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  1. Detailansicht für Treffer 1 öffnen
    Figure 2—figure supplement 2. The number of genes gaining a minimum of 5% CHG methylation (CHG-gain genes) is correlated with AtCMT3 transgene expression levels. ; AtCMT3 expression was determined by RNA-seq (first panel) or qRT-PCR (second panel). For qRT-PCR AtCMT3 expression was normalized to TUB4 expression (Thhalv10003210m). See also Figure 2D and Supplementary file 4.
    2019
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  2. Detailansicht für Treffer 2 öffnen
    Figure 3. Gains in CHG methylation do not alter H3K9me2 levels or distribution. ; (A) Genome browser view of CHG methylation levels and H3K9me2 ChIP sequencing levels in the T3 and T5 generations of the AtCMT3-L1 and L2 lineages. Arrows indicate gains of CHG methylation over gene bodies in the AtCMT3-L2 generations that do not show H3K9me2 enrichment. Scales on methylation tracks designate the weighted percent methylation, with 1 = 100% on the top strand and −1 = 100% on the bottom strand. Scales on the H3K9me2 tracks indicate the number of mapped reads and are not adjusted for library size (See C-F for comparison of normalized reads). DNA methylation is only shown in the CHG context. For DNA methylation in all contexts see Figure 3—figure supplement 1. (B) Metaplot of % CHG methylation over H3K9me2 ChIP peaks identified in wild type plants. (C–F) Metaplot of H3K9me2 ChIP-sequencing enrichment over H3K9me2 ChIP peaks defined in wild type plants and over CHG-gain genes in AtCMT3-L1T3 (C), AtCMT3-L1T5 (D), AtCMT3-L2T3 (E), and AtCMT3-L2T5 (F). Reads were normalized to library size. See Supplementary file 5 for lists of CHG-gain genes in each lineage.
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  3. Detailansicht für Treffer 3 öffnen
    Figure 3—figure supplement 2. Gains in CHG methylation do not alter H3K9me1 levels or distribution. ; (A) Genome browser view of CHG methylation levels and H3K9me1 ChIP sequencing levels in the T2c generation of the AtCMT3-L3 lineage. In wild type and AtCMT3-L3T2c, H3K9me1 can be found enriched in regions also enriched for H3K9me2. The arrow indicates a gene body that gains CHG methylation in AtCMT3-L3 but does not show H3K9me1 enrichment. Scales on methylation tracks designate the weighted percent methylation, with 1 = 100% on the top strand and −1 = 100% on the bottom strand. Scales on the H3K9me1 tracks indicate the number of mapped reads and are not normalized. Cytosine methylation is divided into CG (red), CHG (blue), and CHH (yellow) sequence contexts. (B) Metaplot of H3K9me1 ChIP-sequencing enrichment over H3K9me2 ChIP peaks defined in wild type plants and over CHG-gain genes in AtCMT3-L3T2c. (C) Metaplot of H3K9me1 ChIP-sequencing enrichment comparing enrichment over CHG-gain genes in AtCMT3-L3T2c to genes that do not gain CHG methylation (UM genes).
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  4. Detailansicht für Treffer 4 öffnen
    Figure 2. AtCMT3 expression results in CHG methylation over repeats and a subset of gene bodies. ; (A) Heatmap of % CHG methylation over hyper-CHG differentially methylated regions (DMRs) defined by comparing all AtCMT3-L1 and L2 generations (T1–T6) to wild type. DMRs are ranked by % CHG methylation levels in wild type plants showing that the majority of gains in CHG methylation occurred over regions with pre-existing CHG methylation classified as repeats or intergenic regions. A subset of regions with no pre-existing CHG methylation, mainly classified as genes, also showed gains in CHG methylation, especially in AtCMT3-L2 individuals. See also Supplementary file 2 and Supplementary file 3. (B) Metaplot summarizing % CHG methylation over repetitive sequences for each Line. (C) Metaplot summarizing % CHG methylation over gene bodies for each Line. (D) The number of genes gaining a minimum of 5% CHG methylation (CHG-gain genes) in each lineage. See Supplementary file 5 for lists of CHG-gain genes.
