Emily Kruchek
Postgraduate research student
Academic and research departments
Department of Mechanical Engineering Sciences, Centre for Biomedical Engineering.My publications
Publications
Beale Andrew D., Kruchek Emily, Kitcatt Stephen J., Henslee Erin A., Parry Jack S.W., Braun Gabriella, Jabr Rita, von Schantz Malcolm, O?Neill John S., Labeed Fatima H. (2019) Casein kinase 1 underlies temperature compensation of circadian rhythms in human red blood cells, Journal of Biological Rhythms SAGE Publications
Temperature compensation and period determination by casein kinase 1 (CK1) are conserved features of eukaryotic circadian rhythms, whereas the clock gene transcription factors that facilitate daily gene expression rhythms differ between phylogenetic kingdoms. Human red blood cells (RBCs) exhibit temperature compensated circadian rhythms which, since RBCs lack nuclei, must occur in the absence of a circadian transcription-translation feedback loop. We tested whether period determination and temperature compensation are dependent on casein kinases in RBCs. As with nucleated cell types, broad spectrum kinase inhibition with staurosporine lengthened the period of the RBC clock at 37°C, with more specific inhibition of CK1 and CK2 also eliciting robust changes in circadian period. Strikingly, inhibition of CK1 abolished temperature compensation and increased the Q10 for the period of oscillation in RBCs, similar to observations in nucleated cells. This indicates that CK1 activity is essential for circadian rhythms irrespective of the presence or absence of clock gene expression cycles.
Beale Andrew D., Kruchek Emily, Kitcatt Stephen J., Henslee Erin A., Parry Jack S.W., Braun Gabriella, Jabr Rita, von Schantz Malcolm, O?Neill John S., Labeed Fatima (2019) Casein Kinase 1 Underlies Temperature Compensation of Circadian Rhythms in Human Red Blood Cells, Journal of Biological Rhythms 34 (2) pp. 144-153 SAGE Publications
Temperature compensation and period determination by casein kinase 1 (CK1) are conserved features of eukaryotic circadian rhythms, whereas the clock gene transcription factors that facilitate daily gene expression rhythms differ between phylogenetic kingdoms. Human red blood cells (RBCs) exhibit temperature-compensated circadian rhythms, which, because RBCs lack nuclei, must occur in the absence of a circadian transcription-translation feedback loop. We tested whether period determination and temperature compensation are dependent on CKs in RBCs. As with nucleated cell types, broad-spectrum kinase inhibition with staurosporine lengthened the period of the RBC clock at 37°C, with more specific inhibition of CK1 and CK2 also eliciting robust changes in circadian period. Strikingly, inhibition of CK1 abolished temperature compensation and increased the Q10 for the period of oscillation in RBCs, similar to observations in nucleated cells. This indicates that CK1 activity is essential for circadian rhythms irrespective of the presence or absence of clock gene expression cycles.