The formation of the cerebral cortex, the seat of higher cognitive function, extends over several weeks in mice and years in humans. Although this process occurs continuously, there are moments during development in which the organism is particularly susceptible to perturbations. These perturbations (e.g. genetic mutations or environmental insults) can alter the developmental trajectory of the organism and can lead to long-lasting changes in their development and cortical function. We are interested in understanding how these perturbations in early development can alter the cell biological behaviour of cortical cells and ultimately their function in later life, using mouse as a model system.

Our research focusses on addressing these two general questions:

How does cellular homeostasis occur during development?

The cerebral cortex consists of many different cell types - neurons, consisting of the excitatory and inhibitory neurons, and glial cells, comprised of microglia, astrocytes and oligodendrocytes. Despite differences in the shapes and sizes of the mammalian cerebral cortex in different species, the cerebral cortex is made up of similar cell types. Each cell type can differ substantially in their origins, birthdates, behaviour and function. How then do these various cell types come together at the right place, time and number during development? To address this, we are currently using single cell and bulk RNA sequencing, viral mediated gene manipulation and functional analysis to identify the cellular and molecular mechanisms underlying cellular homeostasis.

How does the disruption of cellular homeostasis lead to disorders?

Multiple labs have demonstrated the importance of glial cells in modulating neurotransmissions and consequently normal cortical function. For example, transient alteration in microglia numbers during early development was sufficient to induce long-lasting changes in mouse behaviour and may underlie some of the cognitive and social deficits typically observed in individuals diagnosed with autism spectrum disorders. We are interested in investigating the impact of disruption of cellular homeostasis and how this may be implicated in neurological disorders throughout the lifetime of the organism. We will be using rodent cognitive and behaviour tasks, anatomical and histochemical analysis together with live cell imaging in order to elucidate the long-term impact of this disruption.

I am currently a MRC CDA fellow. I have previously worked as a behavioural pharmacologist at GlaxoSmithKline (Singapore) before pursuing my PhD in the lab of Wieland B. Huttner at the Max Planck Institute of Molecular Cell Biology and Genetics (MPI-CBG), Dresden, Germany. For my PhD, I have studied the molecular mechanisms underlying the expansion of the mammalian neocortex during evolution and also developed a new tool (microinjection) to manipulate the neural stem and progenitor cells. For my postdoc, I then moved to the lab of Oscar Marín at King’s College London. Here I studied how the interneuron cell survival is regulated during development and how its dysregulation can lead to neurodevelopmental disorders such as autism and epilepsy. By combining my expertise in stem cell biology, system biology and animal behaviour, my lab is currently interested in understanding how the various cortical cells in the mammalian six layered cortex communicate and regulate each others development.