Journal
PLOS GENETICS
Volume 8, Issue 7, Pages -Publisher
PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.pgen.1002808
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Funding
- Fred Eiserling and Judith Lengyel Graduate Doctorate Fellowship
- Marie Curie International Outgoing Fellowship for Career Development within the 7th European Community Framework Program
- Le Fonds de recherche en sante du Quebec/Genome Quebec through a Louis-Berlinguet Postdoctoral Fellowship
- NSF [1121245]
- National Institutes of Health [GM075060]
- Direct For Biological Sciences [1121245] Funding Source: National Science Foundation
- Div Of Molecular and Cellular Bioscience [1121245] Funding Source: National Science Foundation
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The relationship between epigenetic marks on chromatin and the regulation of DNA replication is poorly understood. Mutations of the H3K27 methyltransferase genes, ARABIDOPSIS TRITHORAX-RELATED PROTEIN5 (ATXR5) and ATXR6, result in re-replication (repeated origin firing within the same cell cycle). Here we show that mutations that reduce DNA methylation act to suppress the re-replication phenotype of atxr5 atxr6 mutants. This suggests that DNA methylation, a mark enriched at the same heterochromatic regions that re-replicate in atxr5/6 mutants, is required for aberrant re-replication. In contrast, RNA sequencing analyses suggest that ATXR5/6 and DNA methylation cooperatively transcriptionally silence transposable elements (TEs). Hence our results suggest a complex relationship between ATXR5/6 and DNA methylation in the regulation of DNA replication and transcription of TEs.
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