Latest documents http://publikationen.ub.uni-frankfurt.de/index/index/ Fri, 24 May 2013 15:28:43 +0200 Fri, 24 May 2013 15:28:43 +0200 http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/30047 periodicalpart http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/30047 Fri, 24 May 2013 15:28:43 +0200 http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/30046 periodicalpart http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/30046 Fri, 24 May 2013 15:28:37 +0200 http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/30045 periodicalpart http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/30045 Fri, 24 May 2013 15:28:33 +0200 http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/30044 periodicalpart http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/30044 Fri, 24 May 2013 15:26:54 +0200 http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/30043 periodicalpart http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/30043 Fri, 24 May 2013 15:26:50 +0200 http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/30042 periodicalpart http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/30042 Fri, 24 May 2013 15:26:47 +0200 http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/30041 periodicalpart http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/30041 Fri, 24 May 2013 15:26:43 +0200 http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/30040 periodicalpart http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/30040 Fri, 24 May 2013 15:26:40 +0200 http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/30039 periodicalpart http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/30039 Fri, 24 May 2013 15:26:11 +0200 http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/30038 periodicalpart http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/30038 Fri, 24 May 2013 15:26:06 +0200 http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/30037 periodicalpart http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/30037 Fri, 24 May 2013 15:26:02 +0200 http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/30036 periodicalpart http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/30036 Fri, 24 May 2013 15:25:58 +0200 http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/30035 periodicalpart http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/30035 Fri, 24 May 2013 15:25:55 +0200 http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/30034 periodicalpart http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/30034 Fri, 24 May 2013 15:25:33 +0200 http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/30033 periodicalpart http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/30033 Fri, 24 May 2013 15:25:30 +0200 http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/30032 periodicalpart http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/30032 Fri, 24 May 2013 15:25:23 +0200 http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/30031 periodicalpart http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/30031 Fri, 24 May 2013 15:25:15 +0200 http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/30030 periodicalpart http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/30030 Fri, 24 May 2013 15:25:11 +0200 http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/30029 periodicalpart http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/30029 Fri, 24 May 2013 15:19:08 +0200 http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/30028 periodicalpart http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/30028 Fri, 24 May 2013 14:54:29 +0200 http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/30005 The current study tested the assumption that floristic and functional diversity patterns are negatively related to soil nitrogen content. We analyzed 20 plots with soil N-contents ranging from 0.63% to 1.06% in a deciduous forest near Munich (Germany). To describe species adaptation strategies to different nitrogen availabilities, we used a plant functional type (PFT) approach. Each identified PFT represents one realized adaptation strategy to the current environment. These were correlated, next to plant species richness and evenness, to soil nitrogen contents. We found that N-efficient species were typical for low soil nitrogen contents, while N-requiring species occur at high N-contents. In contrast to our initial hypotheses, floristic and functional diversity measures (number of PFTs) were positively related to nitrogen content in the soil. Every functional group has its own adaptation to the prevailing environmental conditions; in consequence, these functional groups can co-exist but do not out-compete one another. The increased number of functional groups at high N-contents leads to increased species richness. Hence, for explaining diversity patterns we need to consider species groups representing different adaptations to the current environmental conditions. Such co-existing ecological strategies may even overcome the importance of competition in their effect on biodiversity. Markus Bernhardt-Römermann; Christine Römermann; Valério de Patta Pillar; Thomas Kudernatsch; Anton Fischer article http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/30005 Fri, 24 May 2013 09:59:40 +0200 http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/30022 Autophagy is a highly regulated program of self-degradation of the cytosolic constituents that has key roles during early development and in adult cell growth and homeostasis. To investigate the role of autophagy in otic neurogenesis, we studied the expression of autophagy genes in early stages of chicken (Gallus gallus) inner ear development and the consequences of inhibiting the autophagic pathway in organotypic cultures of explanted chicken otic vesicles (OVs). Here we show the expression of autophagy-related genes (Atg) Beclin-1 (Atg6), Atg5 and LC3B (Atg8) in the otocyst and the presence of autophagic vesicles by using transmission electron microscopy in the otic neurogenic zone. The inhibition of the transcription of LC3B by using antisense morpholinos and of class III phosphatidylinositol 