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Genomic instability is a common feature of human cancer. A new study identifies a putative gene expression signature of chromosome instability in solid tumors, with implications for both understanding the underlying mechanisms and improving prediction of clinical outcomes.
Dysregulation of the JAK-STAT pathway is implicated in human cancer and leads to a hematopoietic tumor phenotype in flies. Now, an enhancer-suppressor screen of the fly tumor model connects the JAK kinase Hopscotch pathway with chromatin-modifying proteins and heterochromatic gene silencing.
A new mutation in wspF allows Pseudomonas fluorescens to colonize a previously unoccupied niche, but its proteomic effects reflect only a fitness cost. Between these two observations lies a better understanding of how organisms build and modify networks of protein expression through evolutionary time.
Each animal species displays a specific life span, rate of aging and pattern of development of age-dependent diseases. The genetic bases of these related features are being studied experimentally in invertebrate and vertebrate model systems as well as in humans through medical records. Three types of mutants are being analyzed: (i) short-lived mutants that are prone to age-dependent diseases and might be models of accelerated aging; (ii) mutants that show overt molecular defects but that do not live shorter lives than controls, and can be used to test specific theories about the molecular causes of aging and age-dependent diseases; and (iii) long-lived mutants that might advance the understanding of the molecular physiology of slow-aging animals and aid the discovery of molecular targets that could be used to manipulate rates of aging to benefit human health. Here, I analyze some of what we know today and discuss what we should try to find out in the future to understand the aging phenomenon.
Systematic mapping of genetic interactions for Caenorhabditis elegans genes involved in signaling pathways implicated in human disease reveals a network of 350 interactions. The topology of this network resembles that mapped previously in yeast, reinforcing the idea that similar networks may underlie the genetic basis of complex human disease.
A new study in mice shows that genetic variants underlying a previously mapped lung cancer susceptibility locus can have opposing effects on cancer risk depending on whether an oncogenic somatic mutation at the same locus subsequently arises in cis or in trans. These findings illustrate the complex interplay between genetic background and somatic events in contributing to cancer risk.
Aicardi-Goutières syndrome (AGS) is an autosomal recessive condition of progressive encephalopathy of early childhood, very similar to congenital viral infections. Two new papers identify four genes mutated in AGS and implicate the processing of DNA and RNA by-products in its pathogenesis.
A new study involving a population of 1,904 heterogeneous mice bred for 50 generations, phenotyped for 101 traits and genotyped for 13,459 SNPs, presents the most comprehensive analysis thus far of complex traits in mice. The work represents a landmark resource for the mouse genetics community and offers important insights into the genetic architecture of complex traits.
The shape of leaves is highly variable. A new study shows that changes in plant homeobox genes seem to underlie some of the variation, although a major regulator of those genes remains unchanged.
A new study shows that the independent adaptation to a ruminant lifestyle in two leaf-eating monkeys relied on parallel amino acid substitutions in ribonuclease gene duplicates. This discovery suggests that, given similar initial conditions, proteins may repeatedly follow similar adaptive evolutionary paths.
The proposal that a distinct subset of colorectal cancers show a marked propensity for promoter CpG island DNA methylation and associated gene silencing has been hotly debated. A new study takes an unbiased approach and not only strongly concludes that a CpG island methylator phenotype exists, but also offers new markers to define a concept that could teach much about the origins of cancer.
Plants generate an amazing variety of small molecules and are arguably nature's finest chemists. A new study identifies over 2,000 small molecule mass peaks in the model plant Arabidopsis thaliana and defines both the genetic diversity and genetic architecture controlling the production of these compounds.
Acquired somatic mutations in the transcription factor GATA1 are a defining feature of acute megakaryocytic leukemia in children with Down syndrome. A new study shows that similar inherited GATA1 mutations do not promote leukemia in the absence of trisomy 21 but lead to defects in multiple hematopoietic lineages.
Among the many neurodegenerative diseases caused by repeat expansions, spinocerebellar ataxia type 8 (SCA8) has been something of a puzzle. Now, a new study shows that the CTG/CAG expansion in ATXN8OS (formerly SCA8) is transcribed in both directions, raising the possibility that two molecular mechanisms contribute to disease.
Flowering at the appropriate time is critical to ensure that plants complete sexual reproduction before the onset of winter in temperate habitats. A new study provides the first strong evidence that variation at a photoreceptor gene contributes to variation in flowering time and does so in a latitude-dependent manner.
The process of gene expression is inherently stochastic and leads to differences in protein abundance from one cell to another. A new study shows that this protein noise is unexpectedly predictable, providing important new insights into the properties and origins of variability in gene expression.
