In the indirect developing sea urchin embryo, the primary mesenchyme cells (PMCs) acquire most of the positional and temporalinformation from the overlying ectoderm for skeletal initiation and growth. In this study, we characterize the function of thenovel gene strim1, which encodes a tripartite motif-containing (TRIM) protein, that adds to the list of genes constituting theepithelial-mesenchymal signaling network. We report that strim1 is expressed in ectoderm regions adjacent to the bilateralclusters of PMCs and that its misexpression leads to severe skeletal abnormalities. Reciprocally, knock down of strim1 functionabrogates PMC positioning and blocks skeletogenesis. Blastomere transplantation experiments establish that the defects in PMCpatterning, number and skeletal growth depend upon strim1 misexpression in ectoderm cells. Furthermore, clonal expression ofstrim1 into knocked down embryos locally restores skeletogenesis. We also provide evidence that the Otp and Pax2/5/8regulators, as well as FGFA, but not VEGF, ligand act downstream to strim1 in ectoderm cells, and that strim1 triggers theexpression of the PMC marker sm30, an ectoderm-signaling dependent gene. We conclude that the strim1 function elicits specificgene expression both in ectoderm cells and PMCs to guide the skeletal biomineralization during morphogenesis.
|Number of pages||12|
|Publication status||Published - 2011|
All Science Journal Classification (ASJC) codes
- Molecular Biology
- Developmental Biology