Abstract
The transmembrane protein CLN3 and the motor protein myosin V are both involved in cell polarity. We have preliminary evidence that these proteins interact but the mechanism is unknown. This project will determine the roles of CLN3 and myosin V in cell polarity, investigating their relationship and determining the underlying molecular and biophysical mechanisms. A variety of model systems (zebrafish, yeast, fruit fly, patient cells) will be employed to determine the extent of conservation of protein function, underlying pathways and biophysical mechanisms, further elucidating the function of CLN3, mutations in which cause a paediatric neurodegenerative disease.
References
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