Surfactant control of gas transfer velocity along an offshore coastal transect: results from a laboratory gas exchange tank

Understanding the physical and biogeochemical controls of air–sea gas exchange is necessary for establishing biogeochemical models for predicting regional- and global-scale trace gas fluxes and feedbacks. To this end we report the results of experiments designed to constrain the effect of surfactants in the sea surface microlayer (SML) on the gas transfer velocity (<i>k</i>_w; cm h⁻¹), seasonally (2012–2013) along a 20 km coastal transect (North East UK). We measured total surfactant activity (SA), chromophoric dissolved organic matter (CDOM) and chlorophyll <i>a</i> (Chl <i>a</i>) in the SML and in sub-surface water (SSW) and we evaluated corresponding <i>k</i>_w values using a custom-designed air–sea gas exchange tank. Temporal SA variability exceeded its spatial variability. Overall, SA varied 5-fold between all samples (0.08 to 0.38 mg L⁻¹ T-X-100), being highest in the SML during summer. SML SA enrichment factors (EFs) relative to SSW were  ∼  1.0 to 1.9, except for two values (0.75; 0.89: February 2013). The range in corresponding <i>k</i>₆₆₀ (<i>k</i>_w for CO₂ in seawater at 20 °C) was 6.8 to 22.0 cm h⁻¹. The film factor <i>R</i>₆₆₀ (the ratio of <i>k</i>₆₆₀ for seawater to <i>k</i>₆₆₀ for “clean”, i.e. surfactant-free, laboratory water) was strongly correlated with SML SA (<i>r</i> ≥ 0.70, <i>p</i> ≤ 0.002, each <i>n</i> = 16). High SML SA typically corresponded to <i>k</i>₆₆₀ suppressions  ∼  14 to 51 % relative to clean laboratory water, highlighting strong spatiotemporal gradients in gas exchange due to varying surfactant in these coastal waters. Such variability should be taken account of when evaluating marine trace gas sources and sinks. Total CDOM absorbance (250 to 450 nm), the CDOM spectral slope ratio (<i>S</i>_R = <i>S</i>_{275 − 295}∕<i>S</i>_{350 − 400}), the 250 : 365 nm CDOM absorption ratio (<i>E</i>₂ : <i>E</i>₃), and Chl <i>a</i> all indicated spatial and temporal signals in the quantity and composition of organic matter in the SML and SSW. This prompts us to hypothesise that spatiotemporal variation in <i>R</i>₆₆₀ and its relationship with SA is a consequence of compositional differences in the surfactant fraction of the SML DOM pool that warrants further investigation

Reduced air–sea CO2 exchange in the Atlantic Ocean due to biological surfactants

This is the author accepted manuscript. The final version is available from Springer Nature via the DOI in this recordOcean CO2 uptake accounts for 20–40% of the post-industrial sink for anthropogenic CO2. The uptake rate is the product of the CO2 interfacial concentration gradient and its transfer velocity, which is controlled by spatial and temporal variability in near-surface turbulence. This variability complicates CO2 flux estimates and in large part reflects variable sea surface microlayer enrichments in biologically derived surfactants that cause turbulence suppression. Here we present a direct estimate of this surfactant effect on CO2 exchange at the ocean basin scale, with derived relationships between its transfer velocity determined experimentally and total surfactant activity for Atlantic Ocean surface seawaters. We found up to 32% reduction in CO2 exchange relative to surfactant-free water. Applying a relationship between sea surface temperature and total surfactant activity to our results gives monthly estimates of spatially resolved ‘surfactant suppression’ of CO2 exchange. Large areas of reduced CO2 uptake resulted, notably around 20° N, and the magnitude of the Atlantic Ocean CO2 sink for 2014 was decreased by 9%. This direct quantification of the surfactant effect on CO2 uptake at the ocean basin scale offers a framework for further refining estimates of air–sea gas exchange up to the global scale.This work was supported by grants from the Leverhulme Trust to R.C.U.G. (RPG-303) and the UK Natural Environment Research Council (NERC) to R.C.U.G. (NE/K00252X/1) and J.D.S. (NE/K002511/1). Both NERC grants are components of RAGNARoCC (Radiatively Active Gases from the North Atlantic Region and Climate Change), which contributes to NERC's Greenhouse Gas Emissions and Feedbacks programme (www.nerc.ac.uk/research/funded/programmes/greenhouse). J.D.S. and I.A. acknowledge additional support from the European Space Agency (grant 4000112091/14/I-LG). R.P. acknowledges support from T. Wagner. This study is a contribution to the international IMBeR project and was supported by UK NERC National Capability funding to Plymouth Marine Laboratory and the National Oceanography Centre, Southampton. This is contribution no. 324 of the AMT programme

