Expression profiling by high throughput sequencing Genome binding/occupancy profiling by high throughput sequencing Methylation profiling by high throughput sequencing Genome variation profiling by high throughput sequencing
Summary
The CMT2 and RNA-directed DNA methylation (RdDM) pathways have been proposed to separately maintain CHH methylation in specific regions of the Arabidopsis thaliana genome. Here, we show that dysfunction of the chromatin remodeller DDM1 causes hundreds of genomic regions to switch from CMT2-dependency to RdDM-dependency in DNA methylation. These converted loci are enriched at the edge regions of long transposable elements (TEs). Furthermore, we found that blocking the pathway switch by disrupting both DDM1 and RdDM causes strong reactivation of TEs and a burst of TE transposition in the first generation of mutant plants, indicating that the pathway conversion is critical to maintaining TE repression and protecting genomic stability. Our findings reveal the existence of a novel pathway conversion-based backup mechanism to guarantee the maintenance of DNA methylation and genome integrity.
Overall design
To investigate potential genetic interactions between the CMT2 and RdDM pathways, we generated single-base resolution maps of the DNA methylomes of the nrpd1, nrpe1, cmt2, ddm1, ddm1nrpd1, ddm1nrpe1, and ddm1cmt2 mutants, RNA sequencing in ddm1, ddm1nrpd1, ddm1nrpe1, and ddm1cmt2 mutants, resequencing in ddm1, nrpd1 and ddmcmt2.
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