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bcl-x is expressed in embryonic and postnatal neural tissues and functions to prevent neuronal cell death
M González-García1, I García, L Ding
1Department of Pathology and Anatomy, University of Michigan Medical School, Ann Arbor 48109, USA.
Abstract:
Previous studies have implicated the bcl-2 protooncogene as a potential regulator of neuronal survival. However, mice lacking functional bcl-2 exhibited normal development and maintenance of the central nervous system (CNS). Since bcl-2 appears dispensable for neuronal survival, we have examined the expression and function of bcl-x, another member of the bcl-2 family of death regulatory genes. Bcl-2 is expressed in neuronal tissues during embryonic development but is down-regulated in the adult CNS. In contrast, Bcl-xL expression is retained in neurons of the adult CNS. Two different forms of bcl-x mRNA and their corresponding products, Bcl-xL and Bcl-x beta, were expressed in embryonic and adult neurons of the CNS. Microinjection of bcl-xL and bcl-x beta cDNAs into primary sympathetic neurons inhibited their death induced by nerve growth factor withdrawal. Thus, Bcl-x proteins appear to play an important role in the regulation of neuronal survival in the adult CNS.
Insights
The bcl-2 gene is not essential for neuronal survival. Instead, bcl-x proteins, including Bcl-xL and Bcl-x beta, are crucial for maintaining neuron health in the adult central nervous system (CNS).
Area of Science:
- Neuroscience
- Molecular Biology
- Genetics
Background:
- The bcl-2 protooncogene was previously thought to regulate neuronal survival.
- Mice deficient in bcl-2 showed normal central nervous system (CNS) development and maintenance.
- This suggests bcl-2 is not critical for neuronal survival.
Purpose of the Study:
- To investigate the role of bcl-x, a related gene in the bcl-2 family, in neuronal survival.
- To determine the expression patterns and functional significance of bcl-x in the CNS.
Main Methods:
- Examined bcl-x gene expression in embryonic and adult CNS tissues.
- Identified two forms of bcl-x mRNA: bcl-xL and bcl-x beta.
- Microinjected bcl-xL and bcl-x beta cDNAs into primary sympathetic neurons.
Main Results:
- Bcl-2 expression is high during embryonic development but decreases in the adult CNS.
- Bcl-xL expression persists in adult CNS neurons.
- Both Bcl-xL and Bcl-x beta inhibited neuronal death caused by nerve growth factor withdrawal in primary sympathetic neurons.
Conclusions:
- Bcl-x proteins, unlike Bcl-2, are important for neuronal survival in the adult CNS.
- Bcl-xL and Bcl-x beta play a significant role in regulating neuronal cell death pathways.