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Development, Vol 120, Issue 10 3033-3042, Copyright © 1994 by Company of Biologists
JOURNAL ARTICLES |
M Gonzalez-Garcia, R Perez-Ballestero, L Ding, L Duan, LH Boise, CB Thompson and G Nunez
Department of Pathology, University of Michigan Medical School, Ann Arbor 48109, USA.
Most examples of cell death in animals are controlled by a genetic program that is activated within the dying cell. The apoptotic process is further regulated by a set of genes that act as repressors of cell death. Of these, bcl-2 is expressed in a variety of embryonic and postnatal tissues which suggests a critical role for bcl-2 in organogenesis and tissue homeostasis. Surprisingly, mutant mice with targeted disruption of bcl-2 appear normal at birth and complete maturation of lymphoid tissues before succumbing to fulminant lymphopenia and polycystic renal disease by 2-5 weeks of age. This suggests that there may be genes other than bcl-2 that can regulate apoptosis during development. To begin to investigate this possibility, we have cloned and characterized the murine bcl-x gene, whose human counterpart displays striking homology to bcl-2. The predicted murine bcl-xL gene product exhibits a high level of amino acid identity (97%) to its human counterpart. Just like Bcl-2, the murine bcl-xL gene product can act as a dominant inhibitor of cell death upon growth factor withdrawal. In addition, the bulk of the bcl-xL product localizes to the periphery of mitochondria as assessed by a bcl-xL-tag expression system, suggesting that both Bcl-2 and Bcl-xL proteins prevent cell death by a similar mechanism. bcl-xL is the most abundant bcl-x mRNA species expressed in embryonic and adult tissues. The levels of bcl-xL mRNA appear higher than those of bcl-2 during embryonal development and in several adult organs including bone marrow, brain, kidney and thymus. In addition to bcl-xL, we have identified another form of bcl-x mRNA, bcl-x beta, that results from an unspliced bcl-x transcript. bcl-x beta mRNA is expressed in various embryonic and postnatal tissues. Surprisingly, the expression of bcl-xS (a negative regulator of programmed cell death) was undetectable by a sensitive S1-nuclease assay and polymerase chain reaction analysis of mouse tissues. Based on its tissue and developmental patterns of expression, it appears that bcl-x may play an important role in the regulation of cell death during development and tissue homeostasis.
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F. W. H. Ng and G. C. Shore Bcl-XL Cooperatively Associates with the Bap31 Complex in the Endoplasmic Reticulum, Dependent on Procaspase-8 and Ced-4 Adaptor J. Biol. Chem., February 6, 1998; 273(6): 3140 - 3143. [Abstract] [Full Text] [PDF]
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P. A. Gregoli and M. C. Bondurant The Roles of Bcl-XL and Apopain in the Control of Erythropoiesis by Erythropoietin Blood, July 15, 1997; 90(2): 630 - 640. [Abstract] [Full Text] [PDF]
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M. Deshmukh and E. M. Johnson Jr. Programmed Cell Death in Neurons: Focus on the Pathway of Nerve Growth Factor Deprivation-Induced Death of Sympathetic Neurons Mol. Pharmacol., June 1, 1997; 51(6): 897 - 906. [Abstract] [Full Text]
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Y.-T. Hsu and R. J. Youle Nonionic Detergents Induce Dimerization among Members of the Bcl-2 Family J. Biol. Chem., May 23, 1997; 272(21): 13829 - 13834. [Abstract] [Full Text] [PDF]
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H. W. Findley, L. Gu, A. M. Yeager, and M. Zhou Expression and Regulation of Bcl-2, Bcl-xl, and Bax Correlate With p53 Status and Sensitivity to Apoptosis in Childhood Acute Lymphoblastic Leukemia Blood, April 15, 1997; 89(8): 2986 - 2993. [Abstract] [Full Text] [PDF]
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L. del Peso, V. M. Gonzalez, N. Inohara, R. E. Ellis, and G. Nunez Disruption of the CED-9{middle dot}CED-4 Complex by EGL-1 Is a Critical Step for Programmed Cell Death in Caenorhabditis elegans J. Biol. Chem., August 25, 2000; 275(35): 27205 - 27211. [Abstract] [Full Text] [PDF]
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