Rising atmospheric carbon dioxide (CO 2 ) conditions are driving unprecedented changes in seawater chemistry, resulting in reduced pH and carbonate ion concentrations in the Earth's oceans. This ocean acidification has negative but variable impacts on individual performance in many marine species. However, little is known about the adaptive capacity of species to respond to an acidified ocean, and, as a result, predictions regarding future ecosystem responses remain incomplete. Here we demonstrate that ocean acidification generates striking patterns of genome-wide selection in purple sea urchins (Strongylocentrotus purpuratus) cultured under different CO 2 levels. We examined genetic change at 19,493 loci in larvae from seven adult populations cultured under realistic future CO 2 levels. Although larval development and morphology showed little response to elevated CO 2 , we found substantial allelic change in 40 functional classes of proteins involving hundreds of loci. Pronounced genetic changes, including excess amino acid replacements, were detected in all populations and occurred in genes for biomineralization, lipid metabolism, and ion homeostasis-gene classes that build skeletons and interact in pH regulation. Such genetic change represents a neglected and important impact of ocean acidification that may influence populations that show few outward signs of response to acidification. Our results demonstrate the capacity for rapid evolution in the face of ocean acidification and show that standing genetic variation could be a reservoir of resilience to climate change in this coastal upwelling ecosystem. However, effective response to strong natural selection demands large population sizes and may be limited in species impacted by other environmental stressors.experimental evolution | population genomics | RNA sequencing | adaptation | environmental mosaic A ccelerating increases in ocean CO 2 concentrations and accompanying declines in pH are expected this century (1, 2), particularly in the California Current System (3). The negative impacts of ocean acidification have been seen in a broad range of species (4-8) and are predicted to lead to future populations of individuals with low growth, reproduction, or survival. However, the capacity of marine populations to adapt to these changes is unknown (9, 10), and, as a result, there may be circumstances in which natural selection could result in populations of individuals with better-than-expected fitness under acidified conditions. Until recently, the tools to scan for standing genetic variation with adaptive potential in the face of climate change have not been broadly available. Here we combine sequencing across the transcriptome of the purple sea urchin Strongylocentrotus purpuratus, growth measurements under experimental acidification, and tests of frequency shifts in 19,493 polymorphisms during development. We detect the widespread occurrence of genetic variation to tolerate ocean acidification.Rapid evolution in changing environments is likely to depend ...
Acute lung injury (ALI) is a devastating syndrome characterized by diffuse alveolar damage, elevated airspace levels of pro-inflammatory cytokines, and flooding of the alveolar spaces with protein-rich edema fluid. Interleukin-1 (IL-1) is one of the most biologically active cytokines in the distal airspaces of patients with ALI. IL-1 has been shown to increase lung epithelial and endothelial permeability. In this study, we hypothesized that IL-1 would decrease vectorial ion and water transport across the distal lung epithelium. Therefore, we measured the effects of IL-1 on transepithelial current, resistance, and sodium transport in primary cultures of alveolar epithelial type II (ATII) cells. IL-1 significantly reduced the amiloride-sensitive fraction of the transepithelial current and sodium transport across rat ATII cell monolayers. Moreover, IL-1 decreased basal and dexamethasone-induced epithelial sodium channel ␣-subunit (␣ENaC) mRNA levels and total and cellsurface protein expression. The inhibitory effect of IL-1 on ␣ENaC expression was mediated by the activation of p38 MAPK in both rat and human ATII cells and was independent of the activation of ␣v6 integrin and transforming growth factor-. These results indicate that IL-1 may contribute to alveolar edema in ALI by reducing distal lung epithelial sodium absorption. This reduction in ion and water transport across the lung epithelium is in large part due to a decrease in ␣ENaC expression through p38 MAPK-dependent inhibition of ␣ENaC promoter activity and to an alteration in ENaC trafficking to the apical membrane of ATII cells. Acute lung injury (ALI)1 is a devastating clinical syndrome manifested by diffuse alveolar damage, capillary injury, and disruption of the alveolar epithelium. The acute phase of ALI is characterized by the influx of protein-rich edema fluid that impairs gas exchange, causing arterial hypoxemia and respiratory failure with an overall mortality rate of 30 -40% (1). Along with an increase in lung endothelial and epithelial permeability to protein, this syndrome is associated with abnormal surfactant production and decreased vectorial fluid transport across the lung epithelial barrier (2, 3). A number of inflammatory mediators have been found to be elevated in the alveolar space during the early phase of ALI, including interleukin (IL)-1, tumor necrosis factor-␣, IL-6, and IL-8 (4). IL-1 is one of the most biologically active cytokines in pulmonary edema and bronchoalveolar lavage fluids of patients with ALI (4 -6). Indeed, IL-1 increases microvascular lung epithelial permeability in in vitro and in vivo models of ALI (7). IL-1 also enhances alveolar epithelial repair by increasing cell spreading (8) and fibroblast activation and proliferation (5). In contrast, the role of IL-1 in distal lung epithelial ion transport remains unclear. In other epithelia such as the colonic epithelium, IL-1 inhibits aldosterone-induced electrogenic sodium absorption and attenuates aldosterone-induced up-regulation of -and ␥-subunit ...
High-throughput sequencing technologies are currently revolutionizing the field of biology and medicine, yet bioinformatic challenges in analysing very large data sets have slowed the adoption of these technologies by the community of population biologists. We introduce the 'Simple Fool's Guide to Population Genomics via RNA-seq' (SFG), a document intended to serve as an easy-to-follow protocol, walking a user through one example of high-throughput sequencing data analysis of nonmodel organisms. It is by no means an exhaustive protocol, but rather serves as an introduction to the bioinformatic methods used in population genomics, enabling a user to gain familiarity with basic analysis steps. The SFG consists of two parts. This document summarizes the steps needed and lays out the basic themes for each and a simple approach to follow. The second document is the full SFG, publicly available at http://sfg.stanford.edu, that includes detailed protocols for data processing and analysis, along with a repository of custom-made scripts and sample files. Steps included in the SFG range from tissue collection to de novo assembly, blast annotation, alignment, gene expression, functional enrichment, SNP detection, principal components and F(ST) outlier analyses. Although the technical aspects of population genomics are changing very quickly, our hope is that this document will help population biologists with little to no background in high-throughput sequencing and bioinformatics to more quickly adopt these new techniques.
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