Heterochromatin formation depends critically on methylation of histone H3 at lysine 9 (H3K9me2/3), with concomitant association of heterochromatin protein 1 (HP1a) and other interacting proteins, including H3K9 methyltransferases (HKMTs) the multiple interactions of these proteins are required for the spreading and maintenance of heterochromatin. In this article we will show how these different approaches have converged to identify many contributors to this system, leading to characterization of both structural proteins and modifying enzymes that play key roles in establishing and maintaining heterochromatin. Genetic, cytological, and biochemical analyses are all possible in Drosophila melanogaster. The silencing that occurs in PEV can be attributed to the packaging of the reporter gene in a heterochromatic form, indicating that endogenous heterochromatin formation, once initiated, can spread to encompass nearby genes. Because the change is caused by a change in the position of the gene in the genome, rather than a change in the gene itself, this phenomenon is termed “position-effect variegation” (PEV). This is a result of the gene being silenced in some of the cells in which it is normally active. Genes that are abnormally juxtaposed with heterochromatin, either by rearrangement or transposition, show a variegating phenotype.
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