Rhythmic potassium transport regulates the circadian clock in human red blood cells

Erin A. Henslee, Priya Crosby, Stephen J. Kitcatt, Jack S. W. Parry, Andrea Bernardini, Rula G. Abdallat, Gabriella Braun, Henry O. Fatoyinbo, Esther J. Harrison, Rachel S. Edgar, Kai F. Hoettges, Akhilesh B. Reddy, Rita I. Jabr, Malcolm von Schantz, John S. O’Neill () and Fatima H. Labeed ()
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Erin A. Henslee: University of Surrey
Priya Crosby: MRC Laboratory of Molecular Biology
Stephen J. Kitcatt: University of Surrey
Jack S. W. Parry: University of Surrey
Andrea Bernardini: University of Surrey
Rula G. Abdallat: University of Surrey
Gabriella Braun: University of Surrey
Henry O. Fatoyinbo: University of Surrey
Esther J. Harrison: University of Surrey
Rachel S. Edgar: MRC Laboratory of Molecular Biology
Kai F. Hoettges: University of Surrey
Akhilesh B. Reddy: The Francis Crick Institute
Rita I. Jabr: University of Surrey
Malcolm von Schantz: University of Surrey
John S. O’Neill: MRC Laboratory of Molecular Biology
Fatima H. Labeed: University of Surrey

Nature Communications, 2017, vol. 8, issue 1, 1-10

Abstract: Abstract Circadian rhythms organize many aspects of cell biology and physiology to a daily temporal program that depends on clock gene expression cycles in most mammalian cell types. However, circadian rhythms are also observed in isolated mammalian red blood cells (RBCs), which lack nuclei, suggesting the existence of post-translational cellular clock mechanisms in these cells. Here we show using electrophysiological and pharmacological approaches that human RBCs display circadian regulation of membrane conductance and cytoplasmic conductivity that depends on the cycling of cytoplasmic K+ levels. Using pharmacological intervention and ion replacement, we show that inhibition of K+ transport abolishes RBC electrophysiological rhythms. Our results suggest that in the absence of conventional transcription cycles, RBCs maintain a circadian rhythm in membrane electrophysiology through dynamic regulation of K+ transport.

Date: 2017
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DOI: 10.1038/s41467-017-02161-4

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