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.
Deng
Xinxian
X
Department of Biological Sciences, Wayne State University, Detroit, MI 48202, USA.
Meller
Victoria H
VH
D000818:Animals; D004303:Dosage Compensation, Genetic / Q000235:genetics*; D029721:Drosophila Proteins / Q000235:genetics*; D004331:Drosophila melanogaster / Q000235:genetics* / Q000378:metabolism; D018628:Gene Dosage; D008297:Male; D009154:Mutation / Q000235:genetics*; D014157:Transcription Factors / Q000235:genetics*; D014158:Transcription, Genetic / Q000235:genetics; D019076:Transgenes / Q000235:genetics
D029721:Drosophila Proteins; D014157:Transcription Factors; C454144:roX1 protein, Drosophila