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Vol. 13, No. 6, pp. 718-728, March 15, 1999
1 Fred-Hutchinson Cancer Research Center, Seattle,
Washington 98109 USA; 2 Institut de Biologie et de
Chimie der Proteines, 69376 Lyon Cedex 07, France;
3 Department of Animal and Food Sciences, University of
Delaware, Newark, Delaware 19717 USA; 4 Departments of Medicine and
Pathology, University of Washington, Seattle, Washington 98109 USA
Apoptotic cell death is developmentally regulated in the chicken
bursa of Fabricius. Although apoptosis is low in the embryonic bursa,
cell death increases markedly after hatching. The expression of Bcl2
family cell death antagonists was examined to identify the genes that
regulate bursal cell apoptosis. The expression of Bcl-xL, A1, and Mcl1
was detected in both embryos and hatched birds, whereas Nr13 was
expressed at high levels in embryonic bursa, and decreased
significantly after hatching, correlating inversely with apoptosis. The
oncogene v-reland phorbol myristate acetate, two known
inhibitors of bursal cell apoptosis, induced Nr13 expression.
Overexpression of Nr13 in DT40 bursal lymphoma cells protected them
from low serum-induced apoptosis. The mechanism of inhibition of
apoptosis by Nr13 is likely to involve a critical BH4 domain and
interaction with death agonist Bax. Deletion of the BH4 domain
converted Nr13 into a death agonist. Bax coimmunoprecipitated with Nr13
and Bax was induced, whereas Nr13 levels diminished when bursal
lymphoblasts were induced to apoptosis by dispersion. Bursal
transplantation studies demonstrated that Nr13 could prevent the in
vivo programmed elimination of bursal stem cells after hatching,
suggesting that Nr13 plays a role in maintaining bursal stem cells.
[Key Words: Nr13; apoptosis; bursa; transplant; stem cells]
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