Cell autonomous and non-autonomous mechanisms relevant for the remodelling of axonal terminals of pacemaker neurons in Drosophila melanogaster

HERRERO A; CERIANI MF

Mar del Plata, 27 Septiembre al 1 Octubre 2015.

Congreso; XXX Congreso anual de la SAN; 2015

Sociedad Argentina de Investigaciones en Neurociencias

A number of years ago we reported that pigment dispersing factor (PDF) neurons, which are essential in the control of rest-activity cycles in Drosophila, undergo circadian remodeling of their axonal projections (Fernández et al., Plos Biol, 2008). We then proposed that such remodeling could provide an additional means of transmitting time of day information in addition to differential neurotransmitter release (i.e., PDF). Axonal arborizations display higher complexity during the day and less so at night, and this structural plasticity ensures changes in the degree of connectivity (Gorostiza et al., Curr Biol, 2014). In this work we characterize the molecular mechanisms that underlie these structural changes in PDF neurons, under the hypothesis that this process would allow the molecular clock to modulate the output of the pacemaker circuit. We examined how downregulation or overexpression of specific clock genes affects structural plasticity, to define whether the cell-autonomous circadian clock accounts for a full structural effect. In addition, we characterized PDF´s impact on this structural plasticity, through the analysis of consequence of RNAi-mediated silencing at different times in the day.. To delve further into the mechanisms underlying PDF´s function we attempted to define the source of the neuropeptide through cluster-specific downregulation.