end-1 encodes an apparent GATA factor that specifies the endoderm precursor in Caenorhabditis elegans embryos.

Titleend-1 encodes an apparent GATA factor that specifies the endoderm precursor in Caenorhabditis elegans embryos.
Publication TypeJournal Article
Year of Publication1997
AuthorsZhu J, Hill RJ, Heid PJ, Fukuyama M, Sugimoto A, Priess JR, Rothman JH
JournalGenes Dev
Volume11
Issue21
Pagination2883-96
Date Published1997 Nov 1
ISSN0890-9369
KeywordsAmino Acid Sequence, Animals, Base Sequence, Caenorhabditis elegans, Caenorhabditis elegans Proteins, Cell Division, Chickens, Codon, Consensus Sequence, Conserved Sequence, Drosophila, Embryo, Nonmammalian, Endoderm, Female, GATA Transcription Factors, Genes, Helminth, Genomic Imprinting, Helminth Proteins, Homozygote, Molecular Sequence Data, Sequence Alignment, Sequence Homology, Amino Acid, Transcription Factors, Xenopus, Zinc Fingers
Abstract

The endoderm in the nematode Caenorhabditis elegans is clonally derived from the E founder cell. We identified a single genomic region (the endoderm-determining region, or EDR) that is required for the production of the entire C. elegans endoderm. In embryos lacking the EDR, the E cell gives rise to ectoderm and mesoderm instead of endoderm and appears to adopt the fate of its cousin, the C founder cell. end-1, a gene from the EDR, restores endoderm production in EDR deficiency homozygotes. end-1 transcripts are first detectable specifically in the E cell, consistent with a direct role for end-1 in endoderm development. The END-1 protein is an apparent zinc finger-containing GATA transcription factor. As GATA factors have been implicated in endoderm development in other animals, our findings suggest that endoderm may be specified by molecularly conserved mechanisms in triploblastic animals. We propose that end-1, the first zygotic gene known to be involved in the specification of germ layer and founder cell identity in C. elegans, may link maternal genes that regulate the establishment of the endoderm to downstream genes responsible for endoderm differentiation.

Alternate JournalGenes Dev.
PubMed ID9353257
PubMed Central IDPMC316658
Grant ListGM 48137 / GM / NIGMS NIH HHS / United States