Expulsion of Symbiotic Algae during Feeding by the Green Hydra – a Mechanism for Regulating Symbiont Density?

Background: Algal-cnidarian symbiosis is one of the main factors contributing to the success of cnidarians, and is crucial for the maintenance of coral reefs. While loss of the symbionts (such as in coral bleaching) may cause the death of the cnidarian host, over-proliferation of the algae may also harm the host. Thus, there is a need for the host to regulate the population density of its symbionts. In the green hydra, Chlorohydra viridissima, the density of symbiotic algae may be controlled through host modulation of the algal cell cycle. Alternatively, Chlorohydra may actively expel their endosymbionts, although this phenomenon has only been observed under experimentally contrived stress conditions. Principal Findings: We show, using light and electron microscopy, that Chlorohydra actively expel endosymbiotic algal cells during predatory feeding on Artemia. This expulsion occurs as part of the apocrine mode of secretion from the endodermal digestive cells, but may also occur via an independent exocytotic mechanism. Significance: Our results demonstrate, for the first time, active expulsion of endosymbiotic algae from cnidarians under natural conditions. We suggest this phenomenon may represent a mechanism whereby cnidarians can expel excess symbiotic algae when an alternative form of nutrition is available in the form of prey

Preferential expulsion of dividing algal cells as a mechanism for regulating algal-cnidarian symbiosis

Volume: 199Start Page: 278End Page: 28

Temperature Stress Causes Host Cell Detachment in Symbiotic Cnidarians: Implications for Coral Bleaching

Volume: 182Start Page: 324End Page: 33

Symbiont dynamics during thermal acclimation using cnidarian-dinoflagellate model holobionts

Warming oceans menace reef ecosystems by disrupting symbiosis between cnidarians and Symbiodinium zooxanthellae, thus triggering bleach episodes. Temperature fluctuations promote adjustments in physiological variables and symbiont composition, which can cause stress responses, but can also yield adaptation if fitter host–symbiont homeostasis are achieved. To understand such processes manipulative studies are required, but many reef-building cnidarians pose limitations to experimental prospects. We exposed Exaiptasia anemones to Gradual Thermal Stress (GTS) and Heat Shock (HS) exposures and monitored chlorophyll and symbiont dynamics to test the phenotypic plasticity of these photosynthetic holobionts. GTS enhanced chlorophyll concentrations and decreased Symbiodinium proliferation. A recovery period after GTS returned chlorophyll to lower concentrations and symbiont divisions to higher rates. HS triggered a stress response characterized by intense symbiont declines through degradation and expulsion, algal compensatory proliferation, and chlorophyll accumulation. Anemones pre-exposed to GTS displayed more acute signs of symbiont paucity after HS, demonstrating that recurrent stress does not always induce bleaching-resistance. Our study is the first documenting Symbiodinium C and D, along with the predominant Clade B1 in Exaiptasia anemones. C subclades found in outdoor specimens faded under laboratory exposures. Clade D emerged after HS treatments, and especially after GTS pre-exposure. This highlights the thermotolerance of D subclades found in E. pallida and shows that bleaching-recovery can involve shifts of background symbiont phylotypes. This study enlightens the capability of Exaiptasia anemones to acclimate to gradually increased temperatures, and explores into how thermal history influences in subsequent stress tolerance in symbiotic cnidarians

Global protein expression dataset acquired during isoniazid-induced cytoprotection against H2O2 challenge in HL-60 cells

Isoniazid (INH) is one of the first-line anti-tuberculosis drugs. Its effect on oxidative stress, however, is unknown. Here we used a model of oxidative stress by employing glucose/glucose oxidase (GOx), which (based on the availability of glucose and oxygen) is known to produce H2O2. This reaction induces oxidative stress culminating in necrotic cell death in HL-60 cells (a human promyelocytic leukemia cell line). The changes in protein levels have been quantified using global proteome expression changes through stable isotope labeling by amino acids in cell culture (SILAC) followed by LC–MS/MS analysis. A total of 1459 and 1712 proteins were identified in forward and reverse experiments, respectively. However, only 390 proteins were reproducibly identified in both samples. These 390 proteins were taken into account for further analysis which has been described in “Cytoprotective effect of isoniazid against H2O2 derived injury in HL-60 cells” [1]

Mitochondrial Proton Leak Regulated by Cyclophilin D Elevates Insulin Secretion in Islets at Nonstimulatory Glucose Levels

Fasting hyperinsulinemia precedes the development of type 2 diabetes. However, it is unclear whether fasting insulin hypersecretion is a primary driver of insulin resistance or a consequence of the progressive increase in fasting glycemia induced by insulin resistance in the prediabetic state. Herein, we have discovered a mechanism that specifically regulates non-glucose-stimulated insulin secretion (NGSIS) in pancreatic islets that is activated by nonesterified free fatty acids, the major fuel used by β-cells during fasting. We show that the mitochondrial permeability transition pore regulator cyclophilin D (CypD) promotes NGSIS, but not glucose-stimulated insulin secretion, by increasing mitochondrial proton leak. Islets from prediabetic obese mice show significantly higher CypD-dependent proton leak and NGSIS compared with lean mice. Proton leak-mediated NGSIS is conserved in human islets and is stimulated by exposure to nonesterified free fatty acids at concentrations observed in obese subjects. Mechanistically, proton leak activates islet NGSIS independently of mitochondrial ATP synthesis but ultimately requires closure of the KATP channel. In summary, we have described a novel nonesterified free fatty acid-stimulated pathway that selectively drives pancreatic islet NGSIS, which may be therapeutically exploited as an alternative way to halt fasting hyperinsulinemia and the progression of type 2 diabetes