The germline sex determination gene mog-2 in Caenorhabditis elegans plays an important role in somatic development and meiosis

mog-2 represents the last of the six mog genes that was short of a known gene sequence. Using a combined approach of genetic mapping and single nucleotide polymorphism (SNP) the mog-2 mutant allele has been identified in Spring 2006. mog-2 was identified as sap-1 (Spliceosomal Associated Protein), which is homologous of the U2A' snRNP. As a first step, the expression of the mog-2 transcript and its mutant alleles have been investigated. To further investigate the MOG-2 role, we have now raised antibodies against MOG-2. While they specifically recognize the wild type protein, no signals were detected in extracts from mutant worms. Moreover, we found that the mutant protein was not produced or was readily degraded, because the mog-2(q75) mRNA was actually produced in an alternatively spliced form. Wild type MOG-2 was expressed in nuclei of the germ line and of somatic cells, thus supporting the notion that it could act on pre-mRNA processing. We have found taht the MOG-2 protein behaves in a different manner than the other MOG proteins. In fact MOG-2 does not bind to MEP-1, while all 5 MOG proteins tested so far associated with MEP-1. Furthermore, the other mog;gld-3 double mutants do not accumulate sperm, nor oocytes, but instead produce high amounts of germ nuclei that divide mitotically and therefore form a tumorous germ line. The mog-2;gld-3 double mutant, however, gives an unexpected result, since the animals do not reach adulthood but instead arrest their development at the first larval stage indicating that mog-2 is synthetically required for larval development. Furthermore, mog-2 single mutant exhibit a delayed larval developmental rate. Unfortunately, the requirement of mog-2 for larval progression has not been completely solved. In spite of different transcript tested, no abnormally spliced products have been found yet. However numerous hypothesis have been put forward and are waiting to be demonstrated. Amidst these the idea that mog-2 could be responsible for the gld-3 mRNA processing that in turn will regulate fbf-2 post-transcriptionally.