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  - 
TY  - JOUR
A1  - Zimmermann, Henriette
A1  - Subota, Ines
A1  - Batram, Christopher
A1  - Kramer, Susanne
A1  - Janzen, Christian J.
A1  - Jones, Nicola G.
A1  - Engstler, Markus
T1  - A quorum sensing-independent path to stumpy development in Trypanosoma brucei
JF  - PLoS Pathogens
N2  - For persistent infections of the mammalian host, African trypanosomes limit their population size by quorum sensing of the parasite-excreted stumpy induction factor (SIF), which induces development to the tsetse-infective stumpy stage. We found that besides this cell density-dependent mechanism, there exists a second path to the stumpy stage that is linked to antigenic variation, the main instrument of parasite virulence. The expression of a second variant surface glycoprotein (VSG) leads to transcriptional attenuation of the VSG expression site (ES) and immediate development to tsetse fly infective stumpy parasites. This path is independent of SIF and solely controlled by the transcriptional status of the ES. In pleomorphic trypanosomes varying degrees of ES-attenuation result in phenotypic plasticity. While full ES-attenuation causes irreversible stumpy development, milder attenuation may open a time window for rescuing an unsuccessful antigenic switch, a scenario that so far has not been considered as important for parasite survival.
KW  - Trypanosoma
KW  - hyperexpression techniques
KW  - parasitic cell cycles
KW  - cloning
KW  - cell cycle and cell division
KW  - cell differentiation
KW  - tetracyclines
KW  - parasitic diseases
Y1  - 2017
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-158230
VL  - 13
IS  - 4
ER  -