Deficiency in DNA methylation increases meiotic crossover rates in euchromatic but not in heterochromatic regions in Arabidopsis

Cathy Melamed-Bessudo*, Avraham A. Levy

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

138 Citations (Scopus)

Abstract

Meiotic recombination is tightly regulated by cis- and trans-acting factors. Although DNA methylation and chromatin remodeling affect chromosome structure, their impact on meiotic recombination is not well understood. To study the effect of DNA methylation on the landscape of chromosomal recombination, we analyzed meiotic recombination in the decreased DNA methylation 1 (ddm1) mutant. DDM1 is a SWI2/SNF2-like chromatin-remodeling protein necessary for DNA methylation and heterochromatin maintenance in Arabidopsis thaliana. The rate of meiotic recombination between markers located in euchromatic regions was significantly higher in both heterozygous (DDM1/ddm1) and homozygous (ddm1/ddm1) backgrounds than in WT plants. The effect on recombination was similar for both male and female meiocytes. Contrary to expectations, ddm1 had no effect on the number of crossovers between markers in heterochromatic pericentric regions that underwent demethylation. These results are surprising, because the pericentromeric regions are hypermethylated and were expected to be the regions most affected by demethylation. Thus, DDM1 loss of function may trigger changes that enhance meiotic recombination in euchromatin regions but are not sufficient to induce the same events in heterochromatic segments. This work uncovers the repressive role of methylation on meiotic recombination in euchromatic regions and suggests that additional factors may have a role in controlling the suppression of recombination in heterochromatin.

Original languageEnglish
Pages (from-to)E981-E988
JournalProceedings of the National Academy of Sciences of the United States of America
Volume109
Issue number16
DOIs
Publication statusPublished - 17 Apr 2012

Funding

European UnionWe thank Prof. Ortrun Mittelsten Scheid for critical comments on the manuscript, Hadar Fuchs and Naomi Avivi-Ragolsky for technical help, and members of the A.A.L. and Paszkowski laboratoriess for useful discussions. This work was supported by a grant from the European Union Seventh Framework Programme (FP7) RECBREED Project.

All Science Journal Classification (ASJC) codes

  • General

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