Abstract
Naturally occurring cell death is believed to play a major role during the development of the nervous system in the establishment of neuronal architecture. Here we study the effects of cell death inhibition by using a transgenic mouse in which the powerful antiapoptotic gene bcl-2 is expressed in neurons. The retina of this mouse reveals that the general neuronal plan has been maintained. However, bcl-2 overexpression leads to altered frequencies of the major cell types in the retina. Thus, it is possible to estimate cell-type-specific rates of apoptosis by observing the increases in numbers of cells in the bcl-2-overexpressing transgenic mouse.
Copyright 2002 Wiley-Liss, Inc.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Amacrine Cells / metabolism
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Amacrine Cells / ultrastructure
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Animals
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Apoptosis / genetics*
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Cell Count
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Cell Differentiation / genetics*
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Gene Expression Regulation, Developmental / physiology*
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Immunohistochemistry
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Interneurons / metabolism
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Interneurons / ultrastructure
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Mice
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Mice, Inbred C57BL
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Mice, Transgenic / abnormalities*
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Mice, Transgenic / growth & development
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Mice, Transgenic / metabolism
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Microscopy, Electron
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Neurons / metabolism*
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Neurons / ultrastructure
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Proto-Oncogene Proteins c-bcl-2 / genetics
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Proto-Oncogene Proteins c-bcl-2 / metabolism*
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Retina / abnormalities*
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Retina / growth & development
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Retina / metabolism
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Retinal Cone Photoreceptor Cells / metabolism
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Retinal Cone Photoreceptor Cells / ultrastructure
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Retinal Rod Photoreceptor Cells / metabolism
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Retinal Rod Photoreceptor Cells / ultrastructure
Substances
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Proto-Oncogene Proteins c-bcl-2