bcl-2 deficiency in mice leads to pleiotropic abnormalities: accelerated lymphoid cell death in thymus and spleen, polycystic kidney, hair hypopigmentation, and distorted small intestine.
Transgenic mice homozygously lacking in the bcl-2 gene were generated using homologous recombination in embryonal stem cells. The complete absence of Bcl-2 alpha and -beta 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.
Kamada
S
S
Department of Medical Genetics, Biomedical Research Center, Osaka University Medical School, Yamadaoka, Japan.
Shimono
A
A
Shinto
Y
Y
Tsujimura
T
T
Takahashi
T
T
Noda
T
T
Kitamura
Y
Y
Kondoh
H
H
Tsujimoto
Y
Y
D000015:Abnormalities, Multiple / Q000235:genetics*; D000818:Animals; D016923:Cell Death / Q000235:genetics*; D005260:Female; D017353:Gene Deletion; D006200:Hair Color / Q000235:genetics*; D007421:Intestine, Small / Q000002:abnormalities* / Q000473:pathology; D008297:Male; D051379:Mice; D008809:Mice, Inbred C3H; D008810:Mice, Inbred C57BL; D008822:Mice, Transgenic; D010641:Phenotype; D007690:Polycystic Kidney Diseases / Q000235:genetics* / Q000473:pathology; D011518:Proto-Oncogene Proteins / Q000172:deficiency* / Q000235:genetics; D019253:Proto-Oncogene Proteins c-bcl-2; D013154:Spleen / Q000002:abnormalities* / Q000473:pathology; D013950:Thymus Gland / Q000002:abnormalities* / Q000473:pathology
D011518:Proto-Oncogene Proteins; D019253:Proto-Oncogene Proteins c-bcl-2