Drivers of fatal bird collisions in an urban center

Millions of nocturnally migrating birds die each year from collisions with built structures, especially brightly illuminated buildings and communication towers. Reducing this source of mortality requires knowledge of important behavioral, meteorological, and anthropogenic factors, yet we lack an understanding of the interacting roles of migration, artificial lighting, and weather conditions in causing fatal bird collisions. Using two decades of collision surveys and concurrent weather and migration measures, we model numbers of collisions occurring at a large urban building in Chicago. We find that the magnitude of nocturnal bird migration, building light output, and wind conditions are the most important predictors of fatal collisions. The greatest mortality occurred when the building was brightly lit during large nocturnal migration events and when winds concentrated birds along the Chicago lakeshore. We estimate that halving lighted window area decreases collision counts by 11× in spring and 6× in fall. Bird mortality could be reduced by ∼60% at this site by decreasing lighted window area to minimum levels historically recorded. Our study provides strong support for a relationship between nocturnal migration magnitude and urban bird mortality, mediated by light pollution and local atmospheric conditions. Although our research focuses on a single site, our findings have global implications for reducing or eliminating a critically important cause of bird mortality.

The cytokine MIF controls daily rhythms of symbiont nutrition in an animal–bacterial association

The recent recognition that many symbioses exhibit daily rhythms has encouraged research into the partner dialogue that drives these biological oscillations. Here we characterized the pivotal role of the versatile cytokine macrophage migration inhibitory factor (MIF) in regulating a metabolic rhythm in the model light-organ symbiosis betweenEuprymna scolopesandVibrio fischeri. As the juvenile host matures, it develops complex daily rhythms characterized by profound changes in the association, from gene expression to behavior. One such rhythm is a diurnal shift in symbiont metabolism triggered by the periodic provision of a specific nutrient by the mature host: each night the symbionts catabolize chitin released from hemocytes (phagocytic immune cells) that traffic into the light-organ crypts, where the population ofV. fischericells resides. Nocturnal migration of these macrophage-like cells, together with identification of anE. scolopesMIF (EsMIF) in the light-organ transcriptome, led us to ask whether EsMIF might be the gatekeeper controlling the periodic movement of the hemocytes. Western blots, ELISAs, and confocal immunocytochemistry showed EsMIF was at highest abundance in the light organ. Its concentration there was lowest at night, when hemocytes entered the crypts. EsMIF inhibited migration of isolated hemocytes, whereas exported bacterial products, including peptidoglycan derivatives and secreted chitin catabolites, induced migration. These results provide evidence that the nocturnal decrease in EsMIF concentration permits the hemocytes to be drawn into the crypts, delivering chitin. This nutritional function for a cytokine offers the basis for the diurnal rhythms underlying a dynamic symbiotic conversation.