Abstract
After the first division of the C. elegans embryo, the posterior blastomere can produce numerous muscles while the anterior blastomere cannot. We show here that maternal-effect lethal mutations in the gene mex-3 cause descendants of the anterior blastomere to produce muscles by a pattern of development similar to that of a descendant of the wild-type posterior blastomere. mex-3 encodes a probable RNA-binding protein that is distributed unequally in early embryos and that is a component of germline-specific granules called P granules. We propose that MEX-3 contributes to anterior-posterior asymmetry by regulating one or more mRNAs involved in specifying the fate of the posterior blastomere.
Publication types
- Research Support, Non-U.S. Gov't
- Research Support, U.S. Gov't, P.H.S.
MeSH terms
- Alleles
- Animals
- Base Sequence
- Blastomeres / cytology*
- Caenorhabditis elegans / embryology*
- Caenorhabditis elegans Proteins*
- Cytoplasm / metabolism
- Cytoplasmic Granules / metabolism
- Gene Expression Regulation, Developmental
- Genes, Helminth
- Genes, Lethal
- Helminth Proteins / physiology*
- Humans
- In Situ Hybridization
- Molecular Sequence Data
- Morphogenesis
- Muscles / embryology
- RNA, Messenger / metabolism
- RNA-Binding Proteins / genetics*
- Sequence Alignment
- Sequence Homology, Amino Acid
Substances
- Caenorhabditis elegans Proteins
- Helminth Proteins
- MEX-3 protein, C elegans
- RNA, Messenger
- RNA-Binding Proteins