Two new studies led by University of Texas (UT) Southwestern (UTSW) scientists outline how individual cells maintain their internal clocks, driven both through heritable and random means. These findings, published online on May 1, 2020 in PNAS (https://www.pnas.org/content/117/19/10350 ) and on May 27, 2020 in eLife (https://elifesciences.org/articles/54186), help explain how organisms’ circadian clocks maintain flexibility and could offer insights into aging and cancer. The open-access PNAS article is titled "Noise-Driven Cellular Heterogeneity in Circadian Periodicity" and the open-access eLife article is titled "Epigenetic Inheritance of Circadian Period in Clonal Cells." Scientists have long known that organisms across the spectrum of life have internal clocks--with cycles about as long as a day--that govern behaviors including sleeping, eating, and immune response. However, individual cells also have their own clocks when removed from the organism, with periods that can vary substantially, stretching up to several hours longer or shorter. How cells maintain these different lengths of internal rhythms has been unknown given that these cells should be the same at the genetic level, explains Joseph Takahashi (photo) (https://profiles.utsouthwestern.edu/profile/105885/joseph-takahashi.html), PhD, Professor and Chair of the Department of Neuroscience at UT Southwestern Medical Center, a member of UTSW’s Peter O’Donnell Jr. Brain Institute, and an Investigator with the Howard Hughes Medical Institute. To investigate this question, Dr. Takahashi and his colleagues worked with mouse cells that were genetically altered so that they glowed whenever a prominent circadian clock gene called Per2 was turned on.
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