Alphaflexivirus Genomes in Stony Coral Tissue Loss Disease-Affected, Disease-Exposed, and Disease-Unexposed Coral Colonies in the U.S. Virgin Islands.

Stony coral tissue loss disease (SCTLD) is decimating Caribbean corals. Here, through the metatranscriptomic assembly and annotation of two alphaflexivirus-like strains, we provide genomic evidence of filamentous viruses in SCTLD-affected, -exposed, and -unexposed coral colonies. These data will assist in clarifying the roles of viruses in SCTLD.

Caspase-2 resides in the mitochondria and mediates apoptosis directly from the mitochondrial compartment.

Caspase-2 plays an important role in apoptosis induced by several stimuli, including oxidative stress. However, the subcellular localization of caspase-2, particularly its presence in the mitochondria, is unclear. It is also not known if cytosolic caspase-2 translocates to the mitochondria to trigger the intrinsic pathway of apoptosis or if caspase-2 is constitutively present in the mitochondria that then selectively mediates this apoptotic effect. Here, we demonstrate the presence of caspase-2 in purified mitochondrial fractions from in vitro-cultured cells and in liver hepatocytes using immunoblots and confocal microscopy. We show that mitochondrial caspase-2 is functionally active by performing fluorescence resonance energy transfer analyses using a mitochondrially targeted substrate flanked by donor and acceptor fluorophores. Cell-free apoptotic assays involving recombination of nuclear, cytosolic and mitochondrial fractions from the livers of wild type and Casp2-/- mice clearly point to a direct functional role for mitochondrial caspase-2 in apoptosis. Furthermore, cytochrome c release from Casp2-/- cells is decreased as compared with controls upon treatment with agents inducing mitochondrial dysfunction. Finally, we show that Casp2-/- primary skin fibroblasts are protected from oxidants that target the mitochondrial electron transport chain. Taken together, our results demonstrate that caspase-2 exists in the mitochondria and that it is essential for mitochondrial oxidative stress-induced apoptosis.

Experimental examination of factors that affect dust generation.

A method is presented to examine factors that affect the amount and size distribution of dust generated by falling granular material in still air. This work was conducted by using an apparatus with separate dust generating and dust measuring sections. The dust generated by a falling material was carried into an elutriation column equipped with a slotted Sierra high-volume impactor at the top. This apparatus can measure dust generation rates for particles between 0.4 and 25 microns in aerodynamic diameter as well as the amount of air entrained by the falling material. Four granular materials were tested, and a simple model was developed to describe the dust generation rate of these materials as a function of particle size, drop height, material flow, and moisture content. Moisture content strongly influenced the interparticle binding forces and the amount of dust generated. Drop height and material flow influenced the material separation forces and also significantly influenced the amount of dust generated.