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  6. Detailansicht für Treffer 6 öffnen
    Figure 1. Expression of AtCMT3 in E.salsugineum results in increased CHG methylation. ; (A) Schematic of the experiment. Two E. salsugineum lines derived from transformations with genomic A. thaliana CMT3 were propagated by single seed decent for six generations (T1–T6). The two lines are referred to as AtCMT3-L1 and AtCMT3-L2, followed by the generation (T1–T6). For additional lines analyzed in this study see Figure 1—figure supplement 1 and Supplementary file 1. (B) Genome browser view of CHG methylation levels derived from whole genome bisulfite sequencing. The image illustrates the gains in CHG methylation that occur in regions that are methylated in wild type, as well as over gene bodies with no pre-existing DNA methylation (boxed in red). Scales on tracks designate the weighted percent methylation, with 1 = 100% on the top strand and −1 = 100% on the bottom strand. Only CHG methylation is shown. For methylation in all contexts see Figure 1—figure supplement 2.
    2019
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  7. Detailansicht für Treffer 7 öffnen
    Figure 5—figure supplement 2. AtCMT3-induced genic CG methylation is maintained at higher levels than background following loss of AtCMT3 expression. ; (A) Comparison of the % methylation of CG sites that were not found to be methylated in the non-transgenic wild type (Shandong ecotype) parent of AtCMT3 transgenic lines. Shown is the % CG methylation calculated in each lineage across hyper CHG DMRs identified in AtCMT3-L2T4 that overlap CHG-gain genes identified in AtCMT3-L2T4 (black bars; same regions assessed in Figure 5B) compared to the average % CG methylation of an equal amount of sequence space extracted from five randomly chosen sets of unmethylated genes that did not gain CHG methylation in AtCMT3-L2T4. The number of genes chosen in each set was equal to the number of AtCMT3-L2T4 CHG gain genes. Note that AtCMT3-L2T5 and T6 exhibited silencing of the AtCMT3 transgene, yet still maintained CG methylation levels higher than that detected on unmethylated genes. Methylation over the same regions was also assessed in additional, non-transgenic E. salsugineum accession (Yukon) to demonstrate that the levels of CG methylation over CHG gain genes in transgenic lines were unlikely to have occurred independently of AtCMT3. (B) Comparison of the % methylation of CG sites that were not found to be methylated in the non-transgenic wild type (Shandong ecotype) parent of AtCMT3 transgenic lines. Shown is the % CG methylation calculated in each lineage across hyper CHG DMRs identified in AtCMT3-L1T5 that overlap CHG-gain genes identified in AtCMT3-L1T5 (black bars; same regions assessed in Figure 5—figure supplement 1E) compared to the average % CG methylation of an equal amount of sequence space extracted from five randomly chosen sets of unmethylated genes that did not gain CHG methylation in AtCMT3-L1T5. The number of genes chosen in each set was equal to the number of AtCMT3-L1T5 CHG gain genes. AtCMT3-L1T5 was crossed to wild type (non-transgenic) and three F2 progeny were assessed: one progeny that retained the transgene (L1T5XWT F2 (+CMT3)) and two where the transgene segregated out (L1T5XWT F2 (-CMT3) #1 and #2). Note that the F2 progeny where the transgene segregated out still maintained CG methylation levels higher than that detected on unmethylated genes. As in (A), methylation over the same regions was also assessed in additional, non-transgenic E. salsugineum accession (Yukon) to demonstrate that the levels of CG methylation over CHG gain genes in transgenic lines were unlikely to have occurred independently of AtCMT3. Error bars are ± one standard deviation of the mean.
    2019
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  8. Detailansicht für Treffer 8 öffnen
    Figure 4—figure supplement 1. Changes in expression are not related to CHG methylation levels. ; Relationship between fold change in expression relative to wild type and CHG methylation levels for genes identified as gaining a minimum of 5% CHG methylation in each respective line. Lines analyzed include those with both RNA sequencing and whole genome bisulfite sequencing data: (A) AtCMT3-L1T3; (B) AtCMT3-L1T4; (C) AtCMT3-L1T5; (D) AtCMT3-L2T3; (E) AtCMT3-L2T5; (F) AtCMT3-L2T6; (G) AtCMT3-L3T2; (H) AtCMT3-L3T2b. Genes with zero FPKM values were removed from the analysis.
