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Biomedical subjects

S F Gilbert

Publications and source records attributed to S F Gilbert.

At least 19 recordsLinked to original sources
PubMed1998

Human cloning.

Explore the source record for details and available documents.

Animals↗
PubMed1998

Bearing crosses: a historiography of genetics and embryology.

As we construct the fusion of medical embryology and medical genetics, it is important to be aware of how the history of genetics has been written to exclude embryology. This article looks at the rhetoric of genetics and how that rhetoric fits a paradigm of supersessionism. Supersessionism is often seen in the history of religion when one sect claims superiority to the original sect from whence it emerged. Such supersessionism portrays embryology as a failed research program, one that genetics now has saved. In some instances, biblical references have alluded to the failed nature of embryology. Although this article does not criticize the data of genetics, it takes issue with the historiography used by geneticists and seeks to show that the mergers between genetics and embryology are those between two equal partners and not between an inferior and superior member.

Animals↗
PubMed1996

Resynthesizing evolutionary and developmental biology.

A new and more robust evolutionary synthesis is emerging that attempts to explain macroevolution as well as microevolutionary events. This new synthesis emphasizes three morphological areas of biology that had been marginalized by the Modern Synthesis of genetics and evolution: embryology, macroevolution, and homology. The foundations for this new synthesis have been provided by new findings from developmental genetics and from the reinterpretation of the fossil record. In this nascent synthesis, macroevolutionary questions are not seen as being soluble by population genetics, and the developmental actions of genes involved with growth and cell specification are seen as being critical for the formation of higher taxa. In addition to discovering the remarkable homologies of homeobox genes and their domains of expression, developmental genetics has recently proposed homologies of process that supplement the older homologies of structure. Homologous developmental pathways, such those involving the wnt genes, are seen in numerous embryonic processes, and they are seen occurring in discrete regions, the morphogenetic fields. These fields (which exemplify the modular nature of developing embryos) are proposed to mediate between genotype and phenotype. Just as the cell (and not its genome) functions as the unit of organic structure and function, so the morphogenetic field (and not the genes or the cells) is seen as a major unit of ontogeny whose changes bring about changes in evolution.

Animals↗
PubMed1995

Activin disrupts epithelial branching morphogenesis in developing glandular organs of the mouse.

We report that activin profoundly alters epithelial branching morphogenesis of embryonic mouse salivary gland, pancreas and kidney rudiments in culture, indicating that it may play a role as a morphogen during mammalian organogenesis. In developing pancreas and salivary gland rudiments, activin causes severe disruption of normal lobulation patterns of the epithelium whereas follistatin, an activin-binding protein, counteracts the effect of activin. In the kidney, activin delays branching of the ureter bud and reduces the number of secondary branches. TGF-beta induces a pattern of aberrant branching in the ureter bud derived epithelium distinct from that seen for activin. Reverse-transcriptase polymerase chain reaction, Northern hybridization and in situ hybridization analyses indicate that these developing tissues express the mRNA transcripts for activin subunits, follistatin or activin receptors. Our results are suggestive of a potential role for the activin-follistatin system as an intrinsic regulator of epithelial branching morphogenesis during mammalian organogenesis.

Activin Receptors↗
PubMed1992

Differential expression of gap junction mRNAs and proteins in the developing murine kidney and in experimentally induced nephric mesenchymes.

