Abstract
Genome architecture is shaped by gene-rich and repeat-rich regions also known as euchromatin and heterochromatin, respectively. Under normal conditions, the repeat-containing regions undergo little or no meiotic crossover (CO) recombination. COs within repeats are risky for the genome integrity. Indeed, they can promote non-allelic homologous recombination (NAHR) resulting in deleterious genomic rearrangements associated with diseases in humans. The assembly of heterochromatin is driven by the combinatorial action of many factors including histones, their modifications, and DNA methylation. In this review, we discuss current knowledge dealing with the epigenetic signatures of the major repeat regions where COs are suppressed. Then we describe mutants for epiregulators of heterochromatin in different organisms to find out how chromatin structure influences the CO rate and distribution.
Highlights
Genome architecture is shaped by gene-rich and repeat-rich regions known as euchromatin and heterochromatin, respectively
Direct and indirect evidence collected in the different organisms far highlight that epigenetic landscape of repeats is related to the suppression of double-strand breaks (DSBs)/COs
Heterochromatin-enriched epigenetic marks likely operate at different levels to avoid meiotic recombination
Summary
Genome architecture is shaped by gene-rich and repeat-rich regions known as euchromatin and heterochromatin, respectively. It has been shown that open chromatin structure is required for SPO11 to access DNA for generating meiotic DSBs (Berchowitz et al 2009; Pan et al 2011). The nucleotide resolution map evidenced that DSBs are suppressed within 5-kb region around centromeres (Pan et al 2011).
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