Anthropogenic climate change is predicted to be a major cause of species extinctions in the next 100 years. But what will actually cause these extinctions? For example, will it be limited physiological tolerance to high temperatures, changing biotic interactions or other factors? Here, we systematically review the proximate causes of climate-change related extinctions and their empirical support. We find 136 case studies of climatic impacts that are potentially relevant to this topic. However, only seven identified proximate causes of demonstrated local extinctions due to anthropogenic climate change. Among these seven studies, the proximate causes vary widely. Surprisingly, none show a straightforward relationship between local extinction and limited tolerances to high temperature. Instead, many studies implicate species interactions as an important proximate cause, especially decreases in food availability. We find very similar patterns in studies showing decreases in abundance associated with climate change, and in those studies showing impacts of climatic oscillations. Collectively, these results highlight our disturbingly limited knowledge of this crucial issue but also support the idea that changing species interactions are an important cause of documented population declines and extinctions related to climate change. Finally, we briefly outline general research strategies for identifying these proximate causes in future studies.

Aim The factors that set species range limits underlie many patterns in ecology, evolution, biogeography and conservation. These factors have been the subject of several reviews, but there has been no systematic review of the causes of warm-edge limits (low elevations and latitudes). Understanding these causes is urgent, given that the factors that set these limits might also drive extinction at warm edges as global climate changes. Many authors have suggested that warm-edge limits are set by biotic factors (particularly competition) whereas others have stressed abiotic factors (particularly temperature). We synthesize the known causes of species' warm-edge range limits, with emphasis on the underlying mechanisms (proximate causes).Location Global.Methods We systematically searched the literature for studies testing the causes of warm-edge range limits.Results We found 125 studies that address the causes of warm-edge limits, from a search including > 4000 studies. Among the species in these studies, abiotic factors are supported more often than biotic factors in setting species range limits at warm edges, in contrast to the widely held view that biotic factors are more important. Studies that test both types of factors support abiotic factors significantly more frequently. In addition, only 23 studies (61 species) identified proximate causes of these limits, and these overwhelmingly support physiological tolerances to abiotic factors (primarily temperature). Only eight species with identified proximate causes were tested for both biotic and abiotic factors, but the majority support abiotic factors.Main conclusions Although it is often assumed that warm-edge limits are set by biotic factors, our review shows that abiotic factors are supported more often among the species in these 125 studies. However, few studies both identify proximate causes and test alternative mechanisms, or examine the interaction between biotic and abiotic factors. Filling these gaps should be a high priority as warm-edge populations are increasingly driven to extinction by climate change.

Tracking SARS-CoV-2 genetic diversity is strongly indicated because diversifying selection may lead to the emergence of novel variants resistant to naturally acquired or vaccine-induced immunity. To monitor New York City (NYC) for the presence of novel variants, we deep sequence most of the receptor binding domain coding sequence of the S protein of SARS-CoV-2 isolated from the New York City wastewater. Here we report detecting increasing frequencies of novel cryptic SARS-CoV-2 lineages not recognized in GISAID’s EpiCoV database. These lineages contain mutations that had been rarely observed in clinical samples, including Q493K, Q498Y, E484A, and T572N and share many mutations with the Omicron variant of concern. Some of these mutations expand the tropism of SARS-CoV-2 pseudoviruses by allowing infection of cells expressing the human, mouse, or rat ACE2 receptor. Finally, pseudoviruses containing the spike amino acid sequence of these lineages were resistant to different classes of receptor binding domain neutralizing monoclonal antibodies. We offer several hypotheses for the anomalous presence of these lineages, including the possibility that these lineages are derived from unsampled human COVID-19 infections or that they indicate the presence of a non-human animal reservoir.

Tracking SARS-CoV-2 genetic diversity is strongly indicated because diversifying selection may lead to the emergence of novel variants resistant to naturally acquired or vaccine-induced immunity. To monitor New York City (NYC) for the presence of novel variants, we amplified regions of the SARS-CoV-2 Spike protein gene from RNA acquired from all 14 NYC wastewater treatment plants (WWTPs) and ascertained the diversity of lineages from these samples using high throughput sequencing. Here we report the detection and increasing frequencies of novel SARS-CoV-2 lineages not recognized in GISAIDs EpiCoV database. These lineages contain mutations rarely observed in clinical samples, including Q493K, Q498Y, H519N and T572N. Many of these mutations were found to expand the tropism of SARS-CoV-2 pseudoviruses by allowing infection of cells expressing the human, mouse, or rat ACE2 receptor. In addition, pseudoviruses containing the Spike amino acid sequence of these lineages were found to be resistant to many different classes of receptor binding domain (RBD) binding neutralizing monoclonal antibodies. We offer several hypotheses for the anomalous presence of these mutations, including the possibility of a non-human animal reservoir. Although wastewater sampling cannot provide direct inference of SARS-CoV-2 clinical sequences, our research revealed several lineages that could be relevant to public health and they would not have been discovered if not for wastewater surveillance.

The evolution of antibiotic resistance in bacteria has become one of the defining problems in modern biology. Bacterial resistance to antimicrobial therapy threatens to eliminate one of the pillars of the practice of modern medicine. Yet, in spite of the importance of this problem, only recently have the dynamics of the shift from antibiotic sensitivity to resistance in a bacterial population been studied. In this study, a novel chemostat method was used to observe the evolution of resistance to streptomycin in a sensitive population of Escherichia coli, which grew while the concentration of antibiotic was constantly increasing. The results indicate that resistant mutants remain at a low frequency for longer than expected and do not begin to rise to a high frequency until the antibiotic concentrations are above the measured MIC, creating a "lull period" in which there were few bacterial cells growing in the chemostats. Overall, mutants resistant to streptomycin were found in >60% of the experimental trial replicates. All of the mutants detected were found to have MICs far above the maximum levels of streptomycin to which they were exposed and reached a high frequency within 96 h.