Cytosine methylation is an important mechanism for dynamical regulation of gene expression and transposable element (TE) mobility during plant developmental processes. Here, we identified the transcription start sites of genes using high-throughput sequencing and then analyzed the DNA methylation status in soybean roots, stems, leaves, and cotyledons of developing seeds at single-base resolution. Profiling of DNA methylation in different organs revealed 2162 differentially methylated regions among organs, and a portion of hypomethylated regions were correlated with high expression of neighboring genes. Because of the different distribution of class I TEs (retrotransposons) and class II TEs (DNA transposons), the promoters of the lowest-expressed genes showed higher levels of CG and CHG methylation but a lower level of CHH methylation. We further found that the CHH methylation level of class II TEs was higher than class I TEs, possibly due to the presence of more smRNAs in class II TEs. In cotyledons of developing seeds, smRNA abundance was roughly positively correlated with hypermethylated regions but negatively related to hypomethylated regions. These studies provide significant insights into the complicated interplays among DNA methylation, smRNA abundance, TE distribution, and gene expression in soybean.

Hepatitis B virus (HBV) infection remains one of the most serious health problems worldwide.Whilst studies have shown that HBV impairs interferon (IFN) production from dendritic cells in chronic hepatitis B patients, it remains unknown whether HBV inhibits IFN production in human hepatocytes. Using transient transfection assays in a primary human hepatocyte cell line (PH5CH8), this study demonstrated that HBV polymerase inhibits IFN-b promoter activity induced by Newcastle disease virus, Sendai virus or poly(I : C) in a dose-dependent manner, whilst ectopic expression of the HBV core and X proteins had no effect on IFN-b promoter activity. In addition, HBV polymerase blocked cellular IFN-b expression and consequent antiviral immunity revealed by an infection protection assay. Furthermore, overexpression of key molecules on the IFN-b induction axis, together with HBV polymerase, resulted in a block of IFN-b promoter activity triggered by RIG-I, IPS-1, TRIF, TBK1 and IKKe, but not by an IFN regulatory factor 3 dominant-positive mutant (IRF3-5D), suggesting that HBV polymerase prevents IFN-b expression at the TBK1/IKKe level. Further studies showed that HBV polymerase inhibited phosphorylation, dimerization and nuclear translocation of IRF3, in response to Sendai virus infection. Finally, it was shown that HBV polymerase-mediated dampening of the interaction between TBK1/IKKe and DDX3 may be involved in the inhibitory effect on IFN-b induction. Taken together, these findings reveal a novel role of HBV polymerase in HBV counteraction of IFN-b production in human hepatocytes.