@article{KoenigZundelKrimmeretal.2019,
  author    = {K{\"o}nig, Kerstin and Zundel, Petra and Krimmer, Elena and K{\"o}nig, Christian and Pollmann, Marie and Gottlieb, Yuval and Steidle, Johannes L. M.},
  title     = {Reproductive isolation due to prezygotic isolation and postzygotic cytoplasmic incompatibility in parasitoid wasps},
  series = {Ecology and Evolution},
  volume    = {9},
  journal   = {Ecology and Evolution},
  doi       = {10.1002/ece3.5588},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-222796},
  pages     = {10694-10706},
  year      = {2019},
  abstract  = {The reproductive barriers that prevent gene flow between closely related species are a major topic in evolutionary research. Insect clades with parasitoid lifestyle are among the most species-rich insects and new species are constantly described, indicating that speciation occurs frequently in this group. However, there are only very few studies on speciation in parasitoids. We studied reproductive barriers in two lineages of Lariophagus distinguendus (Chalcidoidea: Hymenoptera), a parasitoid wasp of pest beetle larvae that occur in human environments. One of the two lineages occurs in households preferably attacking larvae of the drugstore beetle Stegobium paniceum ("DB-lineage"), the other in grain stores with larvae of the granary weevil Sitophilus granarius as main host ("GW-lineage"). Between two populations of the DB-lineage, we identified slight sexual isolation as intraspecific barrier. Between populations from both lineages, we found almost complete sexual isolation caused by female mate choice, and postzygotic isolation, which is partially caused by cytoplasmic incompatibility induced by so far undescribed endosymbionts which are not Wolbachia or Cardinium. Because separation between the two lineages is almost complete, they should be considered as separate species according to the biological species concept. This demonstrates that cryptic species within parasitoid Hymenoptera also occur in Central Europe in close contact to humans.},
  language  = {en}
}
@article{MederKoenigOzretićetal.2016,
  author    = {Meder, Lydia and K{\"o}nig, Katharina and Ozretić, Luka and Schultheis, Anne M. and Ueckeroth, Frank and Ade, Carsten P. and Albus, Kerstin and Boehm, Diana and Rommerscheidt-Fuss, Ursula and Florin, Alexandra and Buhl, Theresa and Hartmann, Wolfgang and Wolf, J{\"u}rgen and Merkelbach-Bruse, Sabine and Eilers, Martin and Perner, Sven and Heukamp, Lukas C. and Buettner, Reinhard},
  title     = {NOTCH, ASCL1, p53 and RB alterations define an alternative pathway driving neuroendocrine and small cell lung carcinomas},
  series = {International Journal of Cancer},
  volume    = {138},
  journal   = {International Journal of Cancer},
  number    = {4},
  doi       = {10.1002/ijc.29835},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-190853},
  pages     = {927-938},
  year      = {2016},
  abstract  = {Small cell lung cancers (SCLCs) and extrapulmonary small cell cancers (SCCs) are very aggressive tumors arising de novo as primary small cell cancer with characteristic genetic lesions in RB1 and TP53. Based on murine models, neuroendocrine stem cells of the terminal bronchioli have been postulated as the cellular origin of primary SCLC. However, both in lung and many other organs, combined small cell/non-small cell tumors and secondary transitions from non-small cell carcinomas upon cancer therapy to neuroendocrine and small cell tumors occur. We define features of "small cell-ness" based on neuroendocrine markers, characteristic RB1 and TP53 mutations and small cell morphology. Furthermore, here we identify a pathway driving the pathogenesis of secondary SCLC involving inactivating NOTCH mutations, activation of the NOTCH target ASCL1 and canonical WNT-signaling in the context of mutual bi-allelic RB1 and TP53 lesions. Additionaly, we explored ASCL1 dependent RB inactivation by phosphorylation, which is reversible by CDK5 inhibition. We experimentally verify the NOTCH-ASCL1-RB-p53 signaling axis in vitro and validate its activation by genetic alterations in vivo. We analyzed clinical tumor samples including SCLC, SCC and pulmonary large cell neuroendocrine carcinomas and adenocarcinomas using amplicon-based Next Generation Sequencing, immunohistochemistry and fluorescence in situ hybridization. In conclusion, we identified a novel pathway underlying rare secondary SCLC which may drive small cell carcinomas in organs other than lung, as well.},
  language  = {en}
}