3-kinase with 3-methyladenine causes an aberrant morphology of the OV with accumulation of apoptotic cells. Moreover, inhibition of autophagy provokes the misregulation of the cell cycle in the otic epithelium, impaired neurogenesis and poor axonal outgrowth. Finally, our results indicate that autophagy provides the energy required for the clearing of neuroepithelial dying cells and suggest that it is required for the migration of otic neuronal precursors. Taken together, our results show for the first time that autophagy is an active and essential process during early inner ear development. Maria Rodriguez Aburto; Hortensia Sánchez-Calderón; Juan M. Hurlé; Isabel Varela-Nieto; Marta Magariños article http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/30022 Thu, 23 May 2013 17:07:25 +0200 http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/30018 Background: Early inner ear development requires the strict regulation of cell proliferation, survival, migration and differentiation, coordinated by the concerted action of extrinsic and intrinsic factors. Deregulation of these processes is associated with embryonic malformations and deafness. We have shown that insulin-like growth factor I (IGF-I) plays a key role in embryonic and postnatal otic development by triggering the activation of intracellular lipid and protein kinases. RAF kinases are serine/threonine kinases that regulate the highly conserved RAS-RAF-MEK-ERK signaling cascade involved in transducing the signals from extracellular growth factors to the nucleus. However, the regulation of RAF kinase activity by growth factors during development is complex and still not fully understood. Methodology/Principal Findings: By using a combination of qRT-PCR, Western blotting, immunohistochemistry and in situ hybridization, we show that C-RAF and B-RAF are expressed during the early development of the chicken inner ear in specific spatiotemporal patterns. Moreover, later in development B-RAF expression is associated to hair cells in the sensory patches. Experiments in ex vivo cultures of otic vesicle explants demonstrate that the influence of IGF-I on proliferation but not survival depends on RAF kinase activating the MEK-ERK phosphorylation cascade. With the specific RAF inhibitor Sorafenib, we show that blocking RAF activity in organotypic cultures increases apoptosis and diminishes the rate of cell proliferation in the otic epithelia, as well as severely impairing neurogenesis of the acoustic-vestibular ganglion (AVG) and neuron maturation. Conclusions/Significance: We conclude that RAF kinase activity is essential to establish the balance between cell proliferation and death in neuroepithelial otic precursors, and for otic neuron differentiation and axonal growth at the AVG. Marta Magariños; Maria Rodriguez Aburto; Hortensia Sánchez-Calderón; Carmen Muñoz-Agudo; Ulf Rüdiger Rapp; Isabel Varela-Nieto article http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/30018 Thu, 23 May 2013 15:08:25 +0200 http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/30019 Background: Otic neurons and sensory cells derive from common progenitors whose transition into mature cells requires the coordination of cell survival, proliferation and differentiation programmes. Neurotrophic support and survival of post-mitotic otic neurons have been intensively studied, but the bases underlying the regulation of programmed cell death in immature proliferative otic neuroblasts remains poorly understood. The protein kinase AKT acts as a node, playing a critical role in controlling cell survival and cell cycle progression. AKT is activated by trophic factors, including insulin-like growth factor I (IGF-I), through the generation of the lipidic second messenger phosphatidylinositol 3-phosphate by phosphatidylinositol 3-kinase (PI3K). Here we have investigated the role of IGF-dependent activation of the PI3K-AKT pathway in maintenance of otic neuroblasts. Methodology/Principal Findings: By using a combination of organotypic cultures of chicken (Gallus gallus) otic vesicles and acoustic-vestibular ganglia, Western blotting, immunohistochemistry and in situ hybridization, we show that IGF-I-activation of AKT protects neural progenitors from programmed cell death. IGF-I maintains otic neuroblasts in an undifferentiated and proliferative state, which is characterised by the upregulation of the forkhead box M1 (FoxM1) transcription factor. By contrast, our results indicate that post-mitotic p27Kip-positive neurons become IGF-I independent as they extend their neuronal processes. Neurons gradually reduce their expression of the Igf1r, while they increase that of the neurotrophin receptor, TrkC. Conclusions/Significance: Proliferative otic neuroblasts are dependent on the activation of the PI3K-AKT pathway by IGF-I for survival during the otic neuronal progenitor phase of early inner ear development. Maria Rodriguez Aburto; Marta Magariños; Yolanda Leon; Isabel Varela-Nieto; Hortensia Sanchez-Calderon article http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/30019 Thu, 23 May 2013 14:55:27 +0200 http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/30013 Autophagy is an evolutionarily conserved catabolic process by which cells degrade their own components through the lysosomal machinery. In physiological conditions, the mechanism is tightly regulated and contributes to maintain a balance between synthesis and degradation in cells undergoing intense metabolic activities. Autophagy is associated with major tissue remodeling processes occurring through the embryonic, fetal and early postnatal periods of vertebrates. Here we survey current information implicating autophagy in cellular death, proliferation or differentiation in developing vertebrates. In developing systems, activation of the autophagic machinery could promote different outcomes depending on the cellular context. Autophagy is thus an extraordinary tool for the developing organs and tissues. Maria Rodriguez Aburto; Juan M. Hurlé; Isabel Varela-Nieto; Marta Magariños article http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/30013 Thu, 23 May 2013 13:03:42 +0200