TL;DR: It is concluded that the cell lineage itself, complex as it is, plays an important role in determining cell fate and is demonstrated to demonstrate substantial cell autonomy in at least some sections of embryogenesis.
TL;DR: Stages of Drosophila Embryogenesis, some Aspects of Segmentation, and a Fate Map of the Blastoderm are described.
Abstract: A Summary of Drosophila Embryogenesis.- Stages of Drosophila Embryogenesis.- Mesoderm Development.- Musculature.- Circulatory System and Fat Body.- Macrophages.- The Gut and its Annexes.- Epidermis.- Peripheral Nervous System.- The Peripheral Nervous System.- Central Nervous System.- Tracheal Tree.- The Gonads.- The Pattern of Embryonic Cell Divisions.- Morphogenetic Movements.- Cephalogenesis.- Some Aspects of Segmentation.- A Fate Map of the Blastoderm.
TL;DR: It is reported that mice homozygous for a disrupted p63 gene have major defects in their limb, craniofacial and epithelial development, and results indicate that p63 is critical for maintaining the progenitor-cell populations that are necessary to sustain epithelialDevelopment and morphogenesis.
Abstract: The p63 gene, a homologue of the tumour-suppressor p53, is highly expressed in the basal or progenitor layers of many epithelial tissues. Here we report that mice homozygous for a disrupted p63 gene have major defects in their limb, craniofacial and epithelial development. p63 is expressed in the ectodermal surfaces of the limb buds, branchial arches and epidermal appendages, which are all sites of reciprocal signalling that direct morphogenetic patterning of the underlying mesoderm. The limb truncations are due to a failure to maintain the apical ectodermal ridge, a stratified epithelium, essential for limb development. The embryonic epidermis of p63-/- mice undergoes an unusual process of non-regenerative differentiation, culminating in a striking absence of all squamous epithelia and their derivatives, including mammary, lacrymal and salivary glands. Taken together, our results indicate that p63 is critical for maintaining the progenitor-cell populations that are necessary to sustain epithelial development and morphogenesis.
TL;DR: Results provide direct genetic evidence that BMP-4 is essential for several different processes in early mouse development, beginning with gastrulation and mesoderm formation.
Abstract: Bone morphogenetic protein-4 (BMP-4) is a member of the TGF-beta superfamily of polypeptide signaling molecules, closely related to BMP-2 and to Drosophila decapentaplegic (DPP). To elucidate the role of BMP-4 in mouse development the gene has been inactivated by homologous recombination in ES cells. Homozygous mutant Bmp-4tm1blh embryos die between 6.5 and 9.5 days p.c., with a variable phenotype. Most Bmp-4tm1blh embryos do not proceed beyond the egg cylinder stage, do not express the mesodermal marker T(Brachyury), and show little or no mesodermal differentiation. Some homozygous mutants develop to the head fold or beating heart/early somite stage or beyond. However, they are developmentally retarded and have truncated or disorganized posterior structures and a reduction in extraembryonic mesoderm, including blood islands. These results provide direct genetic evidence that BMP-4 is essential for several different processes in early mouse development, beginning with gastrulation and mesoderm formation. Moreover, in the presumed absence of zygotic ligand, it appears that homozygous mutants can be rescued partially by related proteins or by maternal BMP-4.
TL;DR: The potential to generate virtually any differentiated cell type from embryonic stem cells (ESCs) offers the possibility to establish new models of mammalian development and to create new sources of cells for regenerative medicine, but it is essential to be able to control ESC differentiation and to direct the development of these cells along specific pathways.