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.

Levels of gene expression show considerable variation in eukaryotes, but no fine-scale maps have been made of the fitness consequences of such variation in controlled genetic backgrounds and environments. To address this, we assayed fitness at many levels of up- and down-regulated expression of a single essential gene, LCB2, involved in sphingolipid synthesis in budding yeast Saccharomyces cerevisiae. Reduced LCB2 expression rapidly decreases cellular fitness, yet increased expression has little effect. The wild-type expression level is therefore perched on the edge of a nonlinear fitness cliff. LCB2 is upregulated when cells are exposed to osmotic stress; consistent with this, the entire fitness curve is shifted upward to higher expression under osmotic stress, illustrating the selective force behind gene regulation. Expression levels of LCB2 are lower in wild yeast strains than in the experimental lab strain, suggesting that higher levels in the lab strain may be idiosyncratic. Reports indicate that the effect sizes of alleles contributing to variation in complex phenotypes differ among environments and genetic backgrounds; our results suggest that such differences may be explained as simple shifts in the position of nonlinear fitness curves.