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Enrichment of H3K9me2 on Unsynapsed Chromatin in Caenorhabditis elegans Does Not Target de Novo Sites.

Guo Y, Yang B, Li Y, Xu X, Maine EM - G3 (Bethesda) (2015)

Bottom Line: Loss of the SET domain protein, MET-2, greatly reduces H3K9me2 abundance and results in germline mortality.These results suggest that MET-2 activity is elevated in him-8 mutants generally as well as targeted preferentially to the unsynapsed X.We hypothesize H3K9me2 may have a structural function critical for germline immortality, and a greater abundance of these marks may be required when a chromosome does not synapse.

View Article: PubMed Central - PubMed

Affiliation: Department of Biology, Syracuse University, Syracuse, New York 13244.

No MeSH data available.


Examples of differential histone H3 lysine 9 dimethylation (H3K9me2) accumulation in the fer-1vs.fer-1;him-8 genome. Tracks represent fer-1 control H3K9me2, fer-1;him-8 H3K9me2, differential sites, input reads, and annotated genes (Refseq). For H3K9me2 tracks, the average of two independent biological replicates is shown as normalized total reads. Representative genome browser tracts show differential sites that (A) have a greater signal in fer-1;him-8 than in fer-1 or (B) have a de novo him-8−specific site of enrichment. Differential regions are boxed. Y-axis scale reflects the number of reads, ranging from a minimum of 0 to a maximum of ≥ 120.
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fig5: Examples of differential histone H3 lysine 9 dimethylation (H3K9me2) accumulation in the fer-1vs.fer-1;him-8 genome. Tracks represent fer-1 control H3K9me2, fer-1;him-8 H3K9me2, differential sites, input reads, and annotated genes (Refseq). For H3K9me2 tracks, the average of two independent biological replicates is shown as normalized total reads. Representative genome browser tracts show differential sites that (A) have a greater signal in fer-1;him-8 than in fer-1 or (B) have a de novo him-8−specific site of enrichment. Differential regions are boxed. Y-axis scale reflects the number of reads, ranging from a minimum of 0 to a maximum of ≥ 120.

Mentions: Although the fer-1 and fer-1;him-8 datasets are similar, we observed differential enrichment at many sites. Overall, ∼99.9% of the enriched sites present in fer-1 were also enriched in fer-1;him-8. We were surprised to observe a statistically significant increase in enrichment at approximately 50% of these sites distributed across the genome (Table 1). A statistically significant reduction in enrichment was observed at approximately 25% of the sites, and enrichment at the remainder of the sites was not significantly different in the two data sets (Table 1). We also identified a small number of de novo sites that are present specifically in him-8. To do so, we first identified sites that might be unique to fer-1 or fer-1;him-8 using MACS2.1 (see the section Materials and Methods), and then visually inspected all sites that had been called as unique to one genotype to validate the peak calling. This approach identified a relatively small set of 348 him-8−specific sites distributed across the genome (Table 1 and Figure 5). These de novo sites tend to be associated with repetitive sequences, although to a slightly lower degree than the conserved sites: 85% of the 348 de novo regions include at least one repetitive sequence, and repetitive sequences comprise 41% of the de novo enrichment. The net effect of the observed differential H3K9me2 deposition is a general increase in H3K9me2 level in him-8. Taken together, our data are consistent with a global increase in H3K9me2 across the him-8 hermaphrodite genome, and a further enhanced increase on the unsynapsed X chromosomes.


Enrichment of H3K9me2 on Unsynapsed Chromatin in Caenorhabditis elegans Does Not Target de Novo Sites.

Guo Y, Yang B, Li Y, Xu X, Maine EM - G3 (Bethesda) (2015)

Examples of differential histone H3 lysine 9 dimethylation (H3K9me2) accumulation in the fer-1vs.fer-1;him-8 genome. Tracks represent fer-1 control H3K9me2, fer-1;him-8 H3K9me2, differential sites, input reads, and annotated genes (Refseq). For H3K9me2 tracks, the average of two independent biological replicates is shown as normalized total reads. Representative genome browser tracts show differential sites that (A) have a greater signal in fer-1;him-8 than in fer-1 or (B) have a de novo him-8−specific site of enrichment. Differential regions are boxed. Y-axis scale reflects the number of reads, ranging from a minimum of 0 to a maximum of ≥ 120.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4555223&req=5

fig5: Examples of differential histone H3 lysine 9 dimethylation (H3K9me2) accumulation in the fer-1vs.fer-1;him-8 genome. Tracks represent fer-1 control H3K9me2, fer-1;him-8 H3K9me2, differential sites, input reads, and annotated genes (Refseq). For H3K9me2 tracks, the average of two independent biological replicates is shown as normalized total reads. Representative genome browser tracts show differential sites that (A) have a greater signal in fer-1;him-8 than in fer-1 or (B) have a de novo him-8−specific site of enrichment. Differential regions are boxed. Y-axis scale reflects the number of reads, ranging from a minimum of 0 to a maximum of ≥ 120.
Mentions: Although the fer-1 and fer-1;him-8 datasets are similar, we observed differential enrichment at many sites. Overall, ∼99.9% of the enriched sites present in fer-1 were also enriched in fer-1;him-8. We were surprised to observe a statistically significant increase in enrichment at approximately 50% of these sites distributed across the genome (Table 1). A statistically significant reduction in enrichment was observed at approximately 25% of the sites, and enrichment at the remainder of the sites was not significantly different in the two data sets (Table 1). We also identified a small number of de novo sites that are present specifically in him-8. To do so, we first identified sites that might be unique to fer-1 or fer-1;him-8 using MACS2.1 (see the section Materials and Methods), and then visually inspected all sites that had been called as unique to one genotype to validate the peak calling. This approach identified a relatively small set of 348 him-8−specific sites distributed across the genome (Table 1 and Figure 5). These de novo sites tend to be associated with repetitive sequences, although to a slightly lower degree than the conserved sites: 85% of the 348 de novo regions include at least one repetitive sequence, and repetitive sequences comprise 41% of the de novo enrichment. The net effect of the observed differential H3K9me2 deposition is a general increase in H3K9me2 level in him-8. Taken together, our data are consistent with a global increase in H3K9me2 across the him-8 hermaphrodite genome, and a further enhanced increase on the unsynapsed X chromosomes.

Bottom Line: Loss of the SET domain protein, MET-2, greatly reduces H3K9me2 abundance and results in germline mortality.These results suggest that MET-2 activity is elevated in him-8 mutants generally as well as targeted preferentially to the unsynapsed X.We hypothesize H3K9me2 may have a structural function critical for germline immortality, and a greater abundance of these marks may be required when a chromosome does not synapse.

View Article: PubMed Central - PubMed

Affiliation: Department of Biology, Syracuse University, Syracuse, New York 13244.

No MeSH data available.