TY  - JOUR
A1  - Chen, Jiangtian
A1  - Reiher, Wencke
A1  - Hermann-Luibl, Christiane
A1  - Sellami, Azza
A1  - Cognigni, Paola
A1  - Kondo, Shu
A1  - Helfrich-Förster, Charlotte
A1  - Veenstra, Jan A.
A1  - Wegener, Christian
T1  - Allatostatin A Signalling in Drosophila Regulates Feeding and Sleep and Is Modulated by PDF
JF  - PLoS Genetics
N2  - Feeding and sleep are fundamental behaviours with significant interconnections and cross-modulations. The circadian system and peptidergic signals are important components of this modulation, but still little is known about the mechanisms and networks by which they interact to regulate feeding and sleep. We show that specific thermogenetic activation of peptidergic Allatostatin A (AstA)-expressing PLP neurons and enteroendocrine cells reduces feeding and promotes sleep in the fruit fly Drosophila. The effects of AstA cell activation are mediated by AstA peptides with receptors homolog to galanin receptors subserving similar and apparently conserved functions in vertebrates. We further identify the PLP neurons as a downstream target of the neuropeptide pigment-dispersing factor (PDF), an output factor of the circadian clock. PLP neurons are contacted by PDF-expressing clock neurons, and express a functional PDF receptor demonstrated by cAMP imaging. Silencing of AstA signalling and continuous input to AstA cells by tethered PDF changes the sleep/activity ratio in opposite directions but does not affect rhythmicity. Taken together, our results suggest that pleiotropic AstA signalling by a distinct neuronal and enteroendocrine AstA cell subset adapts the fly to a digestive energy-saving state which can be modulated by PDF.
KW  - neurons
KW  - neuroimaging
KW  - circadian rhythms
KW  - food consumption
KW  - sleep
KW  - biological locomotion
KW  - Drosophila melanogaster
KW  - signal peptides
Y1  - 2016
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-178170
VL  - 12
IS  - 9
ER  - 
TY  - JOUR
A1  - Fischer, Robin
A1  - Helfrich-Förster, Charlotte
A1  - Peschel, Nicolai
T1  - GSK-3 Beta Does Not Stabilize Cryptochrome in the Circadian Clock of Drosophila
JF  - PLoS ONE
N2  - Cryptochrome (CRY) is the primary photoreceptor of Drosophila’s circadian clock. It resets the circadian clock by promoting light-induced degradation of the clock protein Timeless (TIM) in the proteasome. Under constant light, the clock stops because TIM is absent, and the flies become arrhythmic. In addition to TIM degradation, light also induces CRY degradation. This depends on the interaction of CRY with several proteins such as the E3 ubiquitin ligases Jetlag (JET) and Ramshackle (BRWD3). However, CRY can seemingly also be stabilized by interaction with the kinase Shaggy (SGG), the GSK-3 beta fly orthologue. Consequently, flies with SGG overexpression in certain dorsal clock neurons are reported to remain rhythmic under constant light. We were interested in the interaction between CRY, Ramshackle and SGG and started to perform protein interaction studies in S2 cells. To our surprise, we were not able to replicate the results, that SGG overexpression does stabilize CRY, neither in S2 cells nor in the relevant clock neurons. SGG rather does the contrary. Furthermore, flies with SGG overexpression in the dorsal clock neurons became arrhythmic as did wild-type flies. Nevertheless, we could reproduce the published interaction of SGG with TIM, since flies with SGG overexpression in the lateral clock neurons shortened their free-running period. We conclude that SGG does not directly interact with CRY but rather with TIM. Furthermore we could demonstrate, that an unspecific antibody explains the observed stabilization effects on CRY.
KW  - neurons
KW  - RNA interference
KW  - hyperexpression techniques
KW  - circadian rhythms
KW  - Drosophila melanogaster
KW  - animal behavior
KW  - phosphorylation
Y1  - 2016
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-180370
VL  - 11
IS  - 1
ER  -