25,609 research outputs found
Picophytoplankton biomass distribution in the global ocean
The smallest marine phytoplankton, collectively termed picophytoplankton, have been routinely enumerated by flow cytometry since the late 1980s during cruises throughout most of the world ocean. We compiled a database of 40 946 data points, with separate abundance entries for Prochlorococcus, Synechococcus and picoeukaryotes. We use average conversion factors for each of the three groups to convert the abundance data to carbon biomass. After gridding with 1? spacing, the database covers 2.4% of the ocean surface area, with the best data coverage in the North Atlantic, the South Pacific and North Indian basins, and at least some data in all other basins. The average picophytoplankton biomass is 12 ± 22 µg Cl-1 or 1.9 g Cm-2. We estimate a total global picophytoplankton biomass of 0.53–1.32 Pg C (17–39% Prochlorococcus, 12–15% Synechococcus and 49–69% picoeukaryotes), with an intermediate/best estimate of 0.74 Pg C. Future efforts in this area of research should focus on reporting calibrated cell size and collecting data in undersampled regions
Nitrogen and phosphorus limitation of oceanic microbial growth during spring in the Gulf of Aqaba
Bioassay experiments were performed to identify how growth of key groups within the microbial community was simultaneously limited by nutrient (nitrogen and phosphorus) availability during spring in the Gulf of Aqaba's oceanic waters. Measurements of chlorophyll a (chl a) concentration and fast repetition rate (FRR) fluorescence generally demonstrated that growth of obligate phototrophic phytoplankton was co-limited by N and P and growth of facultative aerobic anoxygenic photoheterotropic (AAP) bacteria was limited by N. Phytoplankton exhibited an increase in chl a biomass over 24 to 48 h upon relief of nutrient limitation. This response coincided with an increase in photosystem II (PSII) photochemical efficiency (F v /F m), but was preceded (within 24 h) by a decrease in effective absorption crosssection (σPSII) and electron turnover time (τ). A similar response for τ and bacterio-chl a was observed for the AAPs. Consistent with the up-regulation of PSII activity with FRR fluorescence were observations of newly synthesized PSII reaction centers via low temperature (77K) fluorescence spectroscopy for addition of N (and N + P). Flow cytometry revealed that the chl a and thus FRR fluorescence responses were partly driven by the picophytoplankton (æ10 μm) community, and in particular Synechococcus. Productivity of obligate heterotrophic bacteria exhibited the greatest increase in response to a natural (deep water) treatment, but only a small increase in response to N and P addition, demonstrating the importance of additional substrates (most likely dissolved organic carbon) in moderating the heterotrophs. These data support previous observations that the microbial community response (autotrophy relative to heterotrophy) is critically dependent upon the nature of transient nutrient enrichment. © Inter-Research 2009
High-Resolution Replication Profiles Define the Stochastic Nature of Genome Replication Initiation and Termination
Copyright © 2013 The Authors. Published by Elsevier Inc. All rights reserved.Peer reviewedPublisher PD
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Mapping lung cancer epithelial-mesenchymal transition states and trajectories with single-cell resolution.
Elucidating the spectrum of epithelial-mesenchymal transition (EMT) and mesenchymal-epithelial transition (MET) states in clinical samples promises insights on cancer progression and drug resistance. Using mass cytometry time-course analysis, we resolve lung cancer EMT states through TGFβ-treatment and identify, through TGFβ-withdrawal, a distinct MET state. We demonstrate significant differences between EMT and MET trajectories using a computational tool (TRACER) for reconstructing trajectories between cell states. In addition, we construct a lung cancer reference map of EMT and MET states referred to as the EMT-MET PHENOtypic STAte MaP (PHENOSTAMP). Using a neural net algorithm, we project clinical samples onto the EMT-MET PHENOSTAMP to characterize their phenotypic profile with single-cell resolution in terms of our in vitro EMT-MET analysis. In summary, we provide a framework to phenotypically characterize clinical samples in the context of in vitro EMT-MET findings which could help assess clinical relevance of EMT in cancer in future studies
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Ischemic axonal injury up-regulates MARK4 in cortical neurons and primes tau phosphorylation and aggregation.
Ischemic injury to white matter tracts is increasingly recognized to play a key role in age-related cognitive decline, vascular dementia, and Alzheimer's disease. Knowledge of the effects of ischemic axonal injury on cortical neurons is limited yet critical to identifying molecular pathways that link neurodegeneration and ischemia. Using a mouse model of subcortical white matter ischemic injury coupled with retrograde neuronal tracing, we employed magnetic affinity cell sorting with fluorescence-activated cell sorting to capture layer-specific cortical neurons and performed RNA-sequencing. With this approach, we identified a role for microtubule reorganization within stroke-injured neurons acting through the regulation of tau. We find that subcortical stroke-injured Layer 5 cortical neurons up-regulate the microtubule affinity-regulating kinase, Mark4, in response to axonal injury. Stroke-induced up-regulation of Mark4 is associated with selective remodeling of the apical dendrite after stroke and the phosphorylation of tau in vivo. In a cell-based tau biosensor assay, Mark4 promotes the aggregation of human tau in vitro. Increased expression of Mark4 after ischemic axonal injury in deep layer cortical neurons provides new evidence for synergism between axonal and neurodegenerative pathologies by priming of tau phosphorylation and aggregation
Picoheterotroph (Bacteria and Archaea) biomass distribution in the global ocean
We compiled a database of 39 766 data points consisting of flow cytometric and microscopical measurements of picoheterotroph abundance, including both Bacteria and Archaea. After gridding with 1° spacing, the database covers 1.3% of the ocean surface. There are data covering all ocean basins and depths except the Southern Hemisphere below 350m or from April until June. The average picoheterotroph biomass is 3.9 ± 3.6 µg Cl-1 with a 20-fold decrease between the surface and the deep sea. We estimate a total ocean inventory of about 1.3 × 1029 picoheterotroph cells. Surprisingly, the abundance in the coastal regions is the same as at the same depths in the open ocean. Using an average of published open ocean measurements for the conversion from abundance to carbon biomass of 9.1 fg cell-1, we calculate a picoheterotroph carbon inventory of about 1.2 Pg C. The main source of uncertainty in this inventory is the conversion factor from abundance to biomass. Picoheterotroph biomass is ? 2 times higher in the tropics than in the polar oceans
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