Tracer Survey in the Cape Verde Region Traceraufnahme in der Kapverdenregion Cruise No. 10, Leg 1 October 31 – December 06, 2008 Ponta Delgada (Portugal) – Mindelo (Cape Verde Islands)

The research cruise MSM10/1 was extremely successful. All programs were able to collect high quality data and the anticipated goals of the expedition were fully met. We have been able to carry out the first comprehensive survey of a tracer release in the Guinea Upwelling region (GUTRE) roughly seven month after the tracer was released at 8°N 23°W in April 2008. We have estimated that a total of 40% of the tracer was found during this cruise. While the horizontal spreading and mixing was larger than anticipated, the vertical extent of the tracer found was small. The low vertical tracer spreading rate estimates are supported by the micro structure profile data. The extensive survey of the upper 1000m of the oxygen minimum zone (OMZ) allowed comparing our sections with several previous surveys. We found that the lowest oxygen values in the core of the OMZ have dropped at record low values below 40 μmol/kg. The preliminary findings from the trace metal work focused on Fe ligand measurements shows a slight higher excess ligand concentration in the surface (50m) for three stations. The two other stations show a slight decrease at this depth. A large number of biochemical samples were taken and were analyzed in Kiel for DNA and RNA diversity. The tracer release experiment provided an ideal environment for repeated biochemical sampling in the same water mass

Supplementary File1_phenotypes

The txt file contains the phenotypes assessed in our study for all mice under control (CTRL) or enriched (conditions). The file is a txt file, comma delimited. Eache mouse is one line. All abbreviations and the phenotypes are explained in the article

Transcriptome sequencing during mouse brain development identifies long non-coding RNAs functionally involved in neurogenic commitment

Transcriptome analysis of somatic stem cells and their progeny is fundamental to identify new factors controlling proliferation versus differentiation during tissue formation. Here, we generated a combinatorial, fluorescent reporter mouse line to isolate proliferating neural stem cells, differentiating progenitors and newborn neurons that coexist as intermingled cell populations during brain development. Transcriptome sequencing revealed numerous novel long non-coding (lnc)RNAs and uncharacterized protein-coding transcripts identifying the signature of neurogenic commitment. Importantly, most lncRNAs overlapped neurogenic genes and shared with them a nearly identical expression pattern suggesting that lncRNAs control corticogenesis by tuning the expression of nearby cell fate determinants. We assessed the power of our approach by manipulating lncRNAs and protein-coding transcripts with no function in corticogenesis reported to date. This led to several evident phenotypes in neurogenic commitment and neuronal survival, indicating that our study provides a remarkably high number of uncharacterized transcripts with hitherto unsuspected roles in brain development. Finally, we focussed on one lncRNA, Miat, whose manipulation was found to trigger pleiotropic effects on brain development and aberrant splicing of Wnt7b. Hence, our study suggests that lncRNA-mediated alternative splicing of cell fate determinants controls stem-cell commitment during neurogenesis. © 2013 European Molecular Biology Organization

FASN-Dependent Lipid Metabolism Links Neurogenic Stem/Progenitor Cell Activity to Learning and Memory Deficits

Altered neural stem/progenitor cell (NSPC) activity and neurodevelopmental defects are linked to intellectual disability. However, it remains unclear whether altered metabolism, a key regulator of NSPC activity, disrupts human neurogenesis and potentially contributes to cognitive defects. We investigated links between lipid metabolism and cognitive function in mice and human embryonic stem cells (hESCs) expressing mutant fatty acid synthase (FASN; R1819W), a metabolic regulator of rodent NSPC activity recently identified in humans with intellectual disability. Mice homozygous for the FASN R1812W variant have impaired adult hippocampal NSPC activity and cognitive defects because of lipid accumulation in NSPCs and subsequent lipogenic ER stress. Homozygous FASN R1819W hESC-derived NSPCs show reduced rates of proliferation in embryonic 2D cultures and 3D forebrain regionalized organoids, consistent with a developmental phenotype. These data from adult mouse models and in vitro models of human brain development suggest that altered lipid metabolism contributes to intellectual disability