Clare Roskell

Institute of Ageing and Chronic Disease University of Liverpool Willian Henry Duncan Building 6 West Derby Street Liverpool L7 8TX


Dr V. Pekovic-Vaughan (University of Liverpool), Professor P. Clegg (University of Liverpool), Dr D. Shanley (University of Newcastle), Dr M. Goldberg (University of Durham)

I graduated from the University of Liverpool with a First Class BSc (Hons) degree in Genetics. I am currently a second year PhD student at the University of Liverpool as part of the Musculoskeletal Biology group in the institute of Ageing and Chronic disease.

My research interests include circadian biology, musculoskeletal diseases and stem cells. Throughout my studies I have always been passionate about stem cell research and their potential use in regenerative medicine for the treatment of a wide variety of diseases. I am currently focusing on understanding how the molecular circadian clock and lamin proteins interact in muscle and stem cells in response to mechanical stretch and how this is disrupted with age and disease.

I attended the North East Postgraduate Conference and conferences for the European Biological Rhythms Society and British Society for Matrix Biology, presenting a poster at the latter conference.

I helped plan activities based around circadian rhythms for a ‘Meet the Scientist’ day at the Museum of Liverpool.

Nuclear lamins as mediators between circadian clocks and mechanical pathways

Circadian rhythms are evolutionarily conserved through 24h biological cycles in physiology, metabolism and behaviour, including sleep/wake and locomotor activity. With 40% of the genome across tissues shown to be clock regulated, disrupted clocks are associated with an increased risk of diseases in humans and premature ageing in mouse models.

The nuclear lamina is a fibrous meshwork underlying the nuclear envelope, consisting of type V intermediate filament proteins called lamins. Mutations in A type lamins cause several inherited human disorders affecting the musculoskeletal system. They provide structural support to the nucleus and control fundamental cellular processes including mechanosensitive gene expression. Moreover, lamins regulate nuclear tethering of transcription factors to fine-tune signalling pathways important for cell differentiation and stress responses. Our hypothesis is that the molecular clock in skeletal muscle cells is responsive to mechanical stimuli and that this mechanism is mediated by lamins through nuclear tethering of clock transcription factors.

Our results have the potential to uncover a novel mechanism of skeletal muscle clock regulation by the nuclear lamina, which could be used to design new therapeutic strategies to reset altered clocks in elderly individuals and patients with musculoskeletal disorders.

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