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The laboratory mouse is widely considered the model organism of choice for studying the diseases of humans, with whom they share 99% of their genes. A distinguished history of mouse genetic experimentation has been further advanced by the development of powerful new tools to manipulate the mouse genome. The recent launch of several international initiatives to analyse the function of all mouse genes through mutagenesis, molecular analysis and phenotyping underscores the utility of the mouse for translating the information stored in the human genome into increasingly accurate models of human disease.
Scientists are seeking permission to generate human embryonic stem cells to study disease by introducing human genetic material into an animal oocyte. This has raised ethical questions that centre on whether the entities being generated are actually human. The answer to these questions will determine how this area of research will be regulated and whether such work will be legal. The function of the extra-nuclear mitochondrial genome lies at the heart of these issues and forms the focus of this commentary.
The irreversibility of cell-cycle transitions is commonly thought to derive from the irreversible degradation of certain regulatory proteins. We argue that irreversible transitions in the cell cycle (or in any other molecular control system) cannot be attributed to a single molecule or reaction, but that they derive from feedback signals in reaction networks. This systems-level view of irreversibility is supported by many experimental observations.
The nucleosome surface is decorated with an array of enzyme-catalysed modifications on histone tails. These modifications have well-defined roles in a variety of ongoing chromatin functions, often by acting as receptors for non-histone proteins, but their longer-term effects are less clear. Here, an attempt is made to define how histone modifications operate as part of a predictive and heritable epigenetic code that specifies patterns of gene expression through differentiation and development.
