Molecular Evolution of Tandemly Repeated Heterochromatic Gene Clusters Involving a Switch of Their Function in the Genome of Drosophila melanogaster

Abstract

Molecular evolution and divergence of paralogous tandem heterochromatic repeats Stellate and Su(Ste) located on the X and Y chromosomes, respectively, are discussed. These repeats appear to emerge as a result of amplification of a unique autosomal euchromatic gene encoding the regulatory β-subunit of the CK2 protein kinase. The autosomal gene and the clusters of heterochromatic repeats are transcribed in testes. A high level of the Stellate expression leads to partial male sterility and abnormal meiosis. The Stellate expression and its adverse effects are suppressed by homologous Su(Ste) repeats. In genome evolution, the open reading frames (ORF) of Stellate and Su(Ste) putative ancestor were maintained by translational selection. Then the coding Su(Ste) function has been damaged and switched to a new one resulting in antisense Su(Ste) transcription and silencing of theStellategenes. Symmetrical (sense and antisense) Su(Ste) transcription causes the formation of a double-strand RNA, which by interference (selective elimination of the homologous gene expression) suppresses the Stellate genes. The biological significance and the driving forces of evolution of the species-specific balanced interaction of Stellateand Su(Ste) repeats remain mysterious.