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DNA damage drives DNA methylation generation and evolution in plant [RNA-seq]

ABSTRACT: In mammals, it has long been hypothesized that DNA damage could induce DNA hypermethylation and contribute to carcinogenesis. However, the evidence that DNA damage is a cause of genome hypermethylation is still insufficient. Here, we demonstrated that, in plant, DNA damage can induce DNA hypermethylation in the context of symmetric CG, CHG as well as asymmetric CHH. Mechanically, DNA damage regulates the DREAM complex, to induce CG and CHG methylation. Moreover, DNA damage also utilizes the RdDM pathway to induce CHH hypermethylation. The hypermethylation sites of CG and CHG resulting from DNA damage tend to localize to gene body, and a large proportion of them are de nove generated. In contrast, the hypermethylation sites of CHH induced by DNA damage were mainly concentrated in the centromere and pre-centromere regions, and most of them are amplification of existing CHH methylation. Importantly, withdrawing the DNA damage or blocking the DNA damage response signal could fully abolish the CHH hypermethylation, partially rescue the CHG hypermethylation, but rarely recover the CG hypermethylation, indicating that DNA damage leaves symmetric DNA methylation as genetic imprinting. Collectively, our results suggest that DNA damage drives DNA methylation generation and evolution in plants.

ORGANISM(S): Arabidopsis thaliana

PROVIDER: GSE270747 | GEO | 2025/01/01

REPOSITORIES: GEO

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Project description:DNA cytosine methylation is a hallmark of epigenetic gene silencing. DNA demethylation requires ROS1, a bifunctional DNA glycosylase/lyases and open chromatin status mediated by IDM1. HDA6 is a RDP3-like histone deacetylase and was confirmed to mediate DNA methylation. In previous screening for ros1 suppressor, we identified two hda6 mutants reverting ros1-caused hypermethylation at RD29A and 35S promoters respectively, indicating the antagonization of DNA methylation between HDA6 and ROS1. To learn antagonized effects between HDA6 and ROS1 at DNA cytosine methylation genome-wide, we performed whole genome bisulfite sequencing to search antagonized targets of HDA6 and ROS1 and their specific targets to evaluate their roles on DNA methylation. To evaluate HDA6’s roles in sRNA biogenesis and nucleosome positioning, we also performed small RNA sequencing and genome-wide mapping of nucleosome positioning of C24, ros1, hda6-9 and hda6-10. Our results indicate that around 43% ros1-caused CG hypermethylation, 74.5% and 84.5% ros1-caused CHG and CHH hypermethylation were reverted by the two hda6 alleles in the ros1 background respectively. These results indicate that most of ROS1-demethylated targets are also HDA6-mediated DNA methylated targets. In addition, we observed that HDA6-affected DNA methylation targets are far more than ROS1-demethylation targets at CHG and CHH context, but not at CG context. sRNA analysis showed that HDA6 inhibits LTR/Gypsy and TE gene 24nt siRNA accumulation, while promotes RC/Helitron 24nt siRNA accumulation. Our Mono-nucleosome positioning data further showed that the two hda6 alleles have striking difference on nucleosome positioning, hda6-10 obviously have different nucleosome positioning patterns with hda6-9. Our results indicate HDA6 not only mediates overall DNA methylation at CG, CHG and CHH context, and antagonizes with ROS1 mediated DNA demethylation, but also regulates nucleosome positioning and small RNA accumulation at some genome specific regions.

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DNA damage drives DNA methylation generation and evolution in plant [RNA-seq]

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