Moonlight shifts the endogenous clock of Drosophila melanogaster.

The ability to be synchronized by light-dark cycles is a fundamental property of circadian clocks. Although there are indications that circadian clocks are extremely light-sensitive and that they can be set by the low irradiances that occur at dawn and dusk, this has not been shown on the cellular level. Here, we demonstrate that a subset of Drosophila's pacemaker neurons responds to nocturnal dim light. At a nighttime illumination comparable to quarter-moonlight intensity, the flies increase activity levels and shift their typical morning and evening activity peaks into the night. In parallel, clock protein levels are reduced, and clock protein rhythms shift in opposed direction in subsets of the previously identified morning and evening pacemaker cells. No effect was observed on the peripheral clock in the eye. Our results demonstrate that the neurons driving rhythmic behavior are extremely light-sensitive and capable of shifting activity in response to the very low light intensities that regularly occur in nature. This sensitivity may be instrumental in adaptation to different photoperiods, as was proposed by the morning and evening oscillator model of Pittendrigh and Daan. We also show that this adaptation depends on retinal input but is independent of cryptochrome.

Gene expression of adenosine receptors along the nephron.

BACKGROUND: In view of the multiple effects of adenosine on kidney function, this study aimed to determine the expression of adenosine receptors (AR) along the rat and mouse nephron. METHODS: For this purpose, we semiquantified mRNA abundance for adenosine A1-, A2A-, A2B-, and A3 receptors by RNAse protection and by reverse transcription-polymerase chain reaction (RT-PCR) in the kidney zones and in the different nephron segments of mice and rats. RESULTS: We found very similar expression patterns for rat and mice. For the kidney zones A1-AR mRNA and A2A-AR mRNA abundance displayed a marked difference, with an increase from cortex to the inner medulla. This was not seen for A2B receptors, which showed in general a rather weak expression. Along the nephron, A1-AR was strongly expressed in the thin limbs of Henle and in the collecting duct system and to a lesser extent in the medullary thick ascending limb. A2A-AR mRNA was clearly detected in glomeruli but not in other nephron segments. A2B-AR mRNA was strongly expressed in the cortical thick ascending limb of Henle and in the distal convoluted tubule. A3-AR mRNA was not found in any nephron segment. CONCLUSION: Our data demonstrate a distinct mutual expression of the AR subtypes along the nephron. A1 receptors are expressed in medullary tubular structures, while A2B receptors are predominant in cortical tubular structures. A2A receptor expression in the kidney appears to be restricted to vascular cells.