Journal
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume 399, Issue 2, Pages 227-231Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2010.07.059
Keywords
MSL spreading; Non-coding RNA; roX1; roX2; Twofold hypertranscription
Categories
Funding
- UMDNJ Foundation
- National Science Foundation [MCB-0818464]
- Direct For Biological Sciences
- Div Of Molecular and Cellular Bioscience [0818464] Funding Source: National Science Foundation
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The male-specific lethal (MSL) complex in Drosophila melanogaster paints the male X chromosome in a manner that is both cis and trans to induce 2-fold hypertranscription of the X chromosome. To characterize the upregulation of gene expression by MSL cis-spreading, we measured the expressional change of neighboring genes by microarray when the genes were bound by MSL complexes that spread from an autosomal roX transgene. Genes within a 200 kb region that includes roX transgenes were upregulated concurrently with MSL cis-spreading. Conversely, there was almost no expressional change in genes from other regions. RT-PCR and ChIP analyses confirmed that the approximately 2-fold gene hypertranscripdoh was due to MSL cis-spreading. We also demonstrated that upregulation of the neighboring gene could rescue haplo-insufficient phenotypes of the Minute mutant, such as short bristle, delayed adult eclosion and decreased viability. These results indicate that the hypertranscription by MSL cis-spreading is a general mechanism that occurs in several tissue types. Our molecular and genetic data suggest that cis-spreading of the MSL complex from high-affinity sites including the roX gene results in upregulation of the neighboring genes, which are targets for dosage compensation in the male X chromosome. (c) 2010 Elsevier Inc. All rights reserved.
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