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One promising way of attempting to understand the complexity of biological processes is to model them mathematically. Such models can help predict the wider biological effects of local interactions and are now producing testable hypotheses about the workings of developmental systems.
Genome-wide technologies, functional experimentation in model systems and clinical validation are beginning to identify genetic and epigenetic alterations that underlie metastatic disease. These genetic determinants are distinct from those that mediate malignant transformation and can be classified into metastasis initiation, metastasis progression and metastasis virulence genes.
Animal models are crucial for understanding the pathogenesis of human disease and provide a system in which to develop and test new therapies. The zebrafish offers unique advantages over other vertebrates and is therefore rapidly emerging as a model organism for a wide range of human diseases, both genetic and acquired, and for therapeutic drug discovery and development.
Successful gastrulation depends on a complex pattern of signalling and gene expression in the early embryo. Uniquely in mammals, this involves both embryonic and extraembryonic tissue. This Review examines how lineages are specified and cell movements are co-ordinated in the early mouse embryo.
Reduction in gene flow between varieties is part of the process of speciation. One underappreciated reason for such a reduction is hybrid necrosis — when the hybrid offspring have phenotypes that resemble the results of pathogen attack and environmental stress.
Did the main features of eukaryotes, including endocytosis, develop before the adoption of endosymbionts? Or was their evolution triggered by an interaction between two typical prokaryotic cells, one of which became the host and the other the endosymbiont? Christian de Duve re-examines this important question in the light of cell-biological and phylogenetic data.
