Thank you for visiting nature.com. You are using a browser version with
limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser (or turn off
compatibility mode in Internet Explorer). In the meantime, to ensure continued support, we are displaying the site
The publication of the draft sequence of the mouse genome creates a powerful new resource for the biomedical community. Access to the sequence will undoubtedly improve the ways in which the various reagents and tools of mouse biology are used for understanding the molecular basis for human physiology, development and disease.
A mouse model for familial adenomatous polyposis has been used to distinguish between possible mechanisms leading to loss of function of the Apc tumor-suppressor gene. Somatic recombination rather than chromosome loss associated with genetic instability is the primary cause of these cancers. Moreover, the data suggest that interphase nuclear architecture is a key factor in facilitating this process.
Individuals display morphological variation when genetic buffering is reduced, allowing phenotypic differences to be selected for during successive generations. A new study shows that perturbations of chromatin-inheritance genes uncover morphological variation, and epigenetic variants can be rapidly selected. This finding extends our understanding of the means by which phenotypic variation is generated and brings chromatin inheritance into the realm of multigenic traits.
The spatially and temporally coordinated interaction between migratory cardiac precursors, endothelial cells and myogenic precursors leads to the formation of the highly differentiated cell lineages in the heart. In a new study, conditional mouse mutants are used to show that Nf1 signaling in cardiac endothelium is essential for proper heart formation.
Theories of cancer biology have long held that the metastatic process originates with rare cells within the primary tumor. A new study using expression array analysis has identified a molecular signature of metastatic potential within the bulk of the primary tumor. This suggests that the majority of tumor cells have the potential to metastasize and presents exciting clinical and therapeutic applications.