Facilitation alters climate change risk on rocky shores.

A huge fraction of global biodiversity resides within biogenic habitats that ameliorate physical stresses. In most cases, details of how physical conditions within facilitative habitats respond to external climate forcing remain unknown, hampering climate change predictions for many of the world's species. Using intertidal mussel beds as a model system, we characterize relationships among external climate conditions and within-microhabitat heat and desiccation conditions. We use these data, along with physiological tolerances of two common inhabitant taxa (the isopod Cirolana harfordi and the porcelain crab Petrolisthes cinctipes), to examine the magnitude of climate risk inside and outside biogenic habitat, applying an empirically derived model of evaporation to simulate mortality risk under a high-emissions climate-warming scenario. We found that biogenic microhabitat conditions responded so weakly to external climate parameters that mortality risk was largely unaffected by climate warming. In contrast, outside the biogenic habitat, desiccation drove substantial mortality in both species, even at temperatures 4.4-8.6°C below their hydrated thermal tolerances. These findings emphasize the importance of warming-exacerbated desiccation to climate-change risk and the role of biogenic habitats in buffering this less-appreciated stressor. Our results suggest that, when biogenic habitats remain intact, climate warming may have weak direct effects on organisms within them. Instead, risk to such taxa is likely to be indirect and tightly coupled with the fate of habitat-forming populations. Conserving and restoring biogenic habitats that offer climate refugia could therefore be crucial to supporting biodiversity in the face of climate warming.

Differing responses of red abalone (Haliotis rufescens) and white abalone (H. sorenseni) to infection with phage-associated Candidatus Xenohaliotis californiensis.

The Rickettsiales-like prokaryote and causative agent of Withering Syndrome (WS)-Candidatus Xenohaliotis californiensis (Ca. Xc)-decimated black abalone populations along the Pacific coast of North America. White abalone-Haliotis sorenseni-are also susceptible to WS and have become nearly extinct in the wild due to overfishing in the 1970s. Candidatus Xenohaliotis californiensis proliferates within epithelial cells of the abalone gastrointestinal tract and causes clinical signs of starvation. In 2012, evidence of a putative bacteriophage associated with Ca. Xc in red abalone-Haliotis rufescens-was described. Recently, histologic examination of animals with Ca. Xc infection in California abalone populations universally appear to have the phage-containing inclusions. In this study, we investigated the current virulence of Ca. Xc in red abalone and white abalone at different environmental temperatures. Using a comparative experimental design, we observed differences over time between the two abalone species in mortality, body condition, and bacterial load by quantitative real time PCR (qPCR). By day 251, all white abalone exposed to the current variant of Ca. Xc held in the warm water (18.5 °C) treatment died, while red abalone exposed to the same conditions had a mortality rate of only 10%, despite a relatively heavy bacterial burden as determined by qPCR of posterior esophagus tissue and histological assessment at the termination of the experiment. These data support the current status of Ca. Xc as less virulent in red abalone, and may provide correlative evidence of a protective phage interaction. However, white abalone appear to remain highly susceptible to this disease. These findings have important implications for implementation of a white abalone recovery program, particularly with respect to the thermal regimes of locations where captively-reared individuals will be outplanted.