The XXXX @entity68092 RNA gene can overcome silent chromatin by recruiting the male-specific lethal dosage compensation complex.

@entity1472 @entity68092 @entity65122 @entity27051 @entity238
The @entity238 @entity27051 complex consists of at least six proteins and two noncoding roX RNAs that mediate dosage compensation. It acts to remodel the male's X chromatin by covalently modifying the @entity1472 terminal tails of histones. The @entity68092 and @entity65122 genes are thought to be nucleation sites for assembly and spreading of @entity27051 complexes into surrounding chromatin where they roughly double the rates of transcription. We generated many transgenic stocks in which the @entity68092 gene was moved from its normal location on the X to new autosomal sites. Approximately 10% of such lines displayed unusual sexually dimorphic expression patterns of the transgene's mini-white eye-color marker. Males often displayed striking mosaic pigmentation patterns similar to those seen in position-effect variegation and yet most inserts were in euchromatic locations. In many of these stocks, female mini-white expression was very low or absent. The male-specific activation of mini-white depended upon the @entity27051 complex. We propose that these transgenes are inserted in several different types of repressive chromatin environments that inhibit mini-white expression. Males are able to overcome this silencing through the action of the @entity27051 complex spreading from the @entity68092 gene and remodeling the local chromatin to allow transcription. The potency with which an ectopic @entity27051 complex overcomes silent chromatin suggests that its normal action on the X must be under strict regulation.
