Transgenic mice homozygously lacking in the bcl-2 gene were generated using homologous recombination in embryonal stem cells. The complete absence of Bcl-2α and -β proteins did not interfere with normal embryonic development. Abnormalities became evident after birth, although the severity varied among homozygous null mice. bcl-2-/- mice displayed pleiotropic abnormalities similar to those in the previously described bcl-2-/- mice, including growth retardation, smaller ears, short lives, polycystic kidney, atrophic thymus and spleen with accelerated apoptotic cell death of lymphocytes, and hair hypopigmentation in the second hair follicle cycle. Our bcl-2-/- mice also revealed novel defects in the small intestine, characterized by retarded development, accelerated exfoliation of epithelial cells, and very few mitotic progenitor cells.


Supported in part by a Grant-in-Aid for the comprehensive 10-Year Strategy for Cancer Control from the Ministry of Health and Welfare, for Scientific Research on Priority Areas, and for Scientific Research from the Ministry of Education, Science and Culture of Japan, and Uehara Memorial Foundation; and by a grant from Osaka University.

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