The expression of three gap junction (GJ) proteins, alpha 1 (Cx43), beta 1 (Cx32), and beta 2 (Cx26), and their transcripts were examined during the ontogeny of the mouse and rat kidney. These proteins were expressed in two non-overlapping patterns. The alpha 1 GJ protein was first observed in mesenchymal cells in the 12-day mouse kidney. By day 14 and thereafter, the alpha 1 protein was detected in the transient S-shaped bodies, but not in the podocytes of the maturing glomeruli. After birth the antigen was retained in a small subset of secretory tubules. The beta 1 and beta 2 GJ proteins were similar in their developmental patterns. They were first detected in a small subset of secretory tubules in the subcortical zone of day 17 embryos. These tubules were identified by immunohistochemical markers to be proximal. At birth, practically all proximal tubules expressed the two antigens. This analysis of GJ proteins was consistent with the results of S1 nuclease protection assays showing that, while the alpha 1 mRNA appeared early during kidney development and declined around birth, the two beta mRNAs appeared later and became intensified during the last days of intrauterine development. In experimentally induced metanephric mesenchymes, a transient expression of the alpha 1 GJ protein was seen during the segregation of the tubular anlagen. beta 1 and beta 2 GJ proteins were not detected in such induced mesenchymes cultivated up to 7 days. These observations provide evidence for the cell-specific utilization of different GJ genes during different stages of kidney organogenesis. The alpha 1 gene is activated during the early segregation of the secretory tubule and might contribute to its compartmentalization, while the beta 1 and beta 2 gene products are not detected until advanced stages of development. The latter gene products might be correlated with the physiological activity of the proximal tubules in vivo, as they are not expressed in experimentally induced tubules detectable with markers for proximal tubules.

Animals↗
PubMed1990

Immunocytochemical analysis of embryonic compartmentation with a monoclonal antibody against a cytokeratin-related antigen.

Mab 113F4, a monoclonal antibody recognizing an antigen in the outer synaptic layer of the chick neural retina, also recognizes an antigen appearing in all three germ layers of the gastrulating chick embryo. However, as neurulation proceeds, the antigen is down-regulated in three distinct patterns. First, the antigen is lost specifically from those trunk ectodermal cells destined to form the neural plate and, later, the neural tube. It remains absent from any neural derivative until day 13 when it appears in the outer synaptic layer of the neural retina, coincident with synaptogenesis in this region. Second, the entirety of the head ectoderm loses this antigen as the head lifts off the blastoderm. This down-regulation is followed later by a similar loss of antigen expression in the trunk ectoderm. Third, expression in the mesoderm becomes limited to the lateral plate and extraembryonic epithelia. Endodermal derivatives continue to express the antigen throughout development. Antigen 113F4 is localized within the cytoplasm and is organized in a fibrillar pattern. The intracellular localization of this antigen and its characteristic spatio-temporal tissue distribution are consistent with the antigen being a cytokeratin or cytokeratin-related antigen. The changes in tissue distribution suggest a possible role in tissue modelling in response to inductive interactions during development.

Animals↗
PubMed1986

Selective culture medium enhances survival of neuroblasts from postnatal rodent brain.

One of the major limitations to the study of the development of the nervous system in aneuploid mammalian embryos is that the aneuploid condition is usually lethal in utero. Liveborn aneuploid individuals often succumb rapidly because they have a constellation of malformations incompatible with postnatal survival. We have developed a selective tissue culture medium (D-val) which can be used with fetal calf serum or in a serum-free defined composition and which permits neuroblasts and glioblasts present in postnatal rodent (rat, mouse) brain to proliferate and differentiate in vitro. These cells contain D-amino acid oxidase, but fibroblasts do not. In this medium, fibroblasts cannot grow and are eliminated from the cultures without the use of deleterious compounds such as antimitotic or chemotherapeutic agents. With this medium, cultures containing neuroblasts can be established from normal rat and mouse brain as late as postnatal days 11-20. Cultures with significant numbers of proliferating cells can also be established from perinatal aneuploid mouse embryos, 'rescuing' the cells for further study.

Animals↗
PubMed1985

Onset of paternal and maternal Gpi-1 expression in preimplantation mouse embryos.

The initial activation of the glucose phosphate isomerase gene, Gpi-1, was studied in mouse embryos produced by transplanting pronuclei between two strains of mice differing in alleles for this enzyme. Protein isozymes encoded by the embryonic cell nuclei were first detected on Day 4 of embryogenesis, and the maternal and paternal genes are seen to be activated simultaneously. Comparison of isozymes produced by these nuclear-transfer embryos and by F1 embryos from these two strains suggests the absence of oocyte mRNA for GPI-1 at the time when these genes are first activated. Thus, the GPI-1 present is derived from newly transcribed mRNA contributed by both maternal and paternal genes. The relative proportion of maternal cytoplasmic GPI-1 enzyme declines from Day 3 to Day 6, such that on Day 6, almost no oocyte GPI-1 is detected.

Alleles↗