The C. eleganshermaphrodite produces both sperm and oocytes. In the larva, the first germ cells differentiate into sperm. In the adult, spermatogenesis is turned off and all germ cells develop as oocytes. Post-transcriptional control appears to be crucial for the sperm/oocyte switch in the C. eleganshermaphrodite. The post-transcriptional repression of
fem-3 RNA through its SUTR is essential for the switch from spermatogenesis to oogenesis. Several genes that are required for the in vivo repression of
fem-3 expression have been identified. We have previously shown that fbf (
fem-3 binding factor) encodes a protein which is able to repress
fem-3 directly by binding to its SUTR, and that
mog-1, -4 and -5, which represent the C. elegans orthologs of the yeast splicing factors PRP16, PRP2 and PRP22 respectively, are also required for the sperm/oocyte switch. However, in spite of the similarities between MOG-1, -4, -5 and the yeast splicing factors, no general splicing defects were found in mog mutants. We have shown that MOG-1, MOG-4 and MOG-5 do not bind to each other, nor to FBF, nor to the
fem-3 3UTR. Nevertheless, we have identified an RNA-binding zinc finger protein that is able to bind the nuclear proteins MOG-1, -4 and -5. This protein, termed MIF-1 (for mog interacting factor 1), is also a nuclear protein whose mRNA is predominantly present in the germ line. The
mif-1 null mutant allele leads to a phenotype that is very similar to that obtained by RNA interference. In both cases worms are sterile, accumulate sperm and have defects in gonadal arm extension. The fact that
mif-1 mutants do not produce oocytes strongly suggest that
mif-1 might correspond to a new factor involved in the sperm/oocyte switch. Using in vitro binding assays and the yeast two hybrid system, we have shown that different parts of MIF-1 are required for the interaction with the distinct MOG proteins.