The first cell types that form in the mammalian embryo, the trophectoderm and the primitive endoderm, give rise to extraembryonic lineages critical for survival of the embryo in the uterine environment. Recent studies have begun to identify transcription factors and cell signalling pathways important to the establishment and maintenance of these lineages. In some instances, the factors involved are specific to extraembryonic cell types, but in other cases, the same molecules are used elsewhere in the development of the embryo itself. Delineation of embryonic versus extraembryonic function can be achieved by careful use of targeted mutagenesis and chimeric analysis.
Secreted polypeptide signalling molecules of the TGF- superfamily play critical roles during mouse development. There are 20 known members of this diverse family in the mouse, including the TGF-s, inhibin/activins, BMPs, GDFs, and nodal. Mutations in genes for some of these ligands have been identified or created by targeted mutagenesis. A complex network of binding proteins, proteases, and receptors is involved in the processing, presentation and biological activity of TGF-β-related ligands. It is likely that variations in these modifying factors will explain how different genetic backgrounds can influence the severity and penetrance of mutant phenotypes.
The flagella of the unicellular green alga Chlamydomonas reinhardtii are controlled by a number of sophisticated homeostatic mechanisms which ensure that the flagella are maintained at a specific length, and that each cell has two flagella of equal length. Mutants with defects in flagellar length control have been obtained, defining at least nine genes that are involved in the control of flagellar length and the equality of flagellar length. The active machinery involved in flagellar length control requires that cells precisely measure the length of their flagella and drastically alter flagellar protein production and assembly when necessary to maintain desired lengths.
