@article{Puetz2019,
  author    = {P{\"u}tz, Stephanie M.},
  title     = {Mbt/PAK4 together with SRC modulates N-Cadherin adherens junctions in the developing Drosophila eye},
  series = {Biology Open},
  volume    = {8},
  journal   = {Biology Open},
  doi       = {10.1242/bio.038406},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-200898},
  pages     = {bio038406},
  year      = {2019},
  abstract  = {Tissue morphogenesis is accompanied by changes of adherens junctions (AJ). During Drosophila eye development, AJ reorganization includes the formation of isolated N-Cadherin AJ between photoreceptors R3/R4. Little is known about how these N-Cadherin AJ are established and maintained. This study focuses on the kinases Mbt/PAK4 and SRC, both known to alter E-Cadherin AJ across phyla. Drosophila p21-activated kinase Mbt and the non-receptor tyrosine kinases Src64 and Src42 regulate proper N-Cadherin AJ. N-Cadherin AJ elongation depends on SRC kinase activity. Cell culture experiments demonstrate binding of both Drosophila SRC isoforms to N-Cadherin and its subsequent tyrosine phosphorylation. In contrast, Mbt stabilizes but does not bind N-Cadherin in vitro. Mbt is required in R3/R4 for zipping the N-Cadherin AJ between these cells, independent of its kinase activity and Cdc42-binding. The mbt phenotype can be reverted by mutations in Src64 and Src42. Because Mbt neither directly binds to SRC proteins nor has a reproducible influence on their kinase activity, the conclusion is that Mbt and SRC signaling converge on N-Cadherin. N-Cadherin AJ formation during eye development requires a proper balance between the promoting effects of Mbt and the inhibiting influences of SRC kinases.},
  language  = {en}
}
@phdthesis{Lyutova2019,
  author    = {Lyutova, Radostina},
  title     = {Functional dissection of recurrent feedback signaling within the mushroom body network of the Drosophila larva},
  doi       = {10.25972/OPUS-18728},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-187281},
  school      = {Universit{\"a}t W{\"u}rzburg},
  year      = {2019},
  abstract  = {Behavioral adaptation to environmental changes is crucial for animals' survival. The prediction of the outcome of one owns action, like finding reward or avoiding punishment, requires recollection of past experiences and comparison with current situation, and adjustment of behavioral responses. The process of memory acquisition is called learning, and the Drosophila larva came up to be an excellent model organism for studying the neural mechanisms of memory formation. In Drosophila, associative memories are formed, stored and expressed in the mushroom bodies. In the last years, great progress has been made in uncovering the anatomical architecture of these brain structures, however there is still a lack of knowledge about the functional connectivity. Dopamine plays essential roles in learning processes, as dopaminergic neurons mediate information about the presence of rewarding and punishing stimuli to the mushroom bodies. In the following work, the function of a newly identified anatomical connection from the mushroom bodies to rewarding dopaminergic neurons was dissected. A recurrent feedback signaling within the neuronal network was analyzed by simultaneous genetic manipulation of the mushroom body Kenyon cells and dopaminergic neurons from the primary protocerebral anterior (pPAM) cluster, and learning assays were performed in order to unravel the impact of the Kenyon cells-to-pPAM neurons feedback loop on larval memory formation. In a substitution learning assay, simultaneous odor exposure paired with optogenetic activation of Kenyon cells in fruit fly larvae in absence of a rewarding stimulus resulted in formation of an appetitive memory, whereas no learning behavior was observed when pPAM neurons were ablated in addition to the KC activation. I argue that the activation of Kenyon cells may induce an internal signal that mimics reward exposure by feedback activation of the rewarding dopaminergic neurons. My data further suggests that the Kenyon cells-to-pPAM communication relies on peptidergic signaling via short neuropeptide F and underlies memory stabilization.},
  subject      = {Lernen},
  language  = {en}
}