期刊
DEVELOPMENT
卷 136, 期 16, 页码 2735-2746出版社
COMPANY BIOLOGISTS LTD
DOI: 10.1242/dev.038307
关键词
Mesoderm; C. elegans; tbx-35; ceh-51; Tissue specification
资金
- NIH National Center for Research Resources (NCRR) [1R03HD054589-01]
- NSF [0416922, 0643325]
- Howard Hughes Medical Institute
- Direct For Biological Sciences [0416922] Funding Source: National Science Foundation
- Direct For Biological Sciences
- Division Of Integrative Organismal Systems [0643325] Funding Source: National Science Foundation
- Division Of Integrative Organismal Systems [0416922] Funding Source: National Science Foundation
The C. elegans MS blastomere, born at the 7-cell stage of embryogenesis, generates primarily mesodermal cell types, including pharynx cells, body muscles and coelomocytes. A presumptive null mutation in the T-box factor gene tbx-35, a target of the MED-1 and MED-2 divergent GATA factors, was previously found to result in a profound decrease in the production of MS-derived tissues, although the tbx-35(-) embryonic arrest phenotype was variable. We report here that the NK-2 class homeobox gene ceh-51 is a direct target of TBX-35 and at least one other factor, and that CEH-51 and TBX-35 share functions. Embryos homozygous for a ceh-51 null mutation arrest as larvae with pharynx and muscle defects, although these tissues appear to be specified correctly. Loss of tbx-35 and ceh-51 together results in a synergistic phenotype resembling loss of med-1 and med-2. Overexpression of ceh-51 causes embryonic arrest and generation of ectopic body muscle and coelomocytes. Our data show that TBX-35 and CEH-51 have overlapping function in MS lineage development. As T-box regulators and NK-2 homeodomain factors are both important for heart development in Drosophila and vertebrates, our results suggest that these regulators function in a similar manner in C. elegans to specify a major precursor of mesoderm.
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