Abstract
The hermaphrodite-specific neurons (HSNs) of the nematode Caenorhabditis elegans are generated embryonically in both hermaphrodites and males but undergo programmed cell death in males. The gene egl-1 encodes a BH3-containing cell death activator that is required for programmed cell death in C. elegans. Gain-of-function (gf) mutations in egl-1 cause the inappropriate programmed cell death of the HSNs in hermaphrodites. These mutations lie 5.6 kb downstream of the egl-1 transcription unit and disrupt the binding of the TRA-1A zinc finger protein, the terminal global regulator of somatic sexual fate. This disruption results in the activation of the egl-1 gene in the HSNs not only in males but also in hermaphrodites. Our findings suggest that in hermaphrodites TRA-1A represses egl-1 transcription in the HSNs to prevent these neurons from undergoing programmed cell death.
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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Animals
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Animals, Genetically Modified
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Apoptosis*
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Base Sequence
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Binding Sites
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Caenorhabditis / genetics*
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Caenorhabditis elegans Proteins*
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DNA, Helminth / chemistry
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DNA, Helminth / genetics
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DNA-Binding Proteins*
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Disorders of Sex Development / genetics
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Female
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Green Fluorescent Proteins
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Helminth Proteins / genetics*
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Helminth Proteins / metabolism*
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Homozygote
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Luminescent Proteins / genetics
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Male
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Mutation
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Neurons / cytology
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Neurons / physiology
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Oligodeoxyribonucleotides
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Repressor Proteins / genetics*
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Repressor Proteins / metabolism
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Sex Determination Processes*
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Transcription Factors / genetics*
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Transcription Factors / metabolism*
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Transcription, Genetic
Substances
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Caenorhabditis elegans Proteins
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DNA, Helminth
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DNA-Binding Proteins
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EGL-1 protein, C elegans
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Helminth Proteins
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Luminescent Proteins
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Oligodeoxyribonucleotides
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Repressor Proteins
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Transcription Factors
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tra-1 protein, C elegans
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Green Fluorescent Proteins