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Originally published as Genetics Published Articles Ahead of Print on July 5, 2005.
Genetics, Vol. 171, 545-555, October 2005, Copyright © 2005
doi:10.1534/genetics.105.044909
Reevaluation of the Role of the med-1 and med-2 Genes in Specifying the Caenorhabditis elegans Endoderm
Barbara Goszczynski and James D. McGhee1
Department of Biochemistry and Molecular Biology, Genes and Development Research Group, University of Calgary, Calgary, Alberta T2N 4N1, Canada
1 Corresponding author: Department of Biochemistry and Molecular Biology, University of Calgary, Health Sciences Centre, Room 2205, 3330 Hospital Dr. NW, Calgary, AB T2N 4N1, Canada.
E-mail: jmcghee{at}ucalgary.ca
The med-1 and med-2 genes encode a pair of essentially identical GATA factor-related transcription factors that have been proposed to be necessary for specification of the C. elegans endoderm (intestine or E lineage) as well as part of the C. elegans mesoderm. med-1 and med-2 are proposed to be the direct downstream targets and the principal effectors of the maternally provided SKN-1 transcription factor; med-1 and med-2 would thus occupy the pivotal interface between maternal and zygotic control of gene expression. The conclusion that med-1 and med-2 are necessary for C. elegans endoderm specification was based on a partially penetrant (
50%) loss of endoderm markers produced by RNA-mediated interference (RNAi). To determine whether this partial penetrance reflects: (i) inefficient RNAi against early zygotic transcripts, (ii) experimental uncertainty in the expected level of endoderm loss in skn-1 nulls, or (iii) additional redundancy in the pathway of endoderm specification, we constructed worm strains that segregate embryos lacking both the med-1 gene (because of a gene-specific deletion) and the med-2 gene (using either of two chromosomal deficiencies). Contrary to expectations, we observe that only 3–20% of med-2(–); med-1(–) embryos do not express markers of endoderm differentiation. Furthermore, we found no evidence for a maternal contribution of the med genes to endoderm specification. We conclude that the major pathway(s) for endoderm specification in C. elegans must be independent of the med-1 and med-2 genes.
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