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Epistasis is an interaction among genes that makes the phenotypic effect of an allele dependent on which alleles are present at other loci. Two new genomic studies find abundant epistasis in the yeast genome, with significant implications for the evolution of sex and for the inference of genetic pathways from genomic data.
DNA methylation is a heritable epigenetic mark found in a wide range of eukaryotes. By mapping DNA methylation within the majority of human promoters, the authors of a new study uncover intriguing insights into genome evolution, cellular differentiation and potential links to tumorigenesis.
The possibility of deep population resequencing of genes has generated excitement over its potentially promising role in understanding complex human traits. A new study has now demonstrated the utility of this approach, reporting the resequencing of a lipid metabolism gene in a large multiethnic population and definitively showing that coding variants in the gene are associated with plasma triglyceride levels.
A new study suggests that manipulating the expression of a Drosophila melanogaster neurofibromatosis-1 ortholog affects organismal lifespan through protein kinase A–mediated regulation of mitochondrial respiration and reactive oxygen species production. These results provide a new and unexpected twist to the study of NF1 signaling.
Recent reports of premature aging in mutant mice with greatly increased rates of mitochondrial DNA mutagenesis (so-called 'mitochondrial mutator mice') appeared to confirm that accumulation of mtDNA mutations is a key mechanism of normal aging. Now, in a dramatic turnaround, a new study reports that levels of point mutations in tissues of aged normal mice are much lower than in the mutator mice, apparently ruling out a causal role in normal aging.
A new approach that scans the modification states of histones along the chromosome allows the identification of enhancer elements in the complex genomes of higher eukaryotes. This is an important step in the functional annotation of the genome.
Signaling pathways are frequently connected through shared intracellular molecules, yet they manage to maintain remarkable specificity to distinct stimuli. A new study identifies mechanisms to explain how this specificity is shaped for MAP kinase modules within the yeast signaling network.
In the current era of large-scale cancer genome sequencing, the interpretation of somatic sequence alterations is a formidable challenge. A new study of known mutations represents an important step in cataloging somatic mutations in individual tumors.
In the nematode Caenorhabditis elegans, dosage compensation is mediated by a subtle twofold downregulation of both X chromosomes. A new study provides a significant advance in our understanding of how the X is targeted for dosage compensation and how this global regulation is integrated with regulation of the expression of each gene.
The DNA methyltransferase DNMT1 is essential for cell viability in various mouse models, but gene targeting in human tumor cells results in a viable line. This dilemma has now been resolved using a new human DNMT1 knockout line, although new questions arise as to the full extent of DNMT1 function in maintaining genome integrity.
Deeply hidden in the bone marrow are rare hematopoietic stem cells that produce all types of blood cells in the circulatory system. A new study shows that the latexin gene affects the size of this population of cells.
Members of the Hedgehog family of secreted proteins are central to animal development, with different levels of Hedgehog signaling activity specifying distinct cellular identities. A new study shows that a microRNA is involved in this process by modulating a component of the Hedgehog signal transduction pathway.
Two new studies show that the Fanconi anemia complementation group N results from biallelic mutations in PALB2, which encodes a recently identified interaction partner of the breast cancer susceptibility protein BRCA2. A third study shows that monoallelic PALB2 mutations are associated with breast cancer susceptibility, providing yet more links between Fanconi anemia, homologous recombination repair and cancer predisposition.
