Prioritizing Stream Barrier Removal to Maximize Connected Aquatic Habitat and Minimize Water Scarcity

Instream barriers, such as dams, culverts, and diversions, alter hydrologic processes and aquatic habitat. Removing uneconomical and aging instream barriers is increasingly used for river restoration. Historically, selection of barrier removal projects used score‐and‐rank techniques, ignoring cumulative change and the spatial structure of stream networks. Likewise, most water supply models prioritize either human water uses or aquatic habitat, failing to incorporate both human and environmental water use benefits. Here, a dual‐objective optimization model identifies barriers to remove that maximize connected aquatic habitat and minimize water scarcity. Aquatic habitat is measured using monthly average streamflow, temperature, channel gradient, and geomorphic condition as indicators of aquatic habitat suitability. Water scarcity costs are minimized using economic penalty functions while a budget constraint specifies the money available to remove barriers. We demonstrate the approach using a case study in Utah\u27s Weber Basin to prioritize removal of instream barriers for Bonneville cutthroat trout, while maintaining human water uses. Removing 54 instream barriers reconnects about 160 km of quality‐weighted habitat and costs approximately US$10 M. After this point, the cost‐effectiveness of removing barriers to connect river habitat decreases. The modeling approach expands barrier removal optimization methods by explicitly including both economic and environmental water uses

A probabilistic model for gene content evolution with duplication, loss, and horizontal transfer

We introduce a Markov model for the evolution of a gene family along a phylogeny. The model includes parameters for the rates of horizontal gene transfer, gene duplication, and gene loss, in addition to branch lengths in the phylogeny. The likelihood for the changes in the size of a gene family across different organisms can be calculated in O(N+hM^2) time and O(N+M^2) space, where N is the number of organisms, $h$ is the height of the phylogeny, and M is the sum of family sizes. We apply the model to the evolution of gene content in Preoteobacteria using the gene families in the COG (Clusters of Orthologous Groups) database

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease