Drosophila melanogaster males have one X chromosome while females have two. This creates an imbalance in X:A gene dosage between the sexes. This imbalance is corrected by increasing transcription from male X-linked genes approximately two-fold. This process involves the Male Specific Lethal (MSL) complex, which is recruited to Chromatin Entry Sites (CES) and transcribed X-linked genes where it modifies chromatin to increase expression. Repetitive sequences strikingly enriched in X euchromatin, the 1.688X satellite repeats, also promote recruitment of the MSL complex to nearby genes. Unlike CES, the 1.688X repeats do not recruit the MSL complex directly. The genetic architecture of recruitment by these DNA elements remains speculative. To facilitate dissection of the mechanism of recruitment, we developed a luciferase reporter system for recruitment of compensation to an autosome. The system was validated by knock down of genes known to participate in compensation. Knock down of factors genetically linked to X recognition reveals that 1.688X repeats recruit through a different mechanism than the CES. Our findings suggest that 1.688X repeats play a larger role during embryogenesis, whereas the contribution of 1.688X repeats and CES is equivalent later in development. Our studies also reveal unexpected complexity and potential interdependence of recruiting elements.
Keywords: Drosophila melanogaster; roX; 1.688X satellite repeats; Chromatin Entry Sites; Dosage compensation; siRNA; small RNA.
© The Author(s) 2024. Published by Oxford University Press on behalf of The Genetics Society of America.