Journal
CURRENT BIOLOGY
Volume 29, Issue 20, Pages 3478-+Publisher
CELL PRESS
DOI: 10.1016/j.cub.2019.08.063
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Funding
- NIH [R01 GM124246, R01 EY026921, P30EY001730, R01 EY027077, R01 EY027711]
- Research to Prevent Blindness
- Mark J. Daily, MD Research Fund
- Goldman Chair of the Abrahamson Pediatric Eye Institute at Cincinnati Children's Hospital Medical Center
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Nearly all mammalian tissues have functional, autonomous circadian clocks, which free-run with non-24 h periods and must be synchronized (entrained) to the 24 h day. This entrainment mechanism is thought to be hierarchical, with photic input to the retina entraining the master circadian clock in the suprachiasmatic nuclei (SCN) and the SCN in turn synchronizing peripheral tissues via endocrine mechanisms. Here, we assess the function of a population of melanocyte precursor cells in hair and vibrissal follicles that express the photopigment neuropsin (OPN5). Organotypic cultures of murine outer ear and vibrissal skin entrain to a light-dark cycle ex vivo, requiring cis-retinal chromophore and Opn5 gene function. Short-wavelength light strongly phase shifts skin circadian rhythms ex vivo via an Opn5-dependent mechanism. In vivo, the normal amplitude of Period mRNA expression in outer ear skin is dependent on both the light-dark cycle and Opn5 function. In Opn4(-/-); Pde6b(rd1/rd1) mice that cannot behaviorally entrain to light-dark cycles, the phase of skin-clock gene expression remains synchronized to the light-dark cycle, even as other peripheral clocks remain phase-locked to the free-running behavioral rhythm. Taken together, these results demonstrate the presence of a direct photic circadian entrainment pathway and direct light-response elements for clock genes in murine skin, similar to pathways previously described for invertebrates and certain non-mammalian vertebrates.
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