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Epigeic spiders were sampled using pitfall traps during one year in an anthropogenic open site within the city of Karlsruhe (Alter Flugplatz Karlsruhe). The area, historically used as a military parade ground and airport, is protected as a Special Area of Conservation (SAC) within the Natura 2000 network of the EU and since 2010 as a German nature reserve. We were interested in the diversity, assemblage structure and distribution of spider species within the area and investigated three different plant formations: sparse grass-dominated vegetation with frequent open sand patches (sandy turf ), closed grassland dominated by the mat-grass (Nardus stricta) and ruderal vegetation with blackberry bushes. 123 species were identified from these captures, including many specialists of xerothermic habitats and rare and endangered species like Alopecosa striatipes, Agroeca lusatica, Haplodrassus dalmatensis, Styloctetor romanus, Typhochrestus simoni and Xysticus striatipes as well as extremely rare species of unclassified red list status like Mysmenella jobi, Theonoe minutissima and Zora parallela. The three investigated habitat types were quite similar concerning α-diversity, while measures of β-diversity indicated a strong species turnover. By performing an ecological habitat analysis (using autecological data on spiders) essential differences between the three habitat types could not be discovered, especially not between mat-grass and sandy turf. However, analysing the guild structures showed that different ways of using habitat resources dominated in the different habitat types. For Nardus-grassland several species could be identified as indicator species. While many xero- and photophiles live in the open grassland, the stenotopic psammophiles of inland dunes in the region were not found. The ruderal area houses a mix of grassland- and forest species.
The usefulness of propylene glycol as capture preservative in pitfall traps, with the aim of using the captured spiders for DNA barcoding, was tested. For this purpose a laboratory experiment on the conserving and/or denaturing effect of propylene glycol on mitochondrial DNA (COI) was set up. For the experiment 110 specimens of the common and abundant wolf spider species Pardosa lugubris were manually captured, killed and incubated from one to four weeks in either pure or watered propylene glycol or 70 % denatured ethanol. Rates of successful sequencing, following a standard protocol, did not differ between samples incubated in propylene glycol and in the more commonly used ethanol. Thus, within four weeks, propylene glycol did not significantly denaturize mitochondrial DNA. In two field studies, pitfall traps with propylene glycol captured more spiders than traps with acetic acid. The effect was significant only in one of two field trials, but then consistent at three different sites and the three dominant spider families. Based on these results and our operating experience, we recommend propylene glycol as a capture preservative for (pitfall) traps to obtain specimens for DNA barcoding identification.
Sphingosine 1-phosphate (S1P) signaling influences numerous cell biological mechanisms such as differentiation, proliferation, survival, migration, and angiogenesis. Intriguingly, our current knowledge is based solely on the role of S1P with an 18-carbon long-chain base length, S1P d18:1. Depending on the composition of the first and rate-limiting enzyme of the sphingolipid de novo metabolism, the serine palmitoyltransferase, other chain lengths have been described in vivo. While cells are also able to produce S1P d20:1, its abundance and function remains elusive so far. Our experiments are highlighting the role of S1P d20:1 in the mouse central nervous system (CNS) and human glioblastoma. We show here that S1P d20:1 and its precursors are detectable in both healthy mouse CNS-tissue and human glioblastoma. On the functional level, we focused our work on one particular, well-characterized pathway, the induction of cyclooxygenase (COX)-2 expression via the S1P receptor 2 (S1P2). Intriguingly, S1P d20:1 only fairly induces COX-2 expression and can block the S1P d18:1-induced COX-2 expression mediated via S1P2 activation in the human glioblastoma cell line LN229. This data indicates that S1P d20:1 might act as an endogenous modulator of S1P signaling via a partial agonism at the S1P2 receptor. While our findings might stimulate further research on the relevance of long-chain base lengths in sphingolipid signaling, the metabolism of S1P d20:1 has to be considered as an integral part of S1P signaling pathways in vivo.
Attention-deficit/hyperactivity disorder (ADHD) is a common, highly heritable neurodevelopmental disorder. Genetic loci have not yet been identified by genome-wide association studies. Rare copy number variations (CNVs), such as chromosomal deletions or duplications, have been implicated in ADHD and other neurodevelopmental disorders. To identify rare (frequency ≤1%) CNVs that increase the risk of ADHD, we performed a whole-genome CNV analysis based on 489 young ADHD patients and 1285 adult population-based controls and identified one significantly associated CNV region. In tests for a global burden of large (>500 kb) rare CNVs, we observed a nonsignificant (P=0.271) 1.126-fold enriched rate of subjects carrying at least one such CNV in the group of ADHD cases. Locus-specific tests of association were used to assess if there were more rare CNVs in cases compared with controls. Detected CNVs, which were significantly enriched in the ADHD group, were validated by quantitative (q)PCR. Findings were replicated in an independent sample of 386 young patients with ADHD and 781 young population-based healthy controls. We identified rare CNVs within the parkinson protein 2 gene (PARK2) with a significantly higher prevalence in ADHD patients than in controls (P=2.8 × 10(-4) after empirical correction for genome-wide testing). In total, the PARK2 locus (chr 6: 162 659 756-162 767 019) harboured three deletions and nine duplications in the ADHD patients and two deletions and two duplications in the controls. By qPCR analysis, we validated 11 of the 12 CNVs in ADHD patients (P=1.2 × 10(-3) after empirical correction for genome-wide testing). In the replication sample, CNVs at the PARK2 locus were found in four additional ADHD patients and one additional control (P=4.3 × 10(-2)). Our results suggest that copy number variants at the PARK2 locus contribute to the genetic susceptibility of ADHD. Mutations and CNVs in PARK2 are known to be associated with Parkinson disease.