Results: 5

1.
Figure 5

Figure 5. Distinct evolutionary implication of labile and persistent epi-polymorphisms.. From: Genetic Modifiers of Chromatin Acetylation Antagonize the Reprogramming of Epi-Polymorphisms.

A scenario is presented where a new epigenotype (black) appears that generate a new phenotypic trait in the course of evolution. If this epigenotype is labile (up), then the trait is likely subjected to selection for a shorter time than if the epigenotype is persistent (low).

Anne-Laure Abraham, et al. PLoS Genet. 2012 September;8(9):e1002958.
2.
Figure 1

Figure 1. Conceptually distinct classes of epi-polymorphisms.. From: Genetic Modifiers of Chromatin Acetylation Antagonize the Reprogramming of Epi-Polymorphisms.

A) Induced SNEPs are defined here as inter-strain differences that arose from a stochastic or environmentally-induced epigenetic change. B) DNA-encoded SNEPs are genetically determined by differences in the DNA sequence. C) After individuals have undergone perturbing environmental conditions, the SNEPs initially present may be lost (called labile), or remain (called persistent).

Anne-Laure Abraham, et al. PLoS Genet. 2012 September;8(9):e1002958.
3.
Figure 4

Figure 4. Genetic control antagonizes epigenetic lability.. From: Genetic Modifiers of Chromatin Acetylation Antagonize the Reprogramming of Epi-Polymorphisms.

A) Fraction of successful aceQTL mapping among labile (n = 1,076) and persistent (n = 1,481) SNEPs. B) Receiver Operating Curve (ROC) analysis of frequency of aceQTL found among SNEPs with increasing persistence. Deviation from the diagonal shows that high persistence correlates with elevated rate of aceQTL discovery. C) Smooth scatter plot of all nucleosomes. X-axis: persistence value of nucleosomes, which reflects the degree of conservation of inter-strain acetylation ratio across the TSA treatment (as in Figure 2C). Y-axis: highest −log10(P) genetic linkage score found on the genome for the acetylation of this nucleosome. High linkage scores are found exclusively at high persistence. Dashed line: aceQTL significance threshold. To allow for identification of outsiders, dark dots represent individual data points (nucleosomes) from areas of lowest densities. D) Nucleosomes were classified according to the genetic heritability h of their acetylation level in the BYxRM cross. Class sizes were n = 14,199 nucleosomes for h = 0, and n = 11,123 nucleosomes for each category of positive h. Curves represent distributions of persistence for each category. A shift towards higher persistence is observed with increasing heritability values.

Anne-Laure Abraham, et al. PLoS Genet. 2012 September;8(9):e1002958.
4.
Figure 2

Figure 2. Reprogramming of SNEPs after a transient exposure to TSA.. From: Genetic Modifiers of Chromatin Acetylation Antagonize the Reprogramming of Epi-Polymorphisms.

(A) Inter-strain differences in H3K14 acetylation after recovery from TSA treatment (y-axis) compared to original inter-strain difference (x-axis). Each dot represents one nucleosome. Persistent, labile and induced SNEPs are colored in magenta, green and blue, respectively. All other nucleosomes are represented by small grey dots. Circle and diamond correspond to SNEPs shown in B). (B) Examples at the MET31 locus. Nucleosome positions (rectangles) are colored according to their level of H3K14 acetylation in BY and RM strains, before TSA treatment (top) and after recovery (bottom). Circle, a labile SNEP that was significant before TSA treatment (P = 3.4×10−8) but no longer after recovery (P = 0.5). Diamond, a persistent SNEP that was significant both before treatment (P = 1.2×10−13) and after recovery (P = 1.2×10−7). (C) Persistence was defined as 1−|log2(RM/BY)before tratment−log2(RM/BY)post recovery| and is shown for ‘isolated’ and ‘non-isolated’ SNEPs, which correspond to cases where no or at least one flanking nucleosome was also a SNEP, respectively (Wilcoxon test: P<2.2×10−16). (D–G) Effect of treatment and recovery in each strain. The x-axis represents the logratio of H3K14 acetylation after recovery from TSA versus before treatment, for every nucleosome considered. (D) Distributions of this logratio value measured in the RM strain (black) and the BY strain (red) in all nucleosomes. The two distributions are centered, showing a similar average effect in the two strains. The larger dispersion of the red curve indicates that more nucleosomes were reprogrammed in the BY strain. (E) Same as (D) but when only nucleosomes corresponding to labile SNEPs are considered. This shows that the reprogramming in the BY strain is not symmetric, with a majority of reprogrammed SNEPs having gained acetylation. (F) The black density curve of (D) was decomposed into three categories of nucleosomes according to the BY/RM ratio of acetylation before treatment: ‘n.s.’, nucleosomes that were not initially SNEPs, ‘low’ and ‘high’, nucleosomes that were initially SNEPs with preferential acetylation in RM or in BY, respectively. (G) Similarly, the red density curve of (D) was decomposed into the same three categories. The fact that the distributions are shifted indicates that SNEP call prior to treatment is predictive of the treatment effect in the BY strain.

Anne-Laure Abraham, et al. PLoS Genet. 2012 September;8(9):e1002958.
5.
Figure 3

Figure 3. Genetic dissection of epigenomic variations.. From: Genetic Modifiers of Chromatin Acetylation Antagonize the Reprogramming of Epi-Polymorphisms.

(A) Genome x Epigenome map of genetic regulations. Each dot represents a significant genetic linkage (FDR = 0.03) between a marker located on the x-axis and acetylation of a nucleosome located on the y-axis. Dots on the diagonal reflect cis regulations. (B) Distribution of trans regulations across aceQTL positions. Bin size: 20 Kb. Dash line: significant enrichment (P<0.05, see Methods). (C) Epigenomic profiles of H3K14ac at the KAR4 locus. Color reflects ChIP-chip intensity relative to BY MATα from low (dark blue) to high (orange) at every informative probe (many per nucleosome). Frames indicate 5 nucleosomes in linkage with MAT, including 3 SNEPs (plain) and 2 nucleosomes not initially called SNEPs (dashed). The 60 segregants are separated by their mating type. (D) Acetylation of nucleosome VI-206633 (y-axis) is controlled by two aceQTLs of opposite effects. Each black dot represents one segregant with genotype as indicated on the x-axis (R:RM, b:BY, markers chrII-346634 and chrVI-213813, respectively). Horizontal bars: group means. Blue and magenta large dots represent replicates on BY and RM strains, respectively. Upper red diamond: mean acetylation value of segregants bb and bR. Lower red diamond: mean acetylation value of segregants Rb and RR. The dashed red line joining these diamonds indicates the effect of the first QTL on chrII (RM allele conferring low value), which counteracts the effect of the second QTL on chrVI (RM allele conferring high value). (E) Comparison of aceQTLs and eQTLs. For each significant aceQTL, all genes located within 10 Kb of the target nucleosome were considered and the one having highest eQTL score to the aceQTL marker was retained. Scores are nominal −log10(P). n.s.: non significant scores were grouped together. (F) Correlated genetic segregation of acetylation of nucleosome chrX-458048 (y-axis) and expression of SPC1 gene (x-axis) containing this nucleosome. Each dot represents one segregant, colored according to the genotype at the locus (red: BY, black: RM). (G) Same as F) but for nucleosome chrIII-28678 and gene KAR4, colored according to genotype at the trans aceQTL (MAT locus). (H) Fraction of successful aceQTL mapping for the two categories of SNEPs defined in Figure 2C.

Anne-Laure Abraham, et al. PLoS Genet. 2012 September;8(9):e1002958.

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