Project description: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.
Project description: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.
Project description: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.
Project description: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.
Project description:Evolution of heterochromatin and heterochromatin genes in the Oryza genomes reveals a new heterochromatin-euchromatin boundary [bisulfite-Seq]
Project description:Evolution of heterochromatin and heterochromatin genes in the Oryza genomes reveals a new heterochromatin-euchromatin boundary [RNA-Seq]
Project description:Evolution of heterochromatin and heterochromatin genes in the Oryza genomes reveals a new heterochromatin-euchromatin boundary [ChIP-Seq]
Project description:Evolution of heterochromatin and heterochromatin genes in the Oryza genomes reveals a new heterochromatin-euchromatin boundary [ncRNA-Seq]
Project description:Histone lysine methylation is an epigenetic mark to index chromosomal subdomains. In Drosophila, H3-K9 di- and trimethylation is mainly controlled by the heterochromatic SU(VAR)3-9 HMTase, a major regulator of position-effect variegation (PEV). In contrast, H3-K27 methylation states are independently mediated by the Pc-group enzyme E(Z). Isolation of 19 point mutants demonstrates that the silencing potential of Su(var)3-9 increases with its associated HMTase activity. A hyperactive Su(var)3-9 mutant, pitkin(D), displays extensive H3-K9 di- and trimethylation within but also outside pericentric heterochromatin. Notably, mutations in a novel Su(var) gene, Su(var)3-1, severely restrict Su(var)3-9-mediated gene silencing. Su(var)3-1 was identified as "antimorphic" mutants of the euchromatic H3-S10 kinase JIL-1. JIL-1(Su(var)3-1) mutants maintain kinase activity and do not detectably impair repressive histone lysine methylation marks. However, analyses with seven different PEV rearrangements demonstrate a general role of JIL-1(Su(var)3-1) in controlling heterochromatin compaction and expansion. Our data provide evidence for a dynamic balance between heterochromatin and euchromatin, and define two distinct mechanisms for Su(var) gene function. Whereas the majority of Su(var)s encode inherent components of heterochromatin that can establish repressive chromatin structures [intrinsic Su(var)s], Su(var)3-1 reflects gain-of-function mutants of a euchromatic component that antagonize the expansion of heterochromatic subdomains [acquired Su(var)s].