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Correct cell fate choice is crucial in development. In post-embryonic development of the hermaphroditic  Caenorhabitis elegans , distinct cell fates must be adopted in two diverse tissues. In the germline, stem cells adopt one of three possible fates: mitotic cell cycle, or gamete formation via meiosis, producing either sperm or oocytes. In the epidermis, the stem cell-like seam cells divide asymmetrically, with the daughters taking on either a proliferative (seam) or differentiated (hypodermal or neuronal) fate. We have isolated a novel conserved  C. elegans  tetratricopeptide repeat containing protein, TRD-1, which is essential for cell fate determination in both the germline and the developing epidermis and has homologs in other species, including humans (TTC27). We show that  trd-1(RNAi)  and mutant animals have fewer seam cells as a result of inappropriate differentiation towards the hypodermal fate. In the germline,  trd-1  RNAi results in a strong masculinization phenotype, as well as defects in the mitosis to meiosis switch. Our data suggests that  trd-1  acts downstream of  tra-2  but upstream of  fem-3  in the germline sex determination pathway, and exhibits a constellation of phenotypes in common with other Mog ( m asculinization  o f  g ermline) mutants. Thus,  trd-1  is a new player in both the somatic and germline cell fate determination machinery, suggestive of a novel molecular connection between the development of these two diverse tissues.

The C. elegans TPR Containing Protein, TRD-1, Regulates Cell Fate Choice in the Developing Germ Line and Epidermis