SDC (Sex and Dosage Compensation) proteins trigger hermaphrodite development by activating dosage compensation and repressing the male sex determination gene
her-1. We have biochemically defined an SDC protein complex including SDC-1, SDC-2, and SDC-3. This complex localizes to the
her-1 promoter, where it represses transcription at least 20-fold. It also associates along the entire length of the hermaphrodite X chromosomes, where it recruits other dosage compensation proteins (DC) such as DPY-26, DPY-27, DPY-28 and MIX-1 to repress X-linked gene expression 2-fold. We are interested in how the SDC complex can recognize and act differentially at these separate sites. Despite the fact that DC proteins are not required for transcriptional repression of
her-1, we have found that the SDC proteins recruit these DC proteins to the
her-1 promoter. We showed this co-localization in transgenic animals that express a GFP-LacI fusion protein from extrachromosomal arrays that also contain both lac operator repeats (lacO) and the
her-1 promoter. Analysis of SDC and DC protein localization to the
her-1 promoter arrays in SDC and DC mutant backgrounds has revealed sequential requirements for recognition and assembly of the SDC and DC proteins onto target sequences. To define how SDC proteins recognize specific target sites, we mapped regions within the
her-1 promoter that are important for SDC protein recognition using the assay above. To test the functional significance of the three regions we identified, we mutated them in the context of a full length
her-1 rescuing construct. Stable transgenic XX strains transformed with a wild-type
her-1 show little masculinization. In contrast, stable transgenic XX strains transformed with mutated
her-1 show varying degrees of transformation to the male fate, including induction of male tail structures and decreased fertility. We interpret this masculinization as an indication of
her-1 derepression. Interestingly, sequences in the regions important to support SDC-2 localization are not homologous to sequences on the X chromosome. Thus, recognition of the X chromosome and the
her-1 promoter appears to be specified by distinct mechanisms.