    2019
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  9. Detailansicht für Treffer 9 öffnen
    Figure 1—figure supplement 4. AtCMT3 expression results in gains in CHG methylation over similar regions between lineages and across generations. ; Matrix showing the number and overlap between hyper-CHG DMRs identified in each individual in AtCMT3-L1 and AtCMT3-L2. The top half of the matrix shows the number of overlapping DMRs and the bottom half shows the p-value calculated based on fisher’s exact test (***p significant
    2019
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  10. Detailansicht für Treffer 10 öffnen
    Figure 2—figure supplement 1. AtCMT3 expression results in gains in CHG methylation over similar genes between lineages and across generations. ; Matrix showing the number and overlap between genes gaining a minimum of 5% CHG methylation identified in each individual in AtCMT3-L1 and AtCMT3-L2. The top half of the matrix shows the number of overlapping genes and the bottom half shows the p-value calculated based on a hypergeometric test (***p significant
    2019
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  12. Detailansicht für Treffer 12 öffnen
    Figure 1. ALN imprinting necessitates non-canonical RdDM. ; (A) Sanger sequencing chromatograms at SNPs of ALN. WT plants (Cvi) were pollinated with WT (Col and Ws) and mutant pollen as indicated. RNA was extracted from endosperm of F1 seeds and subjected to RT-PCR followed by Sanger sequencing. Nucleotides at SNP sites are highlighted in red: ‘C’ originates from Cvi and ‘T’ originates from Ws and Col. Representative results are shown from experiments repeated at least 5 times for each genotype. (B) DNA methylation on the ALN 5’ and 3’ flanking regions in endosperm of mature seed. Black box arrows and yellow box arrows show genes and TEs respectively. Blue lines show regions where DNA methylation was studied. Red line (300 bp) shows ALN’s highly methylated 5’ upstream region (referred as ‘POGO region’). All remaining methylation data shown in this figure only correspond to the 300 bp POGO region. Red, blue and green vertical lines represent CG, CHG, and CHH methylation levels, respectively. (C) Percentages of CHH methylation levels corresponding to the POGO region in different RdDM mutants (Materials and methods). drm1drm2 is in Ws background; ago4ago6 is generated after crossing ago4 with ago6 in Ler and C24 background, respectively; all other mutants are in Col-0 background. Percentages of DNA methylation at CG and CHG sites are shown in Figure 1—figure supplement 1. (D) DNA methylation levels in maternal and paternal alleles. DNA extracted from endosperm and embryo of F1 seeds obtained after reciprocally crossing Cvi and Col WT plants was analyzed by sodium bisulfite sequencing. SNPs were used to distinguish maternal and paternal alleles. Filled and open circles represent methylated and unmethylated cytosines, respectively. (E) Percentage of DNA methylation in the POGO region in different tissues. (F) Percentage of DNA methylation in the POGO region in female and male gametes. The data were extracted from published whole genomic DNA methylation data of female (Park et al., 2016) and male (Ibarra et al., 2012) gametes.
    2019
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  13. Detailansicht für Treffer 13 öffnen
    Figure 5. CHG methylation over gene bodies is associated with gains in non-CHG methylation. ; (A) Heatmap of % methylation levels across CHG DMRs overlapping the CHG-gain genes in AtCMT3-L2T4 divided into selected trinucleotide contexts. See Figure 5—figure supplement 1A for further parsing of the data into all 16 possible trinucleotide contexts. (B) Assessment of the relationship of genic cytosine methylation to AtCMT3 expression across AtCMT3-L2 generations. Line plots show the number of methylated cytosines in each context relative to AtCMT3-L2T4 across CHG DMRs overlapping CHG-gain genes identified in AtCMT3-L2T4. Bar plots show the expression of the AtCMT3 transgene. For further parsing of the CHG and CHH contexts into CWG vs. CCG and CWA vs. other CHH, see Figure 5—figure supplement 1B–C. (C) Assessment of the relationship of repeat and intergenic cytosine methylation to AtCMT3 expression across AtCMT3-L2 generations. Line plots show the number of methylated cytosines relative to AtCMT3-L2T4 across hyper CHG DMRs identified in AtCMT3-L2T4 that overlap repeats or intergenic regions. Bar plots show the expression of the AtCMT3 transgene.