Nitrous oxide emissions from the Arabian Sea: A synthesis

We computed high-resolution (1º latitude x 1º longitude) seasonal and annual nitrous oxide (N2O) concentration fields for the Arabian Sea surface layer using a database containing more than 2400 values measured between December 1977 and July 1997. N2O concentrations are highest during the southwest (SW) monsoon along the southern Indian continental shelf. Annual emissions range from 0.33 to 0.70 Tg N2O and are dominated by fluxes from coastal regions during the SW and northeast monsoons. Our revised estimate for the annual N2O flux from the Arabian Sea is much more tightly constrained than the previous consensus derived using averaged in-situ data from a smaller number of studies. However, the tendency to focus on measurements in locally restricted features in combination with insufficient seasonal data coverage leads to considerable uncertainties of the concentration fields and thus in the flux estimates, especially in the coastal zones of the northern and eastern Arabian Sea. The overall mean relative error of the annual N2O emissions from the Arabian Sea was estimated to be at least 65%

Defining the molecular pathology of pancreatic body and tail adenocarcinom

Background: Pancreatic ductal adenocarcinoma (PDAC) remains a dismal disease, with very little improvement in survival over the past 50 years. Recent large-scale genomic studies have improved understanding of the genomic and transcriptomic landscape of the disease, yet very little is known about molecular heterogeneity according to tumour location in the pancreas; body and tail PDACs especially tend to have a significantly worse prognosis. The aim was to investigate the molecular differences between PDAC of the head and those of the body and tail of the pancreas. Methods: Detailed correlative analysis of clinicopathological variables, including tumour location, genomic and transcriptomic data, was performed using the Australian Pancreatic Cancer Genome Initiative (APGI) cohort, part of the International Cancer Genome Consortium study. Results: Clinicopathological data were available for 518 patients recruited to the APGI, of whom 421 underwent genomic analyses; 179 of these patients underwent whole-genome and 96 RNA sequencing. Patients with tumours of the body and tail had significantly worse survival than those with pancreatic head tumours (12·1 versus 22·0 months; P = 0·001). Location in the body and tail was associated with the squamous subtype of PDAC. Body and tail PDACs enriched for gene programmes involved in tumour invasion and epithelial-to-mesenchymal transition, as well as features of poor antitumour immune response. Whether this is due to a molecular predisposition from the outset, or reflects a later time point on the tumour molecular clock, requires further investigation using well designed prospective studies in pancreatic cancer. Conclusion: PDACs of the body and tail demonstrate aggressive tumour biology that may explain worse clinical outcomes

FAK regulates IL-33 expression by controlling chromatin accessibility at c-Jun motifs

Focal adhesion kinase (FAK) localizes to focal adhesions and is overexpressed in many cancers. FAK can also translocate to the nucleus, where it binds to, and regulates, several transcription factors, including MBD2, p53 and IL-33, to control gene expression by unknown mechanisms. We have used ATAC-seq to reveal that FAK controls chromatin accessibility at a subset of regulated genes. Integration of ATAC-seq and RNA-seq data showed that FAK-dependent chromatin accessibility is linked to differential gene expression, including of the FAK-regulated cytokine and transcriptional regulator interleukin-33 (Il33), which controls anti-tumor immunity. Analysis of the accessibility peaks on the Il33 gene promoter/enhancer regions revealed sequences for several transcription factors, including ETS and AP-1 motifs, and we show that c-Jun, a component of AP-1, regulates Il33 gene expression by binding to its enhancer in a FAK kinase-dependent manner. This work provides the first demonstration that FAK controls transcription via chromatin accessibility, identifying a novel mechanism by which nuclear FAK regulates biologically important gene expression

Deleterious coding variants in multi-case families with non-syndromic cleft lip and/or palate phenotypes

8 páginasNonsyndromic Cleft Lip and/or Palate (NSCLP) is regarded as a multifactorial condition in which clefting is an isolated phenotype, distinguished from the largely monogenic, syndromic forms which include clefts among a spectrum of phenotypes. Nonsyndromic clefting has been shown to arise through complex interactions between genetic and environmental factors. However, there is increasing evidence that the broad NSCLP classification may include a proportion of cases showing familial patterns of inheritance and contain highly penetrant deleterious variation in specific genes. Through exome sequencing of multi-case families ascertained in Bogota, Colombia, we identify 28 non-synonymous single nucleotide variants that are considered damaging by at least one predictive score. We discuss the functional impact of candidate variants identified. In one family we find a coding variant in the MSX1 gene which is predicted damaging by multiple scores. This variant is in exon 2, a highly conserved region of the gene. Previous sequencing has suggested that mutations in MSX1 may account for ~2% of NSCLP. Our analysis further supports evidence that a proportion of NSCLP cases arise through monogenic coding mutations, though further work is required to unravel the complex interplay of genetics and environment involved in facial clefting

The Atlantic Ocean surface microlayer from 50°N to 50°S is ubiquitously enriched in surfactants at wind speeds up to 13 m s−1

