Cookies on this website
We use cookies to ensure that we give you the best experience on our website. If you click 'Continue' we will assume that you are happy to receive all cookies and you will not see this message again. Click 'Find out more' for information on how to change your cookie settings.

My connections

Melissa Bailey

Postgraduate Student

Research Summary

research summary

I am a graduate student in the 4 year Wellcome Trust Doctoral programme in Neuroscience, funded by the Rhodes Trust. I started my DPhil in 2012, working jointly with the Monaco Group in the Wellcome Trust Centre for Human Genetics funded by a Wellcome Trust Programme Grant. My primary interests lie in the genetic and epigenetic contribution to neurodevelopmental disorders. 

My research focuses on elucidating the role of the candidate dyslexia susceptibility (CDS) gene KIAA0319-Like (KIAA0319L) in neurodevelopment. My work is in conjunction with Dr Isabel Martinez-GarayDr Antonio Velayos-Baeza and Luiz Guidi, as part of our group's interest into migration and differentiation associated disorders. Developmental dyslexia (DD) is the most common childhood learning disorder, however the biological causes of the disorder remain poorly understood. Postmortem histological and neuroimaging studies suggest that impaired neuronal migration is a cellular antecedent to DD. To date, all CDS genes studied, including Kiaa0319L, have been shown to function as neuronal migration genes in the rat, through embryonic RNAi-mediated knockdown of CDS homolog genes. These results suggest that neuronal migration errors may also contribute to the DD phenotype. However, recent studies in mice suggest that neuronal migration is neither an essential nor an exclusive function of CDS genes in the cerebral cortex.

My working hypothesis is that Kiaa0319L function is not restricted to neuronal migration, and may be involved in later events during development. Using transgenic mouse technologies, I am characterising the mechanisms underlying the role of Kiaa0319L in neurodevelopment. As part of an Oxford-McGill Neuroscience Collaboration with the laboratory of Dr Anne McKinney, I am examining the effect of KIAA0319L protein levels on dendritogenesis, and spine development.

False False

Brief Biography

Through my undergraduate degree at the University of Manitoba, I worked with Dr Stephanie Booth in the Division of Molecular PathoBiolog at the National Microbiology Laboratory in Winnipeg, Canada. There I contributed to a functional study on microRNAs up regulated during prion disease, and their involvement in the post-transcriptional modification of cholesterol 24-hydroxylase, a monooxygenase involved in the elimination of cholesterol from the brain. In 2009, I was awarded one of ten international summer internships, and worked with Dr Verdon Taylor at the Max-Planck Institute of Immunobiology & Epigenetics in Freiburg, Germany. My research focused on the Notch signaling pathway and the role of the Notch ligand Jagged1 (Jag1) in maintaining neural stem cells in an undifferentiated state. 

In 2010, I was awarded an NSERC Undergraduate Student Research Award to work with Dr Mark Fry, in the Department of Biological Sciences, at the University of Manitoba. I contributed to his research on the electrophysiological properties of neurons of the sensory circumventricular organs and examined the intrinsic electrophysiological properties of dopaminergic neurons of the arcuate nucleus in response to ghrelinIn 2011, I completed my honours thesis on the epigentic regulation of neural stem cells (NSCs) fate determination with Dr Mojgan Rastegar in the Department of Biochemistry & Medical Genetics, at the University of Manitoba. I earned an Undergraduate Summer Studentship Award through the Manitoba Institute of Child Health, which allowed me to continue my work on Rett syndrome, and MeCP2 expression in differentiated brain-derived NSCs.

I earned my MSc in Neuroscience at Oxford, completing a project with Dr Natalie Voets at the FMRIB Centre where I examined functional and structural connectivity changes in epilepsy using resting‐state fMRI, diffusion tensor imaging and neuropsychological data. I also worked with Dr Colin Akerman, using optogenetic techniques and whole-cell voltage-clamp recordings to investigate whether intracellular chloride levels affect GABAA receptor currents in neurons.