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  14. Detailansicht für Treffer 14 öffnen
    Figure 5—figure supplement 1. CHG methylation over gene bodies is associated with gains in non-CHG methylation. ; (A) Heatmap of % methylation levels across CHG hyper-DMRs overlapping the CHG-gain genes in AtCMT3-L2T4 divided into all 16 possible trinucleotide contexts. (B–C) Assessment of the relationship of genic cytosine methylation to AtCMT3 expression across AtCMT3-L2 generations. Line plots show the number of methylated cytosines in (B) CWG vs. CCG contexts and (C) CWA vs. other CHH contexts relative to AtCMT3-L2T4 across CHG DMRs overlapping CHG-gain genes defined in AtCMT3-L2T4. Bar plots show the expression of the AtCMT3 transgene. See also Figure 5A–B. (D) Assessment of the relationship of genic cytosine methylation to AtCMT3 expression across AtCMT3-L1 generations. Line plots show the number of methylated cytosines in each context relative to AtCMT3-L1T4 across CHG DMRs overlapping CHG-gain genes identified in AtCMT3-L1T4. Bar plots show the expression of the AtCMT3 transgene. (E–F) Assessment of the number of methylated cytosines relative to AtCMT3-L1T5 across hyper CHG DMRs identified in AtCMT3-L1T5 that overlap CHG-gain genes identified in AtCMT3-L1T5 (E) or repeats or intergenic regions (F). AtCMT3-L1T5 was crossed to wild type (non-transgenic) and three F2 progeny were assessed: one progeny that retained the transgene (L1T5XWT F2 (+CMT3)) and two where the transgene segregated out (L1T5XWT F2 (-CMT3) #1 and #2). The gel image below the line plot is the result of PCR conducted on genomic DNA from each line with primers to detect the AtCMT3 transgene.
    2019
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  15. Detailansicht für Treffer 15 öffnen
    Figure 1—figure supplement 3. CG, CHG, and CHH DMRs co-localize. ; (A–L) Upset plots showing the number and overlap between hyper DMRs identified for each sequence context, CG, CHG, and CHH, within each generation of each lineage, AtCMT3-L1 and AtCMT3-L2: (A) AtCMT3-L1T1; (B) AtCMT3-L1T2; (C) AtCMT3-L1T3; (D) AtCMT3-L1T4; (E) AtCMT3-L1T5; (F) AtCMT3-L1T6; (G) AtCMT3-L1T1; (H) AtCMT3-L2T2; (I) AtCMT3-L2T3; (J) AtCMT3-L2T4; (K) AtCMT3-L2T5; (L) AtCMT3-L2T6.
    2019
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  17. Detailansicht für Treffer 17 öffnen
    Figure 2—figure supplement 1. Quantitative description of the chromatin environment at EIN2 in ein6-1 een-1 mutants. ; (A) Protein domain structure of EEN as well as a multiple amino acid sequence alignment of EEN, IES6 and human IES6 (hIES6). The YL1-C domain is indicated in blue. (B) Aggregated H3K27me3 profile of 2369 Group I genes shows H3K27me3 occupancy from 1 kb upstream to 2 kb downstream of the TSS in Ler, ein6-1, een-1 and ein6-1 een-1 seedlings. (C) Genome browser screenshot shows differential enrichment of H3K27me3 at an example Group I gene and Group II gene. To ensure an accurate comparison of individual chromatin features between genotypes, the tracks were normalized to the respective sequencing depth. (D) H3K27me3 occupancy of 54 Group II genes in Ler, ein6-1, een-1 and ein6-1 een-1 seedlings is shown as an aggregated H3K27me3 profile from 1 kb upstream to 2 kb downstream of the TSS. The H3K27me3 occupancy was calculated as the ratio between the two respective merged ChIP replicates and the two merged Ler IgG control replicates. (E) Quantification of H3K27me3 levels in the 5’UTR intron, gene body and 3’UTR of the EIN2 gene are shown. The H3K27me3 occupancy in these regions was calculated as the ratio between the respective merged ChIP-seq samples and merged Ler IgG control samples. (F) Spearman’s correlation plot shows correlation of read coverages between the antibody validation H2A.Z datasets from this study (Col-0, pie1-1, Col-0 HTA11:HTA11-GFP (αH2A.Z) and Col-0 HTA11:HTA11-GFP (αGFP)) and three publicly available H2A.Z ChIP-seq datasets (Carter et al., 2018; Wollmann et al., 2017; Coleman-Derr and Zilberman, 2012). Clustering is determined by the degree of correlation. (G) Heatmap shows the H2A.Z occupancy at all Arabidopsis genes in the indicated genotypes. Levels of H2A.Z from 1 kb upstream to 2 kb downstream of the TSS are shown. (H) Genome browser screenshot shows differential enrichment of H2A.Z in Col-0, pie1-1 and Col-0 HTA11:HTA11-GFP seedlings. Moreover, H2A.Z enrichment is also shown for three publicly available H2A.Z ChIP-seq datasets (Carter et al., 2018; Wollmann et al., 2017; Coleman-Derr and Zilberman, 2012). Genetic background and used antibodies are indicated. The Col-0 IgG track serves as a control and the Ler 5mC track indicates methylated cytosines (CG in yellow, CHG in blue, CGG in pink). The shape difference of H2A.Z domains in the Coleman-Derr and Zilberman, 2012 dataset can be explained by the MNase treatment of the chromatin. (I) Levels of H2A.Z in the 5’UTR intron, gene body and 3’UTR of EIN2 in Ler, ein6-1, een-1 and ein6-1 een-1 seedlings are shown. The H2A.Z occupancy in these regions was calculated as the ratio between the respective merged ChIP-seq samples and merged Ler IgG control samples.