We report the first measurements of surfactant activity (SA) in the sea surface microlayer (SML) and in subsurface waters (SSW) at the ocean basin scale, for two Atlantic Meridional Transect from cruises 50°N to 50°S during 2014 and 2015. Northern Hemisphere (NH) SA was significantly higher than Southern Hemisphere (SH) SA in the SML and in the SSW. SA enrichment factors (EF = SASML/SASSW) were also higher in the NH, for wind speeds up to ~13 m s−1, questioning a prior assertion that Atlantic Ocean wind speeds >12 m s−1 poleward of 30°N and 30°S would preclude high EFs and showing the SML to be self-sustaining with respect to SA. Our results imply that surfactants exert a control on air-sea CO2 exchange across the whole North Atlantic CO2 sink region and that the contribution made by high wind, high latitude oceans to air-sea gas exchange globally should be reexamined

Nitrous oxide emissions from the Arabian Sea: A synthesis

We computed high-resolution (1º latitude x&nbsp; 1º longitude) seasonal and annual nitrous oxide (N₂O) concentration fields for the Arabian Sea surface layer using a database containing more than 2400 values measured between December 1977 and July 1997. N₂O concentrations are highest during the southwest (SW) monsoon along the southern Indian continental shelf. Annual emissions range from 0.33 to 0.70 Tg N₂O and are dominated by fluxes from coastal regions during the SW and northeast monsoons. Our revised estimate for the annual N₂O flux from the Arabian Sea is much more tightly constrained than the previous consensus derived using averaged in-situ data from a smaller number of studies. However, the tendency to focus on measurements in locally restricted features in combination with insufficient seasonal data coverage leads to considerable uncertainties of the concentration fields and thus in the flux estimates, especially in the coastal zones of the northern and eastern Arabian Sea. The overall mean relative error of the annual N₂O emissions from the Arabian Sea was estimated to be at least 65%

Role of PLEXIND1/TGFβ signaling axis in pancreatic ductal adenocarcinoma progression correlates with the mutational status of KRAS

PLEXIND1 is upregulated in several cancers, including pancreatic ductal adenocarcinoma (PDAC). It is an established mediator of semaphorin signaling, and neuropilins are its known coreceptors. Herein, we report data to support the proposal that PLEXIND1 acts as a transforming growth factor beta (TGFβ) coreceptor, modulating cell growth through SMAD3 signaling. Our findings demonstrate that PLEXIND1 plays a pro-tumorigenic role in PDAC cells with oncogenic KRAS (KRASmut). We show in KRASmut PDAC cell lines (PANC-1, AsPC-1,4535) PLEXIND1 downregulation results in decreased cell viability (in vitro) and reduced tumor growth (in vivo). Conversely, PLEXIND1 acts as a tumor suppressor in the PDAC cell line (BxPC-3) with wild-type KRAS (KRASwt), as its reduced expression results in higher cell viability (in-vitro) and tumor growth (in vivo). Additionally, we demonstrate that PLEXIND1-mediated interactions can be selectively disrupted using a peptide based on its C-terminal sequence (a PDZ domain-binding motif), an outcome that may possess significant therapeutic implications. To our knowledge, this is the first report showing that (1) PLEXIND1 acts as a TGFβ coreceptor and mediates SMAD3 signaling, and (2) differential roles of PLEXIND1 in PDAC cell lines correlate with KRASmut and KRASwt status

Advances in understanding of air–sea exchange and cycling of greenhouse gases in the upper ocean

This is the final version. Available on open access from University of California Press via the DOI in this recordThe air–sea exchange and oceanic cycling of greenhouse gases (GHG), including carbon dioxide (CO2), nitrous oxide (N2O), methane (CH4), carbon monoxide (CO), and nitrogen oxides (NOx = NO + NO2), are fundamental in controlling the evolution of the Earth’s atmospheric chemistry and climate. Significant advances have been made over the last 10 years in understanding, instrumentation and methods, as well as deciphering the production and consumption pathways of GHG in the upper ocean (including the surface and subsurface ocean down to approximately 1000 m). The global ocean under current conditions is now well established as a major sink for CO2, a major source for N2O and a minor source for both CH4 and CO. The importance of the ocean as a sink or source of NOx is largely unknown so far. There are still considerable uncertainties about the processes and their major drivers controlling the distributions of N2O, CH4, CO, and NOx in the upper ocean. Without having a fundamental understanding of oceanic GHG production and consumption pathways, our knowledge about the effects of ongoing major oceanic changes—warming, acidification, deoxygenation, and eutrophication—on the oceanic cycling and air–sea exchange of GHG remains rudimentary at best. We suggest that only through a comprehensive, coordinated, and interdisciplinary approach that includes data collection by global observation networks as well as joint process studies can the necessary data be generated to (1) identify the relevant microbial and phytoplankton communities, (2) quantify the rates of ocean GHG production and consumption pathways, (3) comprehend their major drivers, and (4) decipher economic and cultural implications of mitigation solutions.European Space AgencyConvex Seascape SurveyEuropean Union Horizon 2020U.S. National Science Foundatio