The sphingosine rheostat is involved in the cnidarian heat stress response but not necessarily in bleaching.

Abstract

Sphingolipids play important roles in mitigating cellular heat and oxidative stress by altering membrane fluidity, receptor clustering and gene expression. Accumulation of signaling sphingolipids that comprise the sphingosine rheostat, pro-apoptotic sphingosine (Sph) and pro-survival sphingosine-1-phosphate (S1P) is key to determining cell fate. Reef-building corals and other symbiotic cnidarians living in shallow tropical waters can experience elevated seawater temperature and high UV irradiance, two stressors that are increasing in frequency and severity with climate change. In symbiotic cnidarians, these stressors disrupt the photosynthetic machinery of the endosymbiont and ultimately result in the collapse of the partnership (dysbiosis), known as cnidarian bleaching. In a previous study, exogenously applied sphingolipids altered heat-induced bleaching in the symbiotic anemone Aiptasia pallida, but endogenous regulation of these lipids is unknown. Here, we characterized the role of the rheostat in the cnidarian heat stress response (HSR) and in dysbiosis. Gene expression of rheostat enzymes sphingosine kinase (AP-SPHK) and S1P phosphatase (AP-SGPP), and concentrations of sphingolipids were quantified from anemones incubated at elevated temperatures. We observed a biphasic HSR in A. pallida. At early exposure, rheostat gene expression and lipid levels were suppressed while gene expression of a heat stress biomarker increased and 40% of symbionts were lost. After longer incubations at the highest temperature, AP-SGPP and then Sph levels both increased. These results indicate that the sphingosine rheostat in A. pallida does not participate in initiation of dysbiosis, but instead functions in the chronic response to prolonged heat stress that promotes host survival.