Maternal deployment of the embryonic SKN-1-->MED-1,2 cell specification pathway in C. elegans.

TitleMaternal deployment of the embryonic SKN-1-->MED-1,2 cell specification pathway in C. elegans.
Publication TypeJournal Article
Year of Publication2007
AuthorsMaduro MF, Broitman-Maduro G, Mengarelli I, Rothman JH
JournalDev Biol
Date Published2007 Jan 15
KeywordsAnimals, Biological Transport, Caenorhabditis elegans, Caenorhabditis elegans Proteins, Cell Differentiation, DNA-Binding Proteins, Embryo, Nonmammalian, Endoderm, GATA Transcription Factors, Gene Expression Regulation, Developmental, Genotype, High Mobility Group Proteins, In Situ Hybridization, Intestines, Mesoderm, Mothers, Mutation, RNA, Messenger, Transcription Factors, Transcription, Genetic, Zygote

We have previously shown that the MED-1,2 divergent GATA factors act apparently zygotically to specify the fates of the MS (mesoderm) and E (endoderm) sister cells, born at the 7-cell stage of C. elegans embryogenesis. In the E cell, MED-1,2 activate transcription of the endoderm-promoting end-1 and end-3 genes. We demonstrate by in situ hybridization that med transcripts accumulate both in the EMS cell and in the maternal germline in a SKN-1-dependent manner. Removal of zygotic med function alone results in a weakly impenetrant loss of endoderm. However, med-1,2(-) embryos made by mothers in which germline med transcripts have been abrogated by transgene cosuppression fail to make endoderm 50% of the time, similar to the phenotype seen by RNAi. We also find that reduction of Med or End activity results in aberrant numbers of intestinal cells in embryos that make endoderm. We further show that regulation of the paralogous end-1 and end-3 genes consists of both shared and distinct inputs, and that END-3 activates end-1 expression. Our data thus reveal three new properties of C. elegans endoderm specification: both maternal and zygotic activities of the med genes act to specify endoderm, defects in endoderm specification also result in defects in gut cell number, and activation of the paralogous end-1 and end-3 genes differs qualitatively in the relative contributions of their upstream regulators.

Alternate JournalDev. Biol.
PubMed ID16979152
Grant ListCA95943 / CA / NCI NIH HHS / United States
HD37487 / HD / NICHD NIH HHS / United States