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Regulation of heterochromatic DNA replication by histone H3 lysine 27 methyltransferases

Yannick Jacob1, Hume Stroud, Chantal Leblanc

  • 1Department of Biology, Indiana University, 915 East Third Street, Bloomington, Indiana 47405, USA.

Nature
|July 16, 2010
PubMed

Insights

Mutations in histone modifiers ARABIDOPSIS TRITHORAX-RELATED PROTEIN5 (ATXR5) and ATXR6 cause DNA re-replication in Arabidopsis. This study reveals a new pathway preventing heterochromatin over-replication and affecting transposon expression.

Area of Science:

  • Molecular Biology
  • Epigenetics
  • Plant Science

Background:

  • Cell cycle regulation prevents DNA replication more than once per cell cycle.
  • Pre-replication complexes at genomic origins are key targets for controlling DNA replication.
  • Histone modifications play crucial roles in regulating gene expression and genome stability.

Purpose of the Study:

  • To investigate the role of histone 3 lysine 27 (H3K27) monomethyltransferases ATXR5 and ATXR6 in preventing DNA re-replication.
  • To identify genomic regions prone to re-replication upon mutation of ATXR5 and ATXR6.
  • To understand the impact of ATXR5 and ATXR6 mutations on transposon expression and plant development.

Main Methods:

  • Genetic analysis of Arabidopsis mutants lacking functional ATXR5 and ATXR6.
  • Whole-genome analysis to identify sites of DNA re-replication.
  • Analysis of H3K27 monomethylation levels at specific genomic loci.
  • Gene expression analysis of transposons.
  • Phenotypic analysis of plant development.

Main Results:

  • Mutations in ATXR5 and ATXR6 lead to re-replication of specific genomic locations in Arabidopsis.
  • Re-replicated regions predominantly correspond to transposons and other repetitive, silent genomic elements.
  • High levels of H3K27 monomethylation were observed at these re-replicated sites.
  • Mutation of the catalytic SET domain of ATXR5/ATXR6 was sufficient to cause the re-replication defect.
  • ATXR5 and ATXR6 mutations resulted in upregulation of transposon expression and developmental abnormalities.

Conclusions:

  • ATXR5 and ATXR6 function in a novel pathway to prevent DNA over-replication of heterochromatin in Arabidopsis.
  • H3K27 monomethylation by ATXR5/ATXR6 is critical for suppressing re-replication at repetitive elements.
  • Dysregulation of this pathway impacts genome stability, transposon activity, and plant development.

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