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Molecularly severe roX1 mutations contribute to dosage compensation in Drosophila
Author(s) -
Deng Xinxian,
Meller Victoria H.
Publication year - 2009
Publication title -
genesis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.093
H-Index - 110
eISSN - 1526-968X
pISSN - 1526-954X
DOI - 10.1002/dvg.20463
Subject(s) - dosage compensation , biology , genetics , gene , complementation , drosophila melanogaster , x inactivation , transgene , x chromosome , allele , chromatin , mutant
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. genesis 47:49–54, 2009. © 2008 Wiley‐Liss, Inc.