ZFIN ID: ZDB-PUB-070212-17
Synchronizing multiphasic circadian rhythms of rhodopsin promoter expression in rod photoreceptor cells
Yu, C.J., Gao, Y., Li, P., and Li, L.
Date: 2007
Source: The Journal of experimental biology   210(4): 676-684 (Journal)
Registered Authors: Li, Lei
Keywords: circadian clock, rod photoreceptor cell, rhodopsin promoter, retina, zebrafish
MeSH Terms:
  • Analysis of Variance
  • Animals
  • Circadian Rhythm/physiology*
  • DNA Primers
  • Dopamine/pharmacology
  • Gene Expression Regulation*
  • Green Fluorescent Proteins/metabolism
  • Promoter Regions, Genetic/genetics
  • Receptors, Dopamine D2/metabolism*
  • Retinal Rod Photoreceptor Cells/metabolism*
  • Reverse Transcriptase Polymerase Chain Reaction
  • Rhodopsin/genetics
  • Rhodopsin/metabolism*
  • Zebrafish/physiology*
PubMed: 17267653 Full text @ J. Exp. Biol.
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ABSTRACT
Endogenous circadian clocks regulate day-night rhythms of animal behavior and physiology. In zebrafish, the circadian clocks are located in the pineal gland and the retina. In the retina, each photoreceptor is considered a circadian oscillator. A critical question is whether the individual circadian oscillators are synchronized. If so, the mechanism that underlies the synchronization needs to be elucidated. We generated a transgenic zebrafish line that expresses short half-life GFP under the transcriptional control of the rhodopsin promoter. Time-lapse imaging of rhodopsin promoter-driven GFP expression revealed that during 24 h in constant darkness, rhodopsin promoter expression in rod photoreceptor cells fluctuated rhythmically. However, the pattern of fluctuation differed between individual cells. In some cells, peak expression was seen in the subjective early morning, whereas in other cells, peak expression was seen in the afternoon or at night. Light transiently decreased rhodopsin expression, thereby synchronizing the multiphasic circadian oscillation. The application of dopamine or dopamine D(2) receptor agonist also synchronized the circadian rhythms of rhodopsin promoter expression. When the D(2) receptors were pharmacologically blocked, light exposure produced no effect. This suggests that the synchronization of the circadian rhythms of rhodopsin promoter expression by light is mediated by dopamine D(2) receptors. The mechanism that underlies the synchronization probably involves dopamine-mediated Ca(2+) signaling pathways. Light, as well as dopamine, lowered Ca(2+) influx into the rod cells, thereby resetting rhodopsin promoter expression to the initial phase.
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