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Evolution of heterochromatin and heterochromatin genes in the Oryza genomes reveals a new heterochromatin-euchromatin boundary [bisulfite-Seq]

ABSTRACT: How heterochromatin genes evolve as ‘gene islands’ to fit into the repressive chromatin environment in plants are poorly understood. To address this question, we performed a comprehensive epigenetic profiling in the genus Oryza with high quality BAC-assembled regional sequences and near gap-free genomes. Comparative analyses of a heterochromatin knob demonstrated the dynamics of chromatin states (heterochromatin versus euchromatin) among the Oryza species in a phylogenetic context. LTR (long-terminal repeat) retrotransposons are the main contributor (~99%) to heterochromatin diversity. Heterochromatin genes are distributed as ‘gene islands’ in heterochromatin, but heterochromatin hardly projects expression disturbance to them. Heterochromatin genes are almost free of H3K9me2 histone modifications in exons, and have similar gene structure and transposon invasion rate in introns to its orthologous euchromatin counterparts. Analyses of the rice HiC data verified the topological existence of ‘gene islands’ and demonstrated that ‘gene islands’ are less spatially co-localized with heterochromatin. By examining evolutionarily recent inserted genes in the Oryza species, we found that the active promoters of six inserted genes can elevate CHH (H=A, C, T) methylation at the insertion sites. Our results reveals that heterochromatin genes evolve as heterochromatin-insulated ‘gene islands’ to escape the repressive influence of heterochromatin, contrasting to the ‘integration’ model in Drosophila. We suggest that active gene promoters may contribute to this insulation by acting as an important heterochromatin-euchromatin boundary in plants.

ORGANISM(S): Oryza brachyantha

PROVIDER: GSE126432 | GEO | 2020/12/02

REPOSITORIES: GEO

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Project description:The establishment of latency is an essential step for the life-long persistent infection and pathogenesis of KaposiM-bM-^@M-^Ys sarcoma-associated herpesvirus (KSHV). While the KSHV genome is chromatin-free in the virions, the viral DNA in latently infected cells has a chromatin structure that is characterized by a specific pattern of activating and repressive histone modifications that ultimately promote latent gene expression while suppressing lytic gene expression. To investigate the molecular events involved in the establishment of the latent chromatin structure during the pre-latency phase of KSHV infection, we performed a comprehensive epigenetic study to analyze the recruitment of chromatin regulatory factors onto the KSHV genome at various time-points following de novo infection of SLK and TIME cells. This showed that the KSHV genome undergoes a biphasic chromatinization following de novo infection. Initially, a transcriptionally active chromatin (euchromatin), characterized by high levels of the H3K4me3 and acetylated H3K27 (H3K27ac) activating histone marks, was deposited on the viral episome and was accompanied by the temporary induction of a limited number of lytic genes. Interestingly, transient expression of the RTA protein facilitated the increases of H3K4me3 and H3K27ac occupancy on the KSHV episome during de novo infection. Between 24-72 hours post-infection, as the levels of these activating histone marks declined on the KSHV genome, the levels of the repressive H3K27me3 and H2AK119ub histone marks increased concomitantly with the decline of lytic gene expression. Importantly, this transition to heterochromatin was dependent on both the Polycomb Repressive Complex 2 and 1. In contrast, upon infection of human gingiva-derived epithelial cells, the KSHV genome underwent a continuously transcription-active euchromatinization, resulting in efficient lytic gene expression. Our data demonstrate that the KSHV genome undergoes a temporally ordered biphasic euchromatin-to-heterochromatin transition in endothelial cells, leading to latent infection, whereas KSHV preferentially adopts a transcriptionally active euchromatin in oral epithelial cells, resulting in lytic gene expression. Our results suggest that the differential epigenetic modification of the KSHV genome in distinct cell types is a potential determining factor for latent infection vs. lytic replication of KSHV. Please see above. 16 hybridizations: ChIP and Input DNA

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Evolution of heterochromatin and heterochromatin genes in the Oryza genomes reveals a new heterochromatin-euchromatin boundary [bisulfite-Seq]

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