Abstract
Mutations in the heterochronic gene lin-28 of C. elegans cause precocious development where diverse events specific to the second larval stage are skipped. lin-28 encodes a cytoplasmic protein with a cold shock domain and retroviral-type (CCHC) zinc finger motifs, consistent with a role for LIN-28 in posttranscriptional regulation. The 3'UTR of lin-28 contains a conserved element that is complementary to the 22 nt regulatory RNA product of lin-4 and that resembles seven such elements in the 3'UTR of the heterochronic gene lin-14. Both lin-4 activity and the lin-4-complementary element (LCE) are necessary for stage-specific regulation of lin-28. Deleting the LCE produces a dominant gain-of-function allele that causes a retarded phenotype, indicating that lin-28 activity is a switch that controls choices of stage-specific fates.
MeSH terms
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Animals
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Caenorhabditis elegans / genetics*
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Caenorhabditis elegans Proteins*
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Chromosome Mapping
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Cloning, Molecular
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Cold Temperature
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Cytoplasm / physiology
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Embryonic Induction / physiology
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Gene Expression Regulation, Developmental / physiology
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Genes, Helminth / physiology*
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Genotype
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Green Fluorescent Proteins
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Helminth Proteins / chemistry
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Helminth Proteins / genetics*
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Helminth Proteins / metabolism
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Luminescent Proteins
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Molecular Sequence Data
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Nuclear Proteins*
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Phenotype
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Protein Structure, Tertiary
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Retroviridae / genetics
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Sequence Homology, Amino Acid
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Transformation, Genetic
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Zinc Fingers / genetics
Substances
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Caenorhabditis elegans Proteins
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Helminth Proteins
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LIN-14 protein, C elegans
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Luminescent Proteins
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Nuclear Proteins
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Green Fluorescent Proteins
Associated data
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GENBANK/U75912
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GENBANK/U75913
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GENBANK/U75914
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GENBANK/U75915