Loss of SUV420H2-Dependent Chromatin Compaction Drives Right-Sided Colon Cancer Progression.

Background & Aims: Epigenetic processes regulating gene expression contribute markedly to epithelial cell plasticity in colorectal carcinogenesis. The lysine methyltransferase SUV420H2 comprises an important regulator of epithelial plasticity and is primarily responsible for trimethylation of H4K20 (H4K20me3). Loss of H4K20me3 has been suggested as a hallmark of human cancer due to its interaction with DNMT1.

Inducible mouse models of colon cancer for the analysis of sporadic and inflammation-driven tumor progression and lymph node metastasis.

Despite advances in the detection and therapy of colorectal cancer (CRC) in recent years, CRC has remained a major challenge in clinical practice. Although alternative methods for modeling CRC have been developed, animal models of CRC remain helpful when analyzing molecular aspects of pathogenesis and are often used to perform preclinical in vivo studies of potential therapeutics. This protocol updates our protocol published in 2007, which provided an azoxymethane (AOM)-based setup for investigations into sporadic (Step 5A) and, when combined with dextran sodium sulfate (Step 5B), inflammation-associated tumor growth.

Regulation of Skeletal Muscle Stem Cell Quiescence by Suv4-20h1-Dependent Facultative Heterochromatin Formation.

Skeletal muscle stem cells (MuSCs) are required for regeneration of adult muscle following injury, a response that demands activation of mainly quiescent MuSCs. Despite the need for dynamic regulation of MuSC quiescence, relatively little is known about the determinants of this property. Here, we show that Suv4-20h1, an H4K20 dimethyltransferase, controls MuSC quiescence by promoting formation of facultative heterochromatin (fHC).

The emerging role of epigenetic modifiers linking cellular metabolism and gene activity in cardiac progenitor cells.

During mammalian heart development, cardiac gene expression is controlled by a complex network consisting of signaling pathways, cardiac transcription factors, and epigenetic modifiers. Emerging evidence suggests that epigenetic modifying enzymes sense and respond to metabolic cues, thereby translating environmental stimuli to cardiac gene expression patterns. Here, we review the impact of metabolic cues on epigenetic changes and survey how epigenetic changes, including DNA modifications, histone modifications, and ATP-dependent chromatin remodeling, affect recruitment of progenitor cells into the cardiac lineage.

Mouse HORMAD1 and HORMAD2, two conserved meiotic chromosomal proteins, are depleted from synapsed chromosome axes with the help of TRIP13 AAA-ATPase.

Meiotic crossovers are produced when programmed double-strand breaks (DSBs) are repaired by recombination from homologous chromosomes (homologues). In a wide variety of organisms, meiotic HORMA-domain proteins are required to direct DSB repair towards homologues. This inter-homologue bias is required for efficient homology search, homologue alignment, and crossover formation.

Entry into and production of the Japanese encephalitis virus from C6/36 cells.

Objectives: The mosquito-borne Japanese encephalitis virus is a leading cause of encephalitis worldwide. However, few studies have investigated the kinetics of Japanese encephalitis virus internalization and production in mosquito cells, and fewer still have investigated the nature of the molecules involved in the binding of the virus to mosquito cells.

Methods: Using the Aedes albopictus/Stegomyia albopicta-derived C6/36 cell line, Japanese encephalitis virus internalization and production were assayed by standard plaque assay, and virus binding was investigated through preinfection enzymatic treatment of cells and virus overlay protein-binding assay of membrane fractions in native and denaturing gels.

Growth and production of the dengue virus in C6/36 cells and identification of a laminin-binding protein as a candidate serotype 3 and 4 receptor protein.

Objectives: Although dengue is one of the most common mosquito-borne viral diseases, few studies have investigated the relationship between the dengue virus and mosquito cells, and this study sought to describe the binding and propagation of the dengue viruses in C6/36 cells.

Methods: The internalization and production of the dengue virus was assayed by standard plaque assay methodologies, while dengue virus receptor proteins were examined by a virus overlay protein-binding assay and candidate gene analysis coupled with virus inhibition studies.

Results: All four serotypes were internalized linearly, and de novo virus production occurred 14-19 h postinfection.