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Mouse HNF-3/fork head homolog-1-like gene: structure, chromosomal location, and expression in adult and embryonic kidney.

Screening of a mouse kidney cDNA library with a HNF-3/fork head domain probe revealed cDNA Hfh-1L containing the highly conserved fork head DNA-binding domain. The Hfh1L cDNA shows 92.7% homology at the nucleic acid level with the fork head gene HFH-1 from rat. Southern blot analyses demonstrated that the Hfh-1L gene is highly conserved in a wide variety of species, including goldfish and frog. Sequencing the corresponding genomic clone, we found that the Hfh-1L gene is most likely intronless. By interspecific back-cross analysis, the Hfh-1L gene was localized to mouse chromosome 13. In order to analyze the expression pattern of Hfh-1L, we performed Northern blot analyses and revealed a 2.7-kb transcript in adult kidney and stomach. In situ hybridization experiments of adult mouse kidney showed Hfh-1L expression in the outer medulla of the kidney and the transitional epithelium. In light of the significance of a number of fork head genes in early embryonic development, the pattern of expression during murine embryogenesis was examined by reverse transcriptase-polymerase chain reaction (RT-PCR), and Hfh-1L transcripts were detected in mouse embryos at every stage tested from day 10.5 to 16.5 postconception (p.c.) and in the developing metanephros of 14.5- and 15.5-day p.c. embryos. This expression pattern suggests that the Hfh-1L gene is involved in the development of the kidney.

Amino Acid Sequence↗

Dephrin, a transmembrane ephrin with a unique structure, prevents interneuronal axons from exiting the Drosophila embryonic CNS.

Ephrin/Eph signalling is crucial for axonal pathfinding in vertebrates and invertebrates. We identified the Drosophila ephrin orthologue, Dephrin, and describe for the first time the role of ephrin/Eph signalling in the embryonic central nervous system (CNS). Dephrin is a transmembrane ephrin with a unique N terminus and an ephrinB-like cytoplasmic tail. Dephrin binds and interacts with DEph, the Drosophila Eph-like receptor, and Dephrin and DEph are confined to different neuronal compartments. Loss of Dephrin or DEph causes the abberant exit of interneuronal axons from the CNS, whereas ectopic expression of Dephrin halts axonal growth. We propose that the longitudinal tracts in the Drosophila CNS are moulded by a repulsive outer border of Dephrin expression.

Animals↗

Submicroscopic structure of glycosaminoglycans in osteocyte capsule of human embryonic bone as revealed by polarization microscopy.

Using qualitative and quantitative polarization microscopical techniques, an axiparallel orientation of chondroitin sulfate molecules and collagen fibrils could be detected in the osteocyte capsule of human embryonic and fetal bones. It is suggested that this spatially oriented microstructure plays a role in ana- and catabolic transport processes of the bone tissue.

Bone and Bones↗

Embryonic development of the hirudinid leech Hirudo medicinalis: structure, development and segmentation of the germinal plate.

The germinal plate of 5- to 12-day-old embryos of the leech Hirudo medicinalis consists of an anterior and a posterior sector that differ both structurally and developmentally. The posterior sector includes the five pairs of teloblasts and five paired longitudinal bandlets of stem cells and their descendant blast cells. The mesoteloblast pair and their descendant cells of the m bandlet divide spirally and give rise to bilaterally paired cell clusters. The four ectoteloblast pairs and their descendant cells of the n, o, p and q bandlet pairs divide unidirectionally and give rise to paired one-cell-thick and four-cell-wide ectodermal arches. The developmentally more advanced anterior sector of the germinal plate consists of differentiating ectodermal and mesodermal cells engaged in organogenesis. The mesodermal cell clusters develop into somites, whereas the expanding ectodermal arches develop into nerve cord ganglia and epidermis. Rostrocaudal expansion of somite tissue results in the formation of obliquely oriented intersegmental septa, causing the ganglia to take on an intersegmental distribution. The first sign that formation of body segments has been completed is the appearance of a bilateral gap in the mesodermal bandlet of the posterior sector of the germinal plate. This gap seems to trigger degeneration of the posterior sector of the germinal plate.

Animals↗

Fine structure of the rabbit submandibular gland during the embryonic development.

