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1.
Figure 4

Figure 4. DCC binding spreads into the autosomal regions of an X;autosome fusion chromosome. From: The C. elegans dosage compensation complex propagates along chromatin dynamically and independently of X-chromosome sequence.

Average z scores of DPY-27 ChIP performed in embryos of three strains that contain an X;V, X;II or X;I chromosome are plotted around each fusion site, which is indicated with a dashed line. Dashed boxes highlight DPY-27 binding at promoters. DPY-27 accumulates at the promoters of both autosomal and X-liked genes to a similar degree near the fusion site.

Sevinç Ercan, et al. Curr Biol. ;19(21):1777-1787.
2.
Figure 5

Figure 5. DPY-27 spreading diminishes as a function of distance from the X. From: The C. elegans dosage compensation complex propagates along chromatin dynamically and independently of X-chromosome sequence.

(A) Possible modes of spreading are represented along a virtual X;autosome fusion chromosome. (B) DPY-27 ChIP z score moving average with a window size of 100 kb and a step size of 10 kb is plotted along the coordinates of fused chromosome in X;V. (C) Same as B, for a normal karyotype. (C) An X;II fusion. (D) An X;I fusion.

Sevinç Ercan, et al. Curr Biol. ;19(21):1777-1787.
3.
Figure 2

Figure 2. The binding of DCC components occurs preferentially at promoters and correlates positively with RNA Polymerase II occupancy. From: The C. elegans dosage compensation complex propagates along chromatin dynamically and independently of X-chromosome sequence.

(A) Data were centered at the translation start sites of each X-linked gene, and the average z score of the probes in a sliding window was plotted. Data from members of the DCC that are homologous to the subunits of condensin are shown in orange. SDC-2 and SDC-3 (in blue) are involved in X-specific recruitment. (B) A moving average of ChIP enrichment at promoters of X-linked genes is plotted as a function of RNA Polymerase II occupancy [36]. (C) The locations of the 38 known rex sites (red bars), sites of SDC-2 binding (Antibody 1), and DCC foci are indicated along the X chromosome. Green bars indicate overlap with rex sites.

Sevinç Ercan, et al. Curr Biol. ;19(21):1777-1787.
4.
Figure 3

Figure 3. The condensin-like portion of the C. elegans Dosage Compensation Complex (DCC) spreads more efficiently relative to subunits involved in early steps of recruitment. From: The C. elegans dosage compensation complex propagates along chromatin dynamically and independently of X-chromosome sequence.

(A) Average z scores of ChIP enrichment are plotted at the rex-1 dpy-23 locus [14, 16]. Data from members of the DCC that are homologous to the subunits of condensin are shown in orange. SDC-2 and SDC-3 (in blue) are involved in X-specific recruitment. DNA fragments shown in red recruit the DCC onto extra-chromosomal arrays [14]. Fragments in grey fail to recruit but are bound in the context of the natural chromosome. The spreading index is calculated by dividing average ChIP score at the dpy-23 promoter by the corresponding value at rex-1. SDC-2 data are from antibody 1. (B) A second polyclonal SDC-2 antibody raised against a different portion of the protein (antibody 2) in two different rabbits (SDQ3146 for rep1 and 2 and SDQ3148 for rep3) was used to generate the ChIP-chip profiles.

Sevinç Ercan, et al. Curr Biol. ;19(21):1777-1787.
5.
Figure 1

Figure 1. DCC binding is dynamically specified according to transcriptional activity during development. From: The C. elegans dosage compensation complex propagates along chromatin dynamically and independently of X-chromosome sequence.