    2019
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  18. Detailansicht für Treffer 18 öffnen
    Figure 2. A repressive chromatin environment at EIN2 down-regulates its expression. ; (A) Genome browser screenshot visualizes the levels of the depicted chromatin features at the EIN2 gene in untreated 3-day-old etiolated Ler, ein6-1, een-1 and ein6-1 een-1 seedlings. Occupancy of H3K27me3, H2A.Z, H3K4me3 and H2Aub was determined with ChIP-seq, mRNA expression was measured with RNA-seq and levels of methylated cytosines (CG in yellow, CHG in blue, CGG in pink) were determined with MethylC-seq. To ensure an accurate comparison of individual chromatin features between genotypes, the tracks were normalized to the respective sequencing depth. Normalization was separately done for each chromatin feature. Biological replicate 1 of the H3K27me3 and H2A.Z ChIP-seq datasets is shown. (B) Venn diagram illustrates the overlap between genes that show a significant increase of H3K27me3 (2-fold enrichment over ein6-1), H2AZ (2-fold enrichment over een-1) and H2Aub (2-fold enrichment over Ler) in ein6-1 een-1 mutants and also a significant decrease of H3K4me3 (1.5-fold enrichment in Ler over ein6-1 een-1). In addition, genes that contain differentially methylated regions (DMRs) with ten or more methylated cytosines in at least one genotype were included as well. (C) Graphical illustration of H3K27me3 and EIN6 occupancy at the EIN2 gene determined with ChIP-seq. Sequencing reads were merged between biological replicates for the H3K27me3 ChIP-seq using untreated 3-day-old etiolated Ler (gray) and ein6-1 een-1 (blue) seedlings (two replicates each) and the EIN6 ChIP-seq (red) using Ler 35S:EIN6-FLAG seedlings (three replicates). The occupancy was calculated as the ratio between the respective merged ChIP and the merged Ler IgG control in 100 bp bins from 2.4 kb upstream to 7.7 kb downstream of the transcriptional start site (TSS) of EIN2 and is shown as log2 fold change. Negative values which reflect lower occupancy in the ChIP sample compared to the IgG control sample were set to zero.
    2019
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  19. Detailansicht für Treffer 19 öffnen
    Figure 1—figure supplement 1. DNA methylation in the POGO region. ; (A) DNA methylation in the POGO region upstream of ALN in the endosperm of WT seeds and RdDM mutant seeds. The studied region is depicted by a red line in Figure 1B. Filled and open circles represent methylated and unmethylated cytosines respectively. (B) Histograms show percentages of CG and CHG, and CHH methylation in the POGO region of WT and different RdDM mutants as indicated. (C) aln x nrpe1 and aln x WT F1 seeds were after-ripened for 7 days. Germination was scored 72 hr upon seed imbibition (eight replicates, n = 50). (D) DNA methylation levels in the POGO region of maternal and paternal alleles. DNA from endosperm and embryo of F1 seeds obtained after reciprocally crossing Cvi and Col WT plants was analyzed by sodium bisulfite sequencing. SNPs were used to distinguish maternal and paternal alleles. (E) DNA methylation in the POGO region in different tissues of WT (Col) plants. (F) Histograms show percentage of DNA methylation in the POGO region in sperm cells and vegetative cell from two independent published whole genomic DNA methylation data of male gamete (Calarco et al., 2012 and Hsieh et al., 2016).
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  20. Detailansicht für Treffer 20 öffnen
    Supplementary file 5. Lists of genes that gained a minimum of 5% CHG methylation in each line.
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xs 0 - 576
sm 576 - 768
md 768 - 992
lg 992 - 1200
xl 1200 - 1366
xxl 1366 -