@article{SchokraieWarnkenHotzWagenblattetal.2012,
  author    = {Schokraie, Elham and Warnken, Uwe and Hotz-Wagenblatt, Agnes and Grohme, Markus A. and Hengherr, Steffen and F{\"o}rster, Frank and Schill, Ralph O. and Frohme, Marcus and Dandekar, Thomas and Schn{\"o}lzer, Martina},
  title     = {Comparative proteome analysis of Milnesium tardigradum in early embryonic state versus adults in active and anhydrobiotic state},
  series = {PLoS One},
  volume    = {7},
  journal   = {PLoS One},
  number    = {9},
  doi       = {10.1371/journal.pone.0045682},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-134447},
  pages     = {e45682},
  year      = {2012},
  abstract  = {Tardigrades have fascinated researchers for more than 300 years because of their extraordinary capability to undergo cryptobiosis and survive extreme environmental conditions. However, the survival mechanisms of tardigrades are still poorly understood mainly due to the absence of detailed knowledge about the proteome and genome of these organisms. Our study was intended to provide a basis for the functional characterization of expressed proteins in different states of tardigrades. High-throughput, high-accuracy proteomics in combination with a newly developed tardigrade specific protein database resulted in the identification of more than 3000 proteins in three different states: early embryonic state and adult animals in active and anhydrobiotic state. This comprehensive proteome resource includes protein families such as chaperones, antioxidants, ribosomal proteins, cytoskeletal proteins, transporters, protein channels, nutrient reservoirs, and developmental proteins. A comparative analysis of protein families in the different states was performed by calculating the exponentially modified protein abundance index which classifies proteins in major and minor components. This is the first step to analyzing the proteins involved in early embryonic development, and furthermore proteins which might play an important role in the transition into the anhydrobiotic state.},
  language  = {en}
}
@article{TuChenLimetal.2012,
  author    = {Tu, Xiaolin and Chen, Jianquan and Lim, Joohyun and Karner, Courtney M. and Lee, Seung-Yon and Heisig, Julia and Wiese, Cornelia and Surendran, Kameswaran and Kopan, Raphael and Gessler, Manfred and Long, Fanxin},
  title     = {Physiological Notch Signaling Maintains Bone Homeostasis via RBPjk and Hey Upstream of NFATc1},
  series = {PLoS Genetics},
  volume    = {8},
  journal   = {PLoS Genetics},
  number    = {3},
  doi       = {10.1371/journal.pgen.1002577},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-133490},
  pages     = {e1002577},
  year      = {2012},
  abstract  = {Notch signaling between neighboring cells controls many cell fate decisions in metazoans both during embryogenesis and in postnatal life. Previously, we uncovered a critical role for physiological Notch signaling in suppressing osteoblast differentiation in vivo. However, the contribution of individual Notch receptors and the downstream signaling mechanism have not been elucidated. Here we report that removal of Notch2, but not Notch1, from the embryonic limb mesenchyme markedly increased trabecular bone mass in adolescent mice. Deletion of the transcription factor RBPjk, a mediator of all canonical Notch signaling, in the mesenchymal progenitors but not the more mature osteoblast-lineage cells, caused a dramatic high-bone-mass phenotype characterized by increased osteoblast numbers, diminished bone marrow mesenchymal progenitor pool, and rapid age-dependent bone loss. Moreover, mice deficient in Hey1 and HeyL, two target genes of Notch-RBPjk signaling, exhibited high bone mass. Interestingly, Hey1 bound to and suppressed the NFATc1 promoter, and RBPjk deletion increased NFATc1 expression in bone. Finally, pharmacological inhibition of NFAT alleviated the high-bone-mass phenotype caused by RBPjk deletion. Thus, Notch-RBPjk signaling functions in part through Hey1-mediated inhibition of NFATc1 to suppress osteoblastogenesis, contributing to bone homeostasis in vivo.},
  language  = {en}
}
@article{AgostonLiHaslingeretal.2012,
  author    = {Agoston, Zsuzsa and Li, Naixin and Haslinger, Anja and Wizenmann, Andrea and Schulte, Dorothea},
  title     = {Genetic and physical interaction of Meis2, Pax3 and Pax7 during dorsal midbrain development},
  series = {BMC Developmental Biology},
  volume    = {12},
  journal   = {BMC Developmental Biology},
  number    = {10},
  doi       = {10.1186/1471-213X-12-10},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-132626},
  year      = {2012},
  abstract  = {Background: During early stages of brain development, secreted molecules, components of intracellular signaling pathways and transcriptional regulators act in positive and negative feed-back or feed-forward loops at the mid-hindbrain boundary. These genetic interactions are of central importance for the specification and subsequent development of the adjacent mid-and hindbrain. Much less, however, is known about the regulatory relationship and functional interaction of molecules that are expressed in the tectal anlage after tectal fate specification has taken place and tectal development has commenced. Results: Here, we provide experimental evidence for reciprocal regulation and subsequent cooperation of the paired-type transcription factors Pax3, Pax7 and the TALE-homeodomain protein Meis2 in the tectal anlage. Using in ovo electroporation of the mesencephalic vesicle of chick embryos we show that (i) Pax3 and Pax7 mutually regulate each other's expression in the mesencephalic vesicle, (ii) Meis2 acts downstream of Pax3/7 and requires balanced expression levels of both proteins, and (iii) Meis2 physically interacts with Pax3 and Pax7. These results extend our previous observation that Meis2 cooperates with Otx2 in tectal development to include Pax3 and Pax7 as Meis2 interacting proteins in the tectal anlage. Conclusion: The results described here suggest a model in which interdependent regulatory loops involving Pax3 and Pax7 in the dorsal mesencephalic vesicle modulate Meis2 expression. Physical interaction with Meis2 may then confer tectal specificity to a wide range of otherwise broadly expressed transcriptional regulators, including Otx2, Pax3 and Pax7.},
  language  = {en}
}
@article{AsoHerbOguetaetal.2012,
  author    = {Aso, Yoshinori and Herb, Andrea and Ogueta, Maite and Siwanowicz, Igor and Templier, Thomas and Friedrich, Anja B. and Ito, Kei and Scholz, Henrike and Tanimoto, Hiromu},
  title     = {Three Dopamine Pathways Induce Aversive Odor Memories with Different Stability},
  series = {PLoS Genetics},
  volume    = {8},
  journal   = {PLoS Genetics},
  number    = {7},
  doi       = {10.1371/journal.pgen.1002768},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-130631},
  pages     = {e1002768},
  year      = {2012},
  abstract  = {Animals acquire predictive values of sensory stimuli through reinforcement. In the brain of Drosophila melanogaster, activation of two types of dopamine neurons in the PAM and PPL1 clusters has been shown to induce aversive odor memory. Here, we identified the third cell type and characterized aversive memories induced by these dopamine neurons. These three dopamine pathways all project to the mushroom body but terminate in the spatially segregated subdomains. To understand the functional difference of these dopamine pathways in electric shock reinforcement, we blocked each one of them during memory acquisition. We found that all three pathways partially contribute to electric shock memory. Notably, the memories mediated by these neurons differed in temporal stability. Furthermore, combinatorial activation of two of these pathways revealed significant interaction of individual memory components rather than their simple summation. These results cast light on a cellular mechanism by which a noxious event induces different dopamine signals to a single brain structure to synthesize an aversive memory.},
  language  = {en}
}