The development of the submandibular gland has been examined in rabbit embryos from the 22nd day to the birth. The 2 main types of secretory cells, which synthetize dense serous granules or large pale mucous granules can be identified from the 24th day of development. A third type of cells, characterized by granules having different densities, has been identified in the preterminal tracts. The possibility that these cells are similar to some small cell with an highly dilated endoplasmic reticulum found in adult rabbit submandibular glands is discussed.

Animals↗

Functional design in the evolution of embryos and larvae.

A function of development is to put the right kind of cells in the right place at the right time. Other functional analyses help define what is right. As examples, functional analyses offer explanations for the unicellular bottleneck in life histories that necessitates embryos, evolutionary divergences in embryonic cell cycles, conditions permissive of loss of larval structures and consequent change in embryonic development, and the decoupled development of larval bodies and juvenile rudiments. Functional analyses also reveal the specifications required of morphogenesis, hence defining developmental phenomena to be explained.

Animals↗

Stem cells and their derivatives can bypass the requirement of myocardin for smooth muscle gene expression.

The Serum Response Factor (SRF) coactivator myocardin stimulates the transcription of multiple muscle genes during cardiac and smooth muscle development. Mouse embryos lacking myocardin die during the earliest stages of smooth muscle development and fail to express multiple smooth muscle marker genes in the embryonic dorsal aorta and other vascular structures. In this study, we used mutant embryonic stem cell lines to further define the role of myocardin in smooth muscle differentiation and vascular development. Misexpression of myocardin in undifferentiated muscle stem cells resulted in efficient activation of smooth muscle genes, and weaker activation of genes involved in cardiac and skeletal muscle differentiation. Remarkably, myocardin(-/-) embryonic stem cell lines differentiated into smooth muscle cells in vitro, although these cells expressed significantly decreased levels of smooth muscle contractile genes. Moreover, genetically labeled myocardin(-/-) ES cells were able to contribute to smooth muscle lineages in vivo. These results indicate that while myocardin function is sufficient for activation of SRF-dependent muscle gene expression in multiple cell types, myocardin-independent mechanism(s) can suffice for expression in some smooth muscle lineages.

Animals↗

Early molecular specification in the hippocampal rudiment: isolation of genes expressed in a region-specific manner in the embryonic telencephalon.

During development, the structure of the telencephalon is dramatically transformed by region-specific proliferation and differentiation of neuroepithelial cells. To understand mechanisms of morphogenesis in the telencephalon, a search was made for genes expressed in a region-specific manner in the dorsal telencephalon of embryonic rats. Dorso-lateral and dorso-medial portions of the telencephalon were taken from rat fetuses on embryonic day (E) 13. Genes expressed in each portion were compared by a modified differential display method. Among more than 4000 cDNA fragments, four fragments termed M1, M1', M2 and M3 were found only after amplification of cDNAs derived from the dorso-medial portion of the telencephalon. Nucleotide sequence and Northern blot analyses showed that M1 and M1' were identical and that M2 and M3 were related genes. In situ hybridization revealed that M1 was expressed in a restricted portion of the hippocampal rudiment with a sharp boundary. M2 and M3 were expressed in the hippocampal rudiment with a more diffuse boundary than that of M1. Expression of M2 and M3 was also found in the most anterior part of the medial diencephalon with a caudal extension along the dorsal midline. These results suggest that at least two types of molecular specification occur in the dorso-medial telencephalon, contributing to the construction of the hippocampal elements during early stages of development.

Animals↗

Occurrence and distribution of matrix metalloproteinase-2-immunoreactivity in human embryonic tissues.

Tissue development and structure is controlled by dynamic and interactive relationships between cells and the extra-cellular matrix (ECM) which they secrete. We have investigated the occurrence and distribution of metalloproteinase-2 (MMP-2), an enzyme involved in the catabolism of ECM components, in human embryonic tissues by immunocytochemistry. Cells displaying MMP-2 immunoreactivity showed a widespread distribution in human embryonic tissues and organs. Cytoplasmic staining was detected in cells deriving from all three embryonic layers. Although further studies are needed to clarify the possible substrates of MMP-2 in developing tissues, these morphological data lend support to the hypothesis that ECM remodelling and degradation may represent a physiological counterpart of ECM deposition that occur during development.

