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
- Animals
- Caenorhabditis elegans / genetics*
- Caenorhabditis elegans Proteins*
- Chromosome Mapping
- Cloning, Molecular
- Cold Temperature
- Cytoplasm / physiology
- Embryonic Induction / physiology
- Gene Expression Regulation, Developmental / physiology
- Genes, Helminth / physiology*
- Genotype
- Green Fluorescent Proteins
- Helminth Proteins / chemistry
- Helminth Proteins / genetics*
- Helminth Proteins / metabolism
- Luminescent Proteins
- Molecular Sequence Data
- Nuclear Proteins*
- Phenotype
- Protein Structure, Tertiary
- Retroviridae / genetics
- Sequence Homology, Amino Acid
- Transformation, Genetic
- Zinc Fingers / genetics
Substances
- Caenorhabditis elegans Proteins
- Helminth Proteins
- LIN-14 protein, C elegans
- Luminescent Proteins
- Nuclear Proteins
- Green Fluorescent Proteins
Associated data
- GENBANK/U75912
- GENBANK/U75913
- GENBANK/U75914
- GENBANK/U75915