Molecularly severe roX1 mutations contribute to dosage compensation in Drosophila

Drosophila melanogaster males maintain a constant ratio of X-linked to autosomal gene products by increasing expression from their single X chromosome. This is achieved through the action of a complex composed of protein and roX RNA. This complex binds in the body of genes and increases expression through chromatin modification. The X-linked roX genes produce RNAs that are essential but redundant for recognition and modification of the male X chromosome. We report that some molecularly severe roX1 mutations with no detectable transcript accumulation contribute dramatically to male rescue by autosomal roX1 transgenes. We propose that this represents genetic complementation between a source of roX RNA (the autosomal transgene) and the severely mutated X-linked allele.