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Functions of TBX-35, CEH-51, and TCF/POP-1 in Mesoderm Specification in Caenorhabditis elegans

  • Author(s): Owraghi, Melissa
  • Advisor(s): Maduro, Morris F
  • et al.
Abstract

Early cells of the nematode Caenorhabditis elegans decide very early which types of tissues they will contribute to. The E and MS blastomeres are sister cells born at the 7-cell stage of embryonic development. E makes the entire endoderm (gut), while MS makes many mesodermal cell types, including pharynx, body muscles and the four embryonically-derived coelomocytes. The E cell is specified by two redundant genes, end-1 and end-3, while MS is specified by the T-box gene tbx-35. However, previous studies indicate that another regulator is involved in MS specification, since tbx-35 mutant embryos continue to make some MS-derived tissues (e.g., coelomocytes). In addition, the embryos that lack NK-2 homeobox gene, ceh-51, previously identified by the Maduro lab to be a direct target of tbx-35, also showed partial specification of MS-derived tissues. Embryos that lack both tbx-35 and ceh-51, however, show a synergistic reduction in MS-specific tissues, suggesting that TBX-35 and CEH-51 work together to specify for tissues downstream in the MS lineage.

The Wnt nuclear effector POP-1 is critical to making MS and E different from one another. The MS-to-E transformation that results from loss of pop-1 function is well documented (Lin et al., 1995), and shows that the main requirement for POP-1 in C. elegans is repression of endoderm fate in MS. Recently, our laboratory has reported that E adopts an MS-like fate in C. briggsae embryos depleted for Cb-pop-1 function. This and other observations prompted us to look for the requirements of POP-1 in specification of MS in C. elegans. We examined pop-1; end-1,3 mutant embryos and found that although such embryos lack endoderm (as expected), they generate additional tissues that are normally made by MS, specifically pharynx muscle, body wall muscle, and coelomocytes. Using a laser microbeam to isolate MS or E, we have found that both cells make these tissues in pop-1; end-1,3 mutants. However, E isolations in the triple mutant embryos also express the hypodermal marker nhr-25::YFP, suggesting that E generates some C-like tissues in the absence of end-1,3. Collectively, these results demonstrate that E is only partially restored to an MS-like fate. The conclusion is that POP-1 is dispensable for some aspects of MS specification in C. elegans end-1,3 mutants, and that there may be a role for POP 1 in blocking MS fate in E.

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