Dr Ko-Fan Chen

From July 2020 I am based at the University of Leicester in my first independent position investigating the visual control of sleep and its interaction with neurodegeneration. I am originally from Taiwan where I completed my BSc and MSc degrees in Biology and Physiology at National Cheng Kung University. I then moved to Ralf Stanewsky’s lab in the UK for my PhD investigating the molecular basis of circadian light entrainment (Queen Mary University of London). For my first postdoc I joined Damian Crowther's lab at the University of Cambridge where I investigated how rhythmic light regimes alter processes underlying age-related neurodegeneration. I also developed a new method for simultaneously detecting the decline of molecular and behavioural oscillations during age-dependant neurodegeneration in a fly model. I then moved to James Jepson’s lab in the UCL Institute of Neurology to investigate Drosophila Dystonia models and to continue exploring how variable light-dark cycles modify normal and disease related sleep-wake behaviour.

We are based in the Department of Genetics and Genome Biology at the University of Leicester. Broadly speaking the lab is interested in two aspects of sleep research: How environmental factors influence sleep and circadian behaviours? and How sleep-related cellular mechanisms modulate progress of human diseases? To answer these research questions we use the fruit fly Drosophila melanogaster as an experimental model allowing us to apply diverse methods to identify evolutionary conserved molecular mechanisms. We work closely with Neurogenetics and Neurodegeneration research network in the department. Please see the following link for more details: https://sites.google.com/view/kofanchen

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2021 Kratschmer, P., Lowe, S. A., Buhl, E., Chen, K. F., Kullmann, D. M., Pittman, A., ... & Jepson, J. E. Impaired Pre‐Motor Circuit Activity and Movement in a Drosophila Model of KCNMA1‐Linked Dyskinesia. Movement Disorders 36(5) 1158-1169.

2021 Putker, M., Wong, D. C., Seinkmane, E., Rzechorzek, N. M., Zeng, A., Hoyle, N. P., .Chen, K. F.. & O’Neill J. S. CRYPTOCHROMES confer robustness not rhythmicity to circadian timekeeping. The EMBO journal 40(7) e106745.

2019 Chen, K.-F.#, Lowe., S, Lamaze, A., Krätschmer, P., Jepson, J.E.C. Neurocalcin regulates nighttime sleep and arousal in Drosophila. eLife 8 e38114

2018 Lamaze, A., Krätschmer, P*., Chen, K.-F.*, Lowe, S., Jepson, J.E.C. Wake-promoting circadian output circuit in Drosophila. Current Biology 28 (19) 3098-3105.

2018 Younan, N.D., Chen, K.-F., Rose, R.S., Crowther, D.C., Viles, J.H. Prion protein stabilizes amyloid-β (Aβ) oligomers and enhances Aβ neurotoxicity in a Drosophila model of Alzheimer’s disease. Journal of Biological Chemistry 293 (34)13090-13099

2016 Khabirova, E.*, Chen, K.-F.#*, O’Neill, J.S., and Crowther, D.C. Flyglow: Single-fly observations of simultaneous molecular and behavioural circadian oscillations in controls and an Alzheimer’s model. Scientific Reports 6. 33759.

2016 Buhl, E., Bradlaugh, A., Ogueta, M., Chen, K.-F., Stanewsky, R., and Hodge, J.J. Quasimodo mediates daily and acute light effects on Drosophila clock neuron excitability. Proceedings of the National Academy of Sciences 113 13486-13491

2014 Chen, K.-F.#, Possidente, B., Lomas, D.A., and Crowther, D.C. The central molecular clock is robust in the face of behavioural arrhythmia in a Drosophila model of Alzheimer’s disease. Disease Models & Mechanisms 7 445-458

2011 Chen, K.-F.*, Peschel, N*., Zavodska, R., Sehadova, H., and Stanewsky, R.. QUASIMODO a Novel GPI-Anchored Zona Pellucida Protein Involved in Light Input to the Drosophila Circadian Clock. Current Biology 21 (9) 719-729

2009 Landskron, J*., Chen, K.-F.*, Wolf, E., and Stanewsky, R.. A role for the PERIOD: PERIOD homodimer in the Drosophila circadian clock. PLOS Biology 7 (4) e1000003

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1. What are the neurogenetic mechanisms underlying light- and vision-promoted sleep?

We are interested in use latest fly behavioural genetics and live imaging methods to explore wider molecular and neural mechanisms by which the visual system facilitates sleep.

2 What is the clock-controlled neuroprotective molecular pathway?

A major hallmark of neurodegeneration is the misfolded protein aggregates leading to ER stress and eventually causes neuronal dysfunction. Intriguingly the presence of the circadian clock may inhibit the formation of pathogenic aggregates depending on the types of misfolded protein aggregates. We will use molecular and neurogenetic tools to identify the underlying neuroprotective molecular mechanisms of circadian clock.

3. Can sleep modulate Neurological disease?

Sleep disruption has been reported in various neurological diseases. Whether such sleep problem exacerbate the disease progress is a open question. Using Drosophila as diease models we will address whether sleep alterations can be identified in diseases such as dystonia and nystagmus. Also we will investigate if reduced sleep quality impacts the severity of neurological diseases. 

I currently contribute and co-convene in lectures and practicals in BS2026. I also cooridnate and supervise 3rd Year research project.

Circadian Rhythm Sleep Neurodegeneration Genetic models of dieases