Growth and survival of zebrafish (Danio rerio) fed different commercial and laboratory diets.

The need to develop standardized diets to support zebrafish (Danio rerio) research is supported by the knowledge that specific dietary ingredients, nutrients, or antinutritional factors in diets have been shown to affect development and growth of adult D. rerio and their offspring. In this study, there were seven dietary treatments consisting of five commercially available diets and two laboratory-prepared diets, three replicates per treatment. Fish were fed ad libitum twice daily for 9 weeks. At 9 weeks, both weight and length were recorded to determine condition indices. D. rerio fed one of the laboratory-prepared diets had significantly higher weights than individuals fed any of the other diets and exhibited significantly higher lengths than those fed five of the six remaining diets. Although there were significant differences in general growth demographics (length/weight) after the 9-week feeding trial, no significant differences in overall health of D. rerio were observed for the different dietary treatments as determined by statistical analysis of condition factor indices (K = [weight x 100]/length(3)). The success achieved with the laboratory-prepared diets represents the foundation for establishing an open-formulation nutritional standard to ensure that the D. rerio model for research does not generate confounding research results caused by nutritional vagaries.

The ING4 tumor suppressor attenuates NF-kappaB activity at the promoters of target genes.

The NF-kappaB family mediates immune and inflammatory responses. In many cancers, NF-kappaB is constitutively activated and induces the expression of genes that facilitate tumorigenesis. ING4 is a tumor suppressor that is absent or mutated in several cancers. Herein, we demonstrate that in human gliomas, NF-kappaB is constitutively activated, ING4 expression is negligible, and NF-kappaB-regulated gene expression is elevated. We demonstrate that an ING4 and NF-kappaB interaction exists but does not prevent NF-kappaB activation, nuclear translocation, or DNA binding. Instead, ING4 and NF-kappaB bind simultaneously at NF-kappaB-regulated promoters, and this binding correlates with reductions in p65 phosphorylation, p300, and the levels of acetylated histones and H3-Me3K4, while enhancing the levels of HDAC-1 at these promoters. Using a knockdown approach, we correlate reductions in ING4 protein levels with increased basal and inducible NF-kappaB target gene expression. Collectively, these data suggest that ING4 may specifically regulate the activity of NF-kappaB molecules that are bound to target gene promoters.