Epithelium↗

The reeler gene: a clue to brain development and evolution.

Reeler mutant mice are characterized by profuse anomalies of cell positioning in the telencephalic and cerebellar cortices as well as by distinct malformations in non-cortical structures such as the inferior olive, the facial nerve nucleus and other brainstem nuclei. Studies of the embryonic development of these structures reveal that the early cell patterns formed by reeler neurons is consistently affected, so that the reeler gene plays an important role in the development of nerve cell patterns. Comparative studies of cortical development in reptiles suggest further that the mammalian type of cortical architectonics has been acquired progressively during brain evolution, and reveal some similarities in early cortical organization between reeler and reptilian, particularly chelonian, embryos, most notably the presence of an inverted gradient of cortical histogenesis. These observations point to a possible role of the reeler gene in cortical evolution. Although the factors responsible for the formation of neural cell patterns are largely unknown, most data point to the importance of cell-cell interactions. Cell-interaction molecules have probably been acquired during brain evolution and the reeler gene could act by perturbing, directly or indirectly, such cell interactions. The characterization and thus the cloning of the reeler gene is therefore important for our understanding of brain development. Recent data on the fine chromosomal mapping of the mutation prior to its positional cloning are reported.

Animals↗

Shh expression is required for embryonic hair follicle but not mammary gland development.

The embryonic mammary gland and hair follicle are both derived from the ventral ectoderm, and their development depends on a number of common fundamental developmental pathways. While the Hedgehog (Hh) signaling pathway is required for hair follicle morphogenesis, the role of this pathway during embryonic mammary gland development remains undetermined. We demonstrate here that, unlike the hair follicle, both Shh and Ihh are expressed in the developing embryonic mouse mammary rudiment as early as E12.5. In Shh(-/-) embryos, hair follicle development becomes arrested at an early stage, while the mammary rudiment, which continues to express Ihh, develops in a manner indistinguishable from that of wild-type littermates. The five pairs of mammary buds in Shh(-/-) female embryos exhibit normal branching morphogenesis at E16.5, forming a rudimentary ductal structure identical to wild-type embryonic mammary glands. We further demonstrate that loss of Hh signaling causes altered cyclin D1 expression in the embryonic dermal mesenchyme. Specifically, cyclin D1 is expressed at E14.5 principally in the condensed mesenchymal cells of the presumptive hair follicles and in both mesenchymal and epithelial cells of the mammary rudiments in wild-type and Shh-deficient embryos. By E18.5, robust cyclin D1 expression is maintained in mammary rudiments of both wild-type and Shh-deficient embryos. In hair follicles of wild-type embryos by E18.5, cyclin D1 expression switches to follicular epithelial cells. In contrast, strong cyclin D1 expression is observed principally in the mesenchymal cells of arrested hair follicles in Shh(-/-) embryos at E18.5. These data reveal that, despite the common embryonic origin of hair follicles and mammary glands, distinct patterns of Hh-family expression occur in these two tissues. Furthermore, these data suggest that cyclin D1 expression in the embryonic hair follicle is mediated by both Hh-independent and Hh-dependent mechanisms.

Animals↗

Gap junction formation during development of the mouse lens.

We have identified a 60 kDa membrane protein (MP60) as a component of the mouse cortical lens fiber gap junction and a monoclonal antibody recognizing this protein has been used to establish the temporal and spatial patterns of gap junction formation during development of the mouse lens. The initial expression of MP60 during embryonic development of the mouse lens correlates with primary fiber elongation and is first seen on the luminal aspect of the extending cells. About 2 days after birth, the relatively large, antibody-positive macular structures characteristic of late embryonic fiber cells begin to disperse into progressively smaller structures within a centrally located region of the lens. This change in the staining pattern with antibody directed against MP60 is consistent with the dispersion of gap junction plaques as confirmed by freeze fracture analysis. Around 5 days after birth, the 60 kDa gap junctional protein in this central region of the lens undergoes a modification resulting in the alteration to the epitope for the monoclonal antibody and a consequent loss of immunorecognition. Our results suggest that gap junctions in the central region of the developing mouse lens undergo sequential changes in immunoreactivity which may reflect potentially distinct functional phases of intercellular communication.

Age Factors↗