Latest Articles Include:
- From the editors
- Nat Rev Genet 10(8):507 (2009)
- Complex disease: Schizophrenia: missing heritability found?
- Nat Rev Genet 10(8):509 (2009)
- MicroRNAs: HITS-CLIP hits the microRNA target
- Nat Rev Genet 10(8):510 (2009)
- Regeneration: Flies get into renewal
- Nat Rev Genet 10(8):510 (2009)
- Technology: The sequencing game
- Nat Rev Genet 10(8):510 (2009)
- In brief: X inactivation, Genome annotation, Epigenetics, Evolution
- Nat Rev Genet 10(8):511 (2009)
- Evolution: Turning up the heat
- Nat Rev Genet 10(8):512 (2009)
- Gene regulation: Sequence, chromatin, action!
- Nat Rev Genet 10(8):512 (2009)
- Cell signalling: Telomerase gets Wnt talking
- Nat Rev Genet 10(8):513 (2009)
- Evolution: Protein kinases mix it up
- Nat Rev Genet 10(8):514 (2009)
- In brief: Phylogenetics, Technology, Epigenetics, Transcriptomics
- Nat Rev Genet 10(8):514 (2009)
- An offer you can't refuse? Ethical implications of non-invasive prenatal diagnosis
- Nat Rev Genet 10(8):515 (2009)
- Quantitative approaches in developmental biology
- Nat Rev Genet 10(8):517-530 (2009)
The tissues of a developing embryo are simultaneously patterned, moved and differentiated according to an exchange of information between their constituent cells. We argue that these complex self-organizing phenomena can only be fully understood with quantitative mathematical frameworks that allow specific hypotheses to be formulated and tested. The quantitative and dynamic imaging of growing embryos at the molecular, cellular and tissue level is the key experimental advance required to achieve this interaction between theory and experiment. Here we describe how mathematical modelling has become an invaluable method to integrate quantitative biological information across temporal and spatial scales, serving to connect the activity of regulatory molecules with the morphological development of organisms. - Fitness and its role in evolutionary genetics
- Nat Rev Genet 10(8):531-539 (2009)
Although the operation of natural selection requires that genotypes differ in fitness, some geneticists may find it easier to understand natural selection than fitness. Partly this reflects the fact that the word 'fitness' has been used to mean subtly different things. In this Review I distinguish among these meanings (for example, individual fitness, absolute fitness and relative fitness) and explain how evolutionary geneticists use fitness to predict changes in the genetic composition of populations through time. I also review the empirical study of fitness, emphasizing approaches that take advantage of recent genetic and genomic data, and I highlight important unresolved problems in understanding fitness. - Evolutionary analysis of the dynamics of viral infectious disease
- Nat Rev Genet 10(8):540-550 (2009)
Many organisms that cause infectious diseases, particularly RNA viruses, mutate so rapidly that their evolutionary and ecological behaviours are inextricably linked. Consequently, aspects of the transmission and epidemiology of these pathogens are imprinted on the genetic diversity of their genomes. Large-scale empirical analyses of the evolutionary dynamics of important pathogens are now feasible owing to the increasing availability of pathogen sequence data and the development of new computational and statistical methods of analysis. In this Review, we outline the questions that can be answered using viral evolutionary analysis across a wide range of biological scales. - Mechanisms of change in gene copy number
- Nat Rev Genet 10(8):551-564 (2009)
Deletions and duplications of chromosomal segments (copy number variants, CNVs) are a major source of variation between individual humans and are an underlying factor in human evolution and in many diseases, including mental illness, developmental disorders and cancer. CNVs form at a faster rate than other types of mutation, and seem to do so by similar mechanisms in bacteria, yeast and humans. Here we review current models of the mechanisms that cause copy number variation. Non-homologous end-joining mechanisms are well known, but recent models focus on perturbation of DNA replication and replication of non-contiguous DNA segments. For example, cellular stress might induce repair of broken replication forks to switch from high-fidelity homologous recombination to non-homologous repair, thus promoting copy number change. - The genetics of quantitative traits: challenges and prospects
- Nat Rev Genet 10(8):565-577 (2009)
A major challenge in current biology is to understand the genetic basis of variation for quantitative traits. We review the principles of quantitative trait locus mapping and summarize insights about the genetic architecture of quantitative traits that have been obtained over the past decades. We are currently in the midst of a genomic revolution, which enables us to incorporate genetic variation in transcript abundance and other intermediate molecular phenotypes into a quantitative trait locus mapping framework. This systems genetics approach enables us to understand the biology inside the 'black box' that lies between genotype and phenotype in terms of causal networks of interacting genes. - Exploiting and antagonizing microRNA regulation for therapeutic and experimental applications
- Nat Rev Genet 10(8):578-585 (2009)
New technologies are emerging that utilize artificial microRNA (miRNA) target sites to exploit or inhibit endogenous miRNA regulation. This approach has been used to improve cell-specific targeting for gene and stem cell therapy studies and for animal transgenics, and also to reduce the toxicity of oncolytic viruses and to attenuate viral vaccines. Artificial targets have also been used to sponge or decoy miRNAs as a way to study their functions. This article considers the benefits of this approach and design considerations for future studies.
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