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 PMID:26392540  

Neuropsin (OPN5)-mediated photoentrainment of local circadian oscillators in mammalian retina and cornea.

Ethan D Buhr | Wendy W S Yue | Xiaozhi Ren | Zheng Jiang | Hsi-Wen Rock Liao | Xue Mei | Shruti Vemaraju | Minh-Thanh Nguyen | Randall R Reed | Richard A Lang | King-Wai Yau | Russell N Van Gelder
Proceedings of the National Academy of Sciences of the United States of America | 2015

The molecular circadian clocks in the mammalian retina are locally synchronized by environmental light cycles independent of the suprachiasmatic nuclei (SCN) in the brain. Unexpectedly, this entrainment does not require rods, cones, or melanopsin (OPN4), possibly suggesting the involvement of another retinal photopigment. Here, we show that the ex vivo mouse retinal rhythm is most sensitive to short-wavelength light but that this photoentrainment requires neither the short-wavelength-sensitive cone pigment [S-pigment or cone opsin (OPN1SW)] nor encephalopsin (OPN3). However, retinas lacking neuropsin (OPN5) fail to photoentrain, even though other visual functions appear largely normal. Initial evidence suggests that OPN5 is expressed in select retinal ganglion cells. Remarkably, the mouse corneal circadian rhythm is also photoentrainable ex vivo, and this photoentrainment likewise requires OPN5. Our findings reveal a light-sensing function for mammalian OPN5, until now an orphan opsin.

Pubmed ID: 26392540

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Associated grants

  • Agency: NEI NIH HHS, United States
    Id: R01 EY014596
  • Agency: NEI NIH HHS, United States
    Id: R01 EY023179
  • Agency: NEI NIH HHS, United States
    Id: EY14596
  • Agency: NEI NIH HHS, United States
    Id: EY001370
  • Agency: NEI NIH HHS, United States
    Id: EY23179
  • Agency: Howard Hughes Medical Institute, United States
  • Agency: NEI NIH HHS, United States
    Id: F32EY02114

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International Mouse Phenotyping Consortium (IMPC) (tool)

RRID:SCR_006158

Center that produces knockout mice and carries out high-throughput phenotyping of each line in order to determine function of every gene in mouse genome. These mice will be preserved in repositories and made available to scientific community representing valuable resource for basic scientific research as well as generating new models for human diseases.

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