In the last four years, a large number of genes encoding g-catenin. The results of all three cadherin mutations are milder than might have been expected from earlier data. E-molecules involved in cell adhesion have been mutated by the methods of homologous recombination in ES cells (see cadherin was originally described as a molecule involved in compaction of the morula-stage embryo. However, E-Tables 1–3). Many of these targeted mutations have been very informative about the roles of various cell adhesion cadherin-null mutant embryos undergo initial compaction normally, apparently because of expression of E-cadherin molecules in development, although many questions remain unanswered. In this brief review, I will not attempt from maternal (//0) mRNA. Subsequently, the cells dissociate, lose polarity, fail to form a blastocyst or trophectoto summarize the results of each mutation; readers are referred to the primary references for details. This is partly derm, and fail to implant. These latter results confirm expectations based on earlier expression and antibody inhibifor reasons of space but mostly because brief summaries do not do justice to the information which can be gleaned from tion data. The unexpected compaction can be explained by the maternal mRNA. The N-cadherin-null mutant emcareful study of each mutant line. Indeed, such summaries can often be misleading and have frequently led to miscon- bryos, somewhat surprisingly, form neural tubes, somites, and myocardium, although all subsequently become defecceptions about the value of targeted mutations. Mutations which unexpectedly allow viability have often been dis- tive, leading to early embryonic lethality. All three tissues express N-cadherin strongly and a simplistic prediction missed as uninformative. As I hope to illustrate, this is a simplistic view. The product of the reductionist molecular would have been that they would not form in its absence. The fact that they do indicates that some other adhesion approach which produces a targeted mutation is a complex molecule (s) is sufficient for early morphogenesis of these organism and only careful, detailed analyses reveal all the structures. This sort of result raises the possibilities of over-information that such mutations can yield. Furthermore, lapping functions and compensation, which will be disall systems involve interactions among diverse and related cussed further below. Expression of other classical cadhergenes and it is frequently the case that comparisons and ins was not detected but, of course, this does not rule out combinations among different mutants are necessary to prononclassical cadherins or unknown molecules. Perhaps duce a deeper understanding. Given the relatively early most surprisingly, P-cadherin-null mice are viable and ferstage of the analyses, it is inevitable that the mutations tile, despite expression of P-cadherin in several organ sysdescribed to date raise as many questions as they answer. tems, including strong expression in the deciduum.