We are investigating the molecular mechanism of action of the suppressor-of-sable [su(s)] system of Drosophila melanogaster: recessive su(s) mutations suppress recessive mutations at the vermilion (v) locus that are caused by insertions of the mobile element 412 in 5' transcribed but untranslated sequences. Current evidence suggests that this suppression is effected by some mechanism that increases the amount of pseudo-wild-type mRNA that is produced by splicing the mobile element sequences from the primary transcript. The cDNA contains an open reading frame that encodes a putative protein of 1322 amino acids, and cellular fractionation studies have shown that the protein is primarily located in the nucleus. This protein has one region of similarity to the RNA Recognition Motif (RRM) that is found in many proteins that are involved in RNA processing and a second region of similarity to the human, Xenopus and Drosophila 70K U1 binding proteins and to the Drosophila suppressor of white-apricot and transformer proteins, all of which are known to be RNA binding proteins. Portions of the cloned 25 kb of DNA have been reintroduced by P element mediated transformation and allow an identification of genetic function with messages produced by the region. A segment of DNA which is homologous with only the su(s) message rescues both the primary phenotype of suppression and a secondary phenotype of cold-sensitive male sterility. Studies of genetic deletions indicate that the females lacking the entire su(s) protein are viable and fertile and that males lacking more than half of the protein are viable and fertile.
