Experimental design–<i>Arabidopsis</i> roots were infected with <i>A</i>. <i>tumefaciens</i>.

<p>DNA was extracted at 0, 6 and 24 hours post infection. Extracted DNA was digested with 3 restriction enzymes: <i>Eco</i>RI (RI), <i>Hind</i>III (H3) and <i>Xba</i>I (Xb). An adapter was ligated to the overhang end of the digested DNA. T-DNA-genomic junctions were amplified using three different primers from within the T-DNA and one primer from the adapter (primers—black arrows, LB–left border, RB–right border). Amplicons were sequenced using high throughput sequencing. Adapter to adapter products were reduced as detailed in O’Malley et al. 2007 [<a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1006875#pgen.1006875.ref027" target="_blank">27</a>].</p

Sequence motifs associated with T-DNA–genome junctions sites.

<p>The motifs CACCAC (P-value = 1e-147, HOMER, E-value = 1.7e-234, MEME) and A-rich (P-value < 1e-21, HOMER, E-value = 2.3e-483, MEME) were associated with T-DNA–genome junction sites.</p

T-DNA-genome junctions form early after infection and are influenced by the chromatin state of the host genome - Table 1

<p>T-DNA-genome junctions form early after infection and are influenced by the chromatin state of the host genome</p> - Table

Association of genomic features with T-DNA-genome junctions under selective and non-selective conditions.

<p>A–The genomic distribution of unselected and selected T-DNA–genome junctions across chromosome 4. The numbers of T-DNA–genome junctions (circles, and smoothed blue line) do not show a correlation with the distribution of transposons (TE, red line) and promoters (green line). T-DNA integrations under selective conditions (orange line) correlates with genes/promoters [<a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1006875#pgen.1006875.ref013" target="_blank">13</a>]. B- The portion of each genomic feature: TE (red), genes (purple), promoters (green) and the remaining regions (other, grey). The portion of genomic features is represented across all the genome (genome wide) and according to the number of T-DNA–genome junctions: without selection (Unselected) and with selection (Selected- data from Alonso et al., 2003 [<a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1006875#pgen.1006875.ref013" target="_blank">13</a>]). Selected events [<a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1006875#pgen.1006875.ref013" target="_blank">13</a>] show an enrichment in promoters (χ² test, compared to unselected events, p = 2.88E-24) and a decrease in TE regions (χ2 test, compared to unselected events, p = 0.005).</p

Epigenetic modifications around T-DNA–genome junctions.

<p>The analysis was performed separately in pericentric (grey background) and in remaining (distal) chromosomal regions. The up and downstream regions to T-DNA–genome junctions (represented as the 0 bp) are shown on the X axis. The Y axis represents the arbitrary level of the epigenetic markers. Blue squares–unselected T-DNA–genome junctions. Orange triangle–integrations under selective conditions [<a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1006875#pgen.1006875.ref013" target="_blank">13</a>]. Black circles–control, random genomic positions.–. A- CG methylation. B–Nucleosome occupancy. C- H3K27me3 modification.</p