Analysis of the mrg-1 gene function required for differentiation of primordial germ cells in the nematode C.elegans

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Germ cells are the only cells that can give rise to next generation and thus are responsible for perpetuation of species. In many animals, establishment of the primordial germ cell (PGC) depends on several maternal factors. However, little is known about the molecular mechanism how maternal factors give the special property of germ cells to PGCs. We show here that a chromodomain protein MRG-1 is required maternally for PGCs to initiate expression of the germline-specific gene pgl-1. MRG-1 is localized to nuclei and associated with chromosomes, suggesting that MRG-1 regulates transcriptional activity of germline-specific genes through chromatin remodeling. Previous study revealed that germline-specific genes become derepressed in somatic cells in animals lacking MEP-1, which is a component of the nucleosome remodeling and histone deacetylase (NuRD) complex (1). We found that depletion of MRG-1 suppresses the Mep-1 phenotype : ectopic expression of germline-specific genes in somatic cells. These studies suggest that MRG-1 gives maternally the potential to express gemline-specific genes to all blastomeres, and the activity is restricted to PGCs by the interaction between MRG-1 and MEP-1. It has been reported that Mep-1 phenotype is also suppressed by mutations in mes-2, mes-3, mes-4 and mes-6 genes. MES proteins are shown to function in histone methylation. Although the sterile phenotype and expression pattern of mrg-1 is quite similar to those of mes genes, mutations in mrg-1 do not affect the localization pattern or the histone methyltransferase activities of MES proteins. These results suggest that MRG-1 acts downstream or parallel with MES proteins. Our findings support a model in which several maternal factors accumulated in the nuclei of PGCs are play an important role to act together to ensure the transcriptional activity of germline-specific genes, at least in part, through chromatin remodeling.