Mice deficient for Rb are nonviable and show defects in neurogenesis and haematopoiesis

Article Abstract:

Mouse embryos lacking the nuclear phosphoprotein (Rb) for the retinoblastoma (RB) tumor-suppressor gene die before the 16th embryonic day and display an array of genetic defects while alive. These defects affect the hematopoietic system which produces an abnormal proliferation of immature nucleated erythrocytes and the nervous system where ectopic mitoses and massive cell death occur. The finding that injecting human RB mini-transgene into the mutant mice rectifies the abnormalities proves that Rb is required for normal embryonic growth in mice.

Causes of, Genetic aspects, Genetic disorders, Phosphoproteins, Retinoblastoma

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p63 is a p53 homologue required for limb and epidermal morphogenesis

Article Abstract:

The function of p63, a homologue of the p53 tumour suppressor, during embryogenesis has been investigated by mutating the p63 gene using embryonic stem cell technology. It was established that p63-deficient newborn mice demonstrate clear limb and skin defects. The downstream targets of p63 probably involve direct or indirect activation of factors associated with ectodermal-mesenchymal communication, which are needed for morphogenesis of the tooth, hair follicle, apical ectodermal ridge and mammary bud.

Morphogenesis

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Rescue of embryonic lethality in Mdm2-deficient mice by absence of p53

Article Abstract:

The Mdm2 proto-oncogene regulates the p53 activity during the embryonic development. This is probably because of the activity of p53 in the absence of Mdm2, which leads to the arrest of the cell cycle at the G1 stage during embryo development. On the other hand, the Mdm2/p53 null mutants show normal morphogenesis. A complex between the Mdm2 oncoprotein and the p53 tumor-suppressor protein is responsible for p53-mediated transregulation of the gene expression.

Observations, Gene expression, Mice as laboratory animals, House mouse, Lethal mutation

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