational manner for genetically-linked neurodevelopmental disorders of the X chromosome, including CDKL5 deficiency (a rare intractable pediatric epilepsy) and Rett syndrome.
Julian been awarded a competitive CDKL5 junior fellowship award and his primary author manuscript has been cited in the top three “must read” publications from the CDKL5 forum. In his current research he is interested in altering the epigenetic landscape of the target gene by means of epigenetic effector domains and analysing its impact on gene reactivation. This includes the removal of repressive histone marks, and the addition of marks that are representative of active promoters and enhancer elements.
His recent work demonstrates that targeted X chromosome reactivation is feasible and can potentially be used as a therapeutic approach to those suffering from X-linked disorders, such as Rett syndrome. In addition he has also been instrumental in novel delivery methods of these epigenetic editors into the brain in a mouse model of Angelman syndrome.
Professor in Biomedical Sciences
Faculty of Medicine
Biography
BSc in Biology (1988) Umea University, Sweden
PhD in Molecular Biology (1994), Umea University, Sweden. Supervisor: Thomas Edlund
Postdoc, Molecular Neurobiology (1994-1999) Salk Institute, La Jolla, USA. Mentor: John B. Thomas
Assistant Professor (1999-2004), Harvard Medical School, Boston, USA
Professor of Developmental Biology (2004-2019), Linkoping University, Sweden
Professor of Developmental Biology (2019-), University of Queensland, Brisbane, Australia
Member of the Royal Swedish Academy of Sciences (2013-)
Qualifications
Australian Institute for Bioengineering and Nanotechnology
Professor Wolvetang is an international leader in pluripotent stem cell biology and human functional neuro-genomics. He leads the Australian organoid facility at AIBN-UQ. His expertise spans reprogramming somatic cells, tissue engineering, genome manipulation with CRISPR, molecular biology, transcriptome analysis, and development of microfluidic devices and nanoparticles for cell analysis and regenerative medicine.
He has been pivotal in advancing induced pluripotent stem cell (iPSC) technology in Australia, focusing on generating iPSCs from patients with neurological disorders. This approach allows for unlimited generation of human brain cells, disease modeling, and drug screening, with potential for patient-specific cellular therapies.
Professor Wolvetang received his PhD in 1992 from the University of Amsterdam. His postdoctoral research at Monash University explored apoptosis, Down syndrome, and Ets transcription factors. He joined the Australian Stem Cell Centre in 2003, leading to a significant Nature Biotechnology publication in 2006. In 2008, he became an independent group leader at the AIBN and a Professor at the University of Queensland, focusing on iPSCs for neurological diseases.
He led the “Reprogramming and Induction of Pluripotency” Collaborative Stream of the Australian Stem Cell Centre and the UQ-stemCARE initiative. His ongoing research integrates cell reprogramming, genome editing, and advanced detection and delivery technologies to model diseases, investigate gene regulatory networks, and develop novel therapeutics.
Please visit https://researchers.uq.edu.au/researcher/2004 to learn more about Professor Wolvetang Awards and Publications
Assistant Professor at the Franlin Biomedical Research Instititue VTC
Dr K. Mukherjee obtained his MBBS degree from Indira Gandhi Medical College in Nagpur, India. Thereafter he switched his career to scientific biomedical research and pursued a Ph.D from National Institute of Immunology, New Delhi, India. The bulk of his postdoctoral work was done under the supervision of the Nobel laureate neuroscientist, Professor Thomas Sudhof at UT Southwestern Medical center at Dallas, USA and Stanford University School of Medicine, Palo Alto, USA. He also received training in the laboratories of prominent neuroscientists, Professor Reinhard Jahn at Max Planck Institute of Biophysical Chemistry, Gottingen, Germany and Professor Leslie Griffith at Brandeis University, Waltham, USA.
Dr. Pars is an early career researcher with an expertise in stem cell research & disease modelling of neurological diseases using human brain organoids. During her scientific training, she has gained experience in various organoid models involving retinal, vascular, and cortical organoids. During her postdoctoral research, Dr. Pars established a drug screening platform for epilepsy patients, using high-density multi-electrode arrays for anti-seizure medication purposes. Her scientific interests are disease modelling of neurodevelopmental diseases using personalised medicine approaches. She is currently working at the Australian Institute for Bioengineering and Nanotechnology (The University of Queensland) as a postdoctoral researcher under the supervision of Prof. Ernst Wolvetang and in collaboration with Prof. Stefan Thor.
Education:
Memberships:
Lavvina is a clinical genetics fellow from NSW, Australia with a background in general paediatrics. She has practiced in multiple tertiary paediatric hospitals in Australia, both in general paediatrics and clinical genetics. She currently provides specialist advice for the NGO, Taking Paediatrics Abroad and is a member of GeneEQUAL, an inclusive research group aiming to improve accessibility of genetic testing and care for people with intellectual disability by co-design.
Lavvina’s clinical interests are in the genetics of autism, intellectual disability and immunogenomics. She is particularly passionate about including the patient groups she works with in research and healthcare decisions.
Lavvina is affiliated with The Children’s Hospital Westmead and the University of New South Wales where she is undertaking a Masters by Research, co-producing a model of genetic healthcare that aligns with the preferences of Autistic people.
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“In some ways, that CASK-linked pathology is degenerative in nature provides a positive outlook. Because microcephaly in CASK-linked pathology progresses postnatally, there may be a temporal window when therapeutic intervention might prevent or slow further brain cell loss. Regression, even in adolescence, has also been observed in some cases of MICPCH [119], again offering the tantalizing possibility that a therapeutic approach might prevent such decline under conditions when degeneration is known to progress. The potential benefits of intervention might extend even further given that non-cell-autonomous toxicity could also affect functioning of the remaining neurons; reduction of such toxicity, especially when coupled with high-intensity rehabilitative measures [120], might offer real hope for a positive impact on functional outcomes.”
