@article{FischerHelfrichFoersterPeschel2016,
  author    = {Fischer, Robin and Helfrich-F{\"o}rster, Charlotte and Peschel, Nicolai},
  title     = {GSK-3 Beta Does Not Stabilize Cryptochrome in the Circadian Clock of Drosophila},
  series = {PLoS ONE},
  volume    = {11},
  journal   = {PLoS ONE},
  number    = {1},
  doi       = {10.1371/journal.pone.0146571},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-180370},
  year      = {2016},
  abstract  = {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.},
  language  = {en}
}
@article{LamazeOeztuerkColakFischeretal.2017,
  author    = {Lamaze, Angelique and {\"O}zt{\"u}rk-{\c{C}}olak, Arzu and Fischer, Robin and Peschel, Nicolai and Koh, Kyunghee and Jepson, James E. C.},
  title     = {Regulation of sleep plasticity by a thermo-sensitive circuit in Drosophila},
  series = {Scientific Reports},
  volume    = {7},
  journal   = {Scientific Reports},
  doi       = {10.1038/srep40304},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-181146},
  pages     = {12},
  year      = {2017},
  abstract  = {Sleep is a highly conserved and essential behaviour in many species, including the fruit fly Drosophila melanogaster. In the wild, sensory signalling encoding environmental information must be integrated with sleep drive to ensure that sleep is not initiated during detrimental conditions. However, the molecular and circuit mechanisms by which sleep timing is modulated by the environment are unclear. Here we introduce a novel behavioural paradigm to study this issue. We show that in male fruit flies, onset of the daytime siesta is delayed by ambient temperatures above 29°C. We term this effect Prolonged Morning Wakefulness (PMW). We show that signalling through the TrpA1 thermo-sensor is required for PMW, and that TrpA1 specifically impacts siesta onset, but not night sleep onset, in response to elevated temperatures. We identify two critical TrpA1-expressing circuits and show that both contact DN1p clock neurons, the output of which is also required for PMW. Finally, we identify the circadian blue-light photoreceptor CRYPTOCHROME as a molecular regulator of PMW, and propose a model in which the Drosophila nervous system integrates information encoding temperature, light, and time to dynamically control when sleep is initiated. Our results provide a platform to investigate how environmental inputs co-ordinately regulate sleep plasticity.},
  language  = {en}
}