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Genes expression in case of PEV caused by chromosomal rearrangement

ABSTRACT: Heterochromatic position effect variegation (PEV) is the epigenetic disruption of genes expression near the new-formed eu-heterochromatic border. We characterized the inversion In(2)A4, demonstrating cis-acting PEV as well as trans-inactivation of the reporter transgenes on the opposite normal chromosome in combination with the inversion. Euchromatic breakpoint of In(2)A4 inversion was localized at 105 bp region (chr2L:21182214-21182318) of the second exon of the Mcm10 gene, the heterochromatic breakpoint is located at the block of dodecasatellite in 2L pericentromeric heterochromatin. In order to check the effects of heterochromatin on neighbor euchromatic genes and estimate the distance of inactivation spreading, we performed RNA-seq analysis of genes expression in larvae and adults females of genotypes A12/A12 (control) and In(2)A4/In(2)A4. Cis-influence of heterochromatin in the inversion causes not only repression, but also activation of genes, and the effects of heterochromatin are different at different developmental stages. Cis-actions affect only a few genes located near the heterochromatin

ORGANISM(S): Drosophila melanogaster

PROVIDER: GSE71842 | GEO | 2015/10/25

SECONDARY ACCESSION(S): PRJNA292305

REPOSITORIES: GEO

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Project description:The mammalian cell nucleus displays a remarkable spatial segregation of active euchromatic from inactive heterochromatic genomic regions. In conventional nuclei, euchromatin is localized in the nuclear interior and heterochromatin at the nuclear periphery. In contrast, rod photoreceptors in nocturnal mammals have inverted nuclei, with a dense heterochromatic core and a thin euchromatic outer shell. This inverted architecture likely converts rod nuclei into microlenses to facilitate nocturnal vision, and may relate to the absence of particular proteins that tether heterochromatin to the lamina. However, both the mechanism of inversion and the role of interactions between different types of chromatin and the lamina in nuclear organization remain unknown. To elucidate this mechanism we performed Hi-C and microscopy on cells with inverted nuclei and their conventional counterparts. Strikingly, despite the inversion evident in microscopy, both types of nuclei display similar Hi-C maps. To resolve this paradox we developed a polymer model of chromosomes and found a universal mechanism that reconciles Hi-C and microscopy for both inverted and conventional nuclei. Based solely on attraction between heterochromatic regions, this mechanism is sufficient to drive phase separation of euchromatin and heterochromatin and faithfully reproduces the 3D organization of inverted nuclei. When interactions between heterochromatin and the lamina are added, the same model recreates the conventional nuclear organization. To further test our models, we eliminated lamina interactions in models of conventional nuclei and found that this triggers a spontaneous process of inversion that qualitatively reproduces the pathway of morphological changes during nuclear inversion in vivo. Together, our experiments and modeling suggest that interactions among heterochromatic regions are central to phase separation of the active and inactive genome in inverted and conventional nuclei, while interactions with the lamina are essential for building the conventional architecture from these segregated phases. Ultimately our data suggest that an inverted organization constitutes the default state of nuclear architecture.

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Genes expression in case of PEV caused by chromosomal rearrangement

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