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The authors review the publications on epigenetic gene silencing models. The topics of interest include the relationship between histone modifications and transcription and a dynamic model of nucleosome mobility and replacement.

This review describes the action of a sequence- specific DNA binding compound, which upon binding to the minor groove of a GAGAA-rich repetitive element causes a mutation that leads to the production of GAGA factor (GAF) DNA binding regulatory protein. Results show that Drosophila larvae fed with such compounds undergo homeotic transformations.

Somatic pairing in diploid nuclei involves a variety of genetic and epigenetic phenomena that include allelic and nonallelic interactions. Several models of these phenomena, also known as 'trans-sensing effects,' are used in the study of phenotypic changes in Drosophila. These include transvection, pairing-dependent repression, trans-inactivation, homolog dragging and trans suppression.

Trinucleotide repeat expansions result in heterochromatin formation in Drosophila and local production of heterochromatin induces gene silencing in higher eukaryotes. Repeated transgenes cause mislocalization of the region into a heterochromatic chromocenter resulting in gene dysfunctions. Fragile X-syndrome is one of the manifestations of nucleotide repeat expansions.

Eukaryotic transcription is a dynamic process in which DNA templates that is tightly wrapped around histones and is read by RNA polymerases. A glimpse of the events that follow transcriptional induction is provided using an integrated cytological system observed in real time.

Dosage compensation refers to the regulated expression of genes, ususally on the sex chromosomes, resulting in equivalency of gene product formation in both sexes. In mammals, this may be achieved by X chromosome inactivation in the female soma, while in Drosophila, male X-linked genes are transcribed at twice the level of their female counterparts. Some recent findings in male X expression are presented and discussed.