Originally published as Genetics Published Articles Ahead of Print on December 6, 2006.

Genetics, Vol. 175, 969-974, February 2007, Copyright © 2007
doi:10.1534/genetics.106.066662

Neither Maternal nor Zygotic med-1/med-2 Genes Play a Major Role in Specifying the Caenorhabditis elegans Endoderm

Vasile V. Captan, 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, Health Sciences Centre, University of Calgary, 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 small, highly similar proteins related to GATA-type transcription factors and have been proposed as necessary for specification of both the mesoderm and the endoderm of Caenorhabditis elegans. However, we have previously presented evidence that neither maternal nor zygotic expression of the med-1/2 genes is necessary to specify the C. elegans endoderm. Contradicting our conclusions, a recent report presented evidence, based on presumed transgene-induced cosuppression, that the med-1/2 genes do indeed show an endoderm-specifying maternal effect. In this article, we reinvestigate med-2(–); med-1(–) embryos using a med-2- specific null allele instead of the chromosomal deficiences used previously and confirm our previous results: the large majority (~84%) of med-2(–); med-1(–) embryos express gut granules. We also reinvestigate the possibility of a maternal med-1/2 effect by direct injection of med dsRNA into sensitized (med-deficient) hermaphrodites using the standard protocol known to be effective in ablating maternal transcripts, but again find no evidence for any significant maternal med-1/2 effect. We do, however, show that expression of gut granules in med-1/2-deficient embryos is exquisitely sensitive to RNAi against the vacuolar ATPase-encoding unc-32 gene [present on the same multicopy med-1(+)-containing transgenic balancer used in support of the maternal med-1/2 effect]. We thus suggest that the experimental evidence for a maternal med-1/2 effect should be reexamined and may instead reflect cosuppression caused by multiple transgenic unc-32 sequences, not med sequences.