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Publication : Phenotypic rescue of a peripheral clock genetic defect via SCN hierarchical dominance.

First Author  Pando MP Year  2002
Journal  Cell Volume  110
Issue  1 Pages  107-17
PubMed ID  12151001 Mgi Jnum  J:77715
Mgi Id  MGI:2182476 Doi  10.1016/s0092-8674(02)00803-6
Citation  Pando MP, et al. (2002) Phenotypic Rescue of a Peripheral Clock Genetic Defect via SCN Hierarchical Dominance. Cell 110(1):107-17
abstractText  The mammalian circadian system contains both central and peripheral oscillators. To understand the communication pathways between them, we have studied the rhythmic behavior of mouse embryo fibroblasts (MEFs) surgically implanted in mice of different genotypes. MEFs from Per1(-/-) mice have a much shorter period in culture than do tissues in the intact animal. When implanted back into mice, however, the Per1(-/-) MEF take on the rhythmic characteristics of the host. A functioning clock is required for oscillations in the target tissues, as arrhythmic clock(c)(/c) MEFs remain arrhythmic in implants. These results demonstrate that SCN hierarchical dominance can compensate for severe intrinsic genetic defects in peripheral clocks, but cannot induce rhythmicity in clock-defective tissues.
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