(A) A schematic representation of the DCC inferred from condensin homology (in parenthesis) and co-immunoprecipitation experiments. Members of the complex homologous to condensin subunits are shown in orange. SDC-2 and SDC-3 (dark blue) are involved in X-specific recruitment. DPY-30 is homologous to a subunit of an H3K4 methyltransferase complex. (B) Average z scores of ChIPs performed in embryos or in L4 worms are plotted. F22A3.1 and F22A3.6 are expressed in L4s but not in embryos. Both RNA Polymerase II and DPY-27 binding are higher in L4s compared to embryos. In embryos, C25B8.4 and C25B8.1 are expressed, and correspondingly are bound by high levels of DPY-27. In L4s, C25B8.4 and C25B8.1 transcription and DPY-27 binding are reduced. (C) RNA abundance for the four genes highlighted in panel B [35]. (D) Change in DPY-27 and RNA Polymerase II binding at promoters was calculated by subtracting the ChIP value in embryos from that of L4s. A moving average of values is plotted. Change in DPY-27 level (y axis) correlates positively with change in RNA Polymerase II binding (x axis) on the X (blue), but not on chromosome III (gray). (E) Average DPY-27 and RNA Polymerase II binding in embryos and L4s at two distinct rex sites.

Sevinç Ercan, et al. Curr Biol. ;19(21):1777-1787.
6.
Figure 6

Figure 6. DCC binding extends ~2 Mb into autosomal regions and is determined by distance from the X and transcriptional activity. From: The C. elegans dosage compensation complex propagates along chromatin dynamically and independently of X-chromosome sequence.

(A) Each point represents a site of DPY-27 binding that occurs in the X;V fusion strain but not in a wild-type strain (Methods). The z score of the maximum value probe value is plotted as a function of distance from the X;V fusion site. (B) Distribution of all DPY-27 peaks in X;V fusion (p value E-10) with respect to underlying genes. The maximum value probe within each peak was assigned to a region by CEAS [32]. P values were obtained by chi-square test using the observed and expected distribution of probes among the annotation classes. Expected value was calculated from the CEAS assignment of all microarray probes. The most commonly bound region is highlighted with an asterisk. (C) A scatter plot of average DPY-27 ChIP z scores at promoters (y axis) and RNA abundance (log2RMA-normalized intensity, x axis) of X-linked genes and genes located within 1 Mb of the fusion site on chromosome V. (D) Average DPY-27 ChIP z scores at chromosome V gene promoters is plotted as a function of distance from the fusion site. The outliers at ~12Mb are histone genes which may cross-hybridize to other histone loci in the genome.

Sevinç Ercan, et al. Curr Biol. ;19(21):1777-1787.
7.
Figure 7

Figure 7. In fusion strains, DPY-27 spreads more efficiently than SDC-3 onto autosomal genes, and autosomal genes bound by the DCC are not strongly repressed. From: The C. elegans dosage compensation complex propagates along chromatin dynamically and independently of X-chromosome sequence.

(A) SDC-3 and DPY-27 binding in the X;V fusion strain, at autosomal loci near the fusion site and at rex-1 on X. The fusion site is indicated with a dashed line. At the recruitment site (rex-1) SDC-3 binds more strongly than DPY-27, but in the same sample, DPY-27 binding is stronger within autosomal regions near the fusion site (compare peaks highlighted with dashed boxes). (B) The distribution of maximum probe values within SDC-3 ChIP peaks in the X;V fusion strain, segregated according to their chromosomal location. Binding foci are shown with a bracket. One autosomal peak (indicated with an asterisk) was identified as a focus. (C) However, this peak was created by a single probe that is identical to a focus on the X. (D) SDC-3 and DPY-27 ChIP profiles shown at an autosomal region that contains three copies of the 10 bp sequence motif (pink, bottom). (E) Real-time PCR analysis of the expression of seven genes in the X:V fusion strain embryos grown in liquid media. Six genes are within 2 megabases of the fusion site on chrV. nhr-47 is more than 15 Mb away. (F) Real time PCR analysis of fkb-6 and myo-2 (a dosage compensated gene on the X). RNA was isolated from embryos obtained from worms grown in liquid or plates, and from mixed stage worms grown on plates. The DCC mutant is strain CB428, dpy-21(e428).

Sevinç Ercan, et al. Curr Biol. ;19(21):1777-1787.

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