Wolvetang Group Honours Projects

 Supervisor Professor Ernst Wolvetang & Dr Julio Aguado Perez

People with Down syndrome (trisomy 21) exhibit accelerated aging of multiple tissues but which of the 135 protein coding genes on chromosome 21 are responsible remains unclear. To discover this we will use CRISPR-enabled genome manipulation technologies in human Down syndrome stem cell models.

 Supervisor Professor Ernst Wolvetang & Dr Mohammed Shaker

Clinical collaborators have identified a novel brain disease in children that leads to focal loss of myelin in the brain. We aim to establish induced pluripotent stem cells from these individuals and assess whether oligodendrocytes are defective in their ability to deposit myelin using in vitro cultured human brain organoids.

 Supervisor Professor Ernst Wolvetang & Dr Sarah Withey

Ataxia telangiectasia is a debilitating disease in children that is due to loss of function of the ATM kinase. ATM regulates DNA repair in the nucleus but also plays an important role in coordinating anti-oxidant defence. Here we will investigate how ATM may be involved in regulating the amount of catalase (a major anti-oxidant defence enzyme) in peroxisomes, using human stem cell derived liver cells.

 Supervisor Professor Ernst Wolvetang & Dr Giovanni Pietrogrande

In this project the student will design, create and test novel Cas9-enabled genome editing technologies with considerable commercial potential developed in the Wolvetang laboratory. The project will assess the accuracy, efficacy and versatility of differently designed versions of this novel platform in a range of cell lines widely used by the biotechnology industry and in human pluripotent stem cells.

 Supervisor Professor Ernst Wolvetang & Dr Mohammed Shaker

How genetic mutations lead to defective cortical development in humans remains poorly understood. In this project the student will use patient-derived and genome edited versions of human induced pluripotent stem cells to create brain organoids, and then assess how and when the migration and specification of cortical cell types becomes derailed in this in vitro model of human brain development. 

 Supervisor Professor Ernst Wolvetang & Dr Hannah Leeson

Mutations in the SPG56/CYP2U1 gene cause hereditary spastic paraplegia. CYP2U1 is expressed in neurons and astrocytes of the cortex, hippocampus and cerebellum and is found to be associated with mitochondria and the ER. Using a variety of brain organoids derived from patient iPSC and from genome edited hiPSC this project aims to gain insight into disease mechanism, identify novel biomarkers, and perhaps even test therapeutics.