Inactivation of mouse Hus1 results in genomic instability and impaired responses to genotoxic stress

Article Abstract:

Mouse Hus1 inactivation has been found to result in genomic instability in an evolutionarily conserved way, and worsened genotoxic stress responses. Inactivation of Hus1 brings on mid-gestational embryo death from apoptosis and defective development of essential extra-embryonic tissues. Embryonic fibroblasts without Hus1 do not proliferate in vitro. Inactivation of P21 lets Hus1-deficient cells continue to grow. With no Hus1 and no p21, cells have significantly raised sensitivity to ultraviolet light and to hydroxyurea, a DNA replication inhibitor. They have only slightly increased sensitivity to ionizing radiation.

Usage, Cell cycle, Mice, mutant strains, Mutant mice, Hydroxyurea

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Hypersensitivity to DNA damage leads to increased apoptosis during early mouse development

Article Abstract:

Hypersensitivity to DNA damage leads to increased apoptosis during early mouse development. Greater apoptosis in early mouse development results from hypersensitivity to DNA damage. The hypersensitivity is a cell fate-dependent mechanism to ensure genome integrity in a period of very great proliferation and differentiation seen in gastrulation in mice.

Embryology, Experimental, Embryological research, Irradiation, Germ cells, Gastrulation

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Loss of Daxx, a promiscuously interacting protein, results in extensive apoptosis in early mouse development

Article Abstract:

Daxx, a promiscuously interacting protein, the loss of which brings extensive apoptosis in early development in mice, is discussed based on generation of a Daxx-deficient mouse for study of the role of Daxx in vivo, from which it was expected that information about a hyperproliferative disorder would come. Daxx does not seem to promote Fas-induced cell death but to directly or indirectly suppress early-embryo apoptosis.

Mice, Mice (Rodents), Developmental genetics, Mammals, Allosteric proteins, Genetic research

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