Impaired neuronal function alters rhythmicity in the circadian circuitry

M DE LA PAZ FERNANDEZ & M. FERNANDA CERIANI

Cold Spring Harbor Laboratories, USA,

Congreso; Neurobiology of Drosophila; 2005

CSHL

The circadian clock serves as a temporal filter to synchronize gene expression, cell metabolism, physiology and behavior to the most critical moments in the day, thus contributing to the adaptation of the organism to a changing environment. While substantial progress has been made in elucidating the molecular processes that impart this temporal control, very little is known to date about the hierarchical organization among the different circadian circuits or whether other neuronal clusters would also be implicated. Circadian release of the neuropeptide pigment dispersing factor (PDF) is central to how the clock controls rhythmic rest-activity cycles. In the present study we have taken advantage of flies exhibiting a distinctive arrhythmic phenotype due to mutation of the calcium-dependent voltage-gated potassium channel slowpoke (slo) to examine the activity of specific neuronal populations in circadian control of behavior. We show that molecular oscillations in the core pacemaker cells are properly running in the null mutant, as are peripheral clocks.  However, altered neuronal function associated to the null mutation specifically impairs PDF accumulation on the dorsal projections running towards the pars intercerebralis and along the midline.  Although the channel is not expressed in the canonical clock neurons within the fly brain, a direct contact between the PDF and SLO-expressing circuits implicates SLO-expressing neurons as part of the circadian network.  Our results demonstrate that control of rhythmic behavior depends on a highly complex neuronal network whose activity coordinates the molecular oscillators within that network.