Overexpression of a Novel Xenopus Rel mRNA Gene Induces Tumors in Early Embryos*

  1. Saoshan Yang,
  2. Ann Lockwood,
  3. Peter Hollett,
  4. Rebecca Ford and
  5. Kenneth Kao
  1. From the Terry Fox Cancer Research Laboratory, Division of Basic Medical Sciences, Faculty of Medicine, Memorial University of Newfoundland, St. John’s, Newfoundland A1B 3V6, Canada

    Abstract

    The Rel family of transcriptional activators form a large diverse group of proteins that are involved in the activation of genes involved in immunity, development, apoptosis and cancer. So far, none of the rel genes cloned in mammals appear to be required for embryonic development. We have cloned and characterized a cDNA from an embryonic cDNA library that encodes a novelXenopus Rel protein, called Xrel3. Xrel3 is a member of the cRel subfamily and is most closely related to but distinct from otherXenopus Rel members. The expression of Xrel3 mRNA was investigated using Northern analysis, RNase protection assay, reverse transcriptase-linked polymerase chain reaction and in situhybridization. Messages are present maternally and are slightly enriched in the equatorial region of the blastula stage embryo. At gastrulation, the accumulation of Xrel3 messages declines to undetectable levels but then increases after neurulation. In situ RNA hybridization was used to determine the spatial location of Xrel3 messenger RNA in embryos. Messages are localized to the developing forebrain, dorsal mid-hindbrain region, the inner ear primordium, or otocyst, and in the notochord. Overexpression by microinjection of Xrel3 RNA induced tumors in the developing embryo that appeared after gastrulation. The location of the tumors depended on the location of the injection site. These results suggest that Xrel3 might have a generalized role in regulation of cell differentiation in the embryo.

    Footnotes

    • * This work was supported by grants from the Medical Research Council of Canada and the National Cancer Institute of Canada.The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked “advertisement” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

    • To whom correspondence should be addressed. Tel.: 709-737-6860; Fax: 709-737-7010; E-mail: kkao{at}plato.ucs.mun.ca.

    • 1 The abbreviations used are: RHD, Rel Homology Domain; RT-PCR, reverse transcriptase-linked polymerase chain reaction.

      • Received February 12, 1998.
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