Developmental regulation of human fetal-to-adult globin gene switching in transgenic mice

Article Abstract:

Different types of the human beta-globin genes, which code for the hemoglobin molecule, are expressed in the different stages of development: embryo, fetal and adult. The mechanism which allows for the switching of the expression of one type to another type is complicated and involves the regulation of gene expression through a sequence of DNA (deoxyribose nucleic acid) known as the locus activating region (LAR). The LAR is responsible for the high level of globin gene expression. Transgenic mice are mice that have been injected with foreign DNA at the embryo stage. It has been shown that transgenic mice that contain the human fetal and adult globin genes, without the LAR, express the genes during the proper times in development. When transgenic mice contain either the human fetal or adult globin gene, each linked to the LAR, the genes are expressed throughout development. The LAR presumably overrides any type of developmental control mechanism. In contrast, transgenic mice that contain both a fetal and an adult globin gene linked to one LAR sequence undergo the switch from the expression of fetal to adult globin. This indicates that only one of the genes can interact with the LAR regulatory sequence, which results in the expression of only one gene at a time. This study adds to the understanding of the control of gene expression, which may lead to the manipulation and control of gene expression in various disease states. (Consumer Summary produced by Reliance Medical Information, Inc.)

Genetic engineering, Hemoglobin, Hemoglobins, Erythrocytes, Red blood cells, Genetically modified mice

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Failure of blood-island formation and vasculogenesis in Flk-1-deficient mice

Article Abstract:

Receptor tyrosine kinase Flk-1 deficient mice can be generated by disruption of the gene using homologous recombination in embryonic stem (ES) cells to confirm Flk-1's essential role in endothelial development and early hematopoiesis. Due to an early defect in the development of hematopoietic and endothelial cells, Flk-1 deficient embryos die in utero between 8.5 days and 9.5 days post-coitum. Organized blood vessels were not observed at any stage in the embryo or yolk sac and only reduced levels of hematopoietic progenitors were observed. AT 7.5 days, Yolk-sac blood islands were absent.

Hematopoiesis, Hemostasis

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Reduced cell motility and enhanced focal adhesion contact formation in cells from FAK-deficient mice

Article Abstract:

Mutant mice embryos in which the focal adhesion kinase (FAK), a protein tyrosine kinase, is absent show poor development of mesoderm because of retarded motility of cells. The anteroposterior axis, notochord and somite are not formed while the head mesenchyme becomes involuted. However, formation of the head, lateral, and extra-embryonic mesenchyme remains normal. The absence of FAK also increases the formation of focal adhesions which causes rise in tyrosine phosphorylation in many proteins.

Observations, Mutation (Biology), Mutation, Protein tyrosine kinase, Protein-tyrosine kinase, Cell proliferation

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