Additional file 3: of A modified sequence capture approach allowing standard and methylation analyses of the same enriched genomic DNA sample

Table S1. Drought tolerance associated genes. 120-mer probes were tiled end-to-end across these genes of particular interest [15–18]. (PDF 81 kb

Additional file 2: of A modified sequence capture approach allowing standard and methylation analyses of the same enriched genomic DNA sample

Figure S2. Design of the 12 Mbp wheat gene capture array. The 110 Mbp design target sequence for the capture probe set is as described by Gardiner et al. (Gardiner et al., 2015). The RNA baits for this SureSelect Methyl-Seq Target Enrichment system are all 120 bp in length, unique, non-repetitive and are evenly placed across the available wheat genic target sequence according to the design illustrated. (PDF 187 kb

Additional file 1: of A modified sequence capture approach allowing standard and methylation analyses of the same enriched genomic DNA sample

Figure S1. Depth of coverage summarised for the non-bisulphite treated samples per extended bait sequence reference contig. Reference extended bait sequence contigs here are organized using POPseq chromosomal pseudomolecules. a) Displays data for the NBTS sample and b) displays data for the NBTF sample. (PDF 1425 kb

Summary of gene expression changes.

<p>(A) Venn diagram of Genes upregulated ≥ 2-fold (log counts per million) compared to the MHB control. (B) Venn diagram of Genes downregulated ≥ 2-fold (log counts per million) compared to the MHB control.</p

Culturability of <i>C</i>. <i>jejuni</i> strains during survival periods in sterile distilled water.

<p>The percentage of the original inoculum retaining culturability is shown at 0 h, 72 h and 240 h at 4°C and at 0 h, 24 h and 48 h at 25°C. The percentage of viable cells at 72 h at 4°C and 24 h at 25°C (indicated by the line graphs) was determined by LIVE/DEAD staining (BacLight, Invitrogen) for <i>C</i>. <i>jejuni</i>. The error bars represent a 5% error, three independent biological replicates were performed.</p

Significant expression changes determined through BitSeq analysis of <i>C</i>. <i>jejuni</i> M1 flagellar assembly components mapped in KEGG.

<p>Results are shown for Time 0, 25°C (24 h) and 4°C (72 h) in sterile distilled water.</p

Expression changes in stress-related genes.

<p>The heatmap shows log fold change (logFC) calculated in edgeR compared to the MHB Control (blue = negative, red = positive, the white traceline in the columns indicates the size of the logFC measurement), and displays normalized counts per million (CPM) in numbers. It includes known stress response genes and genes up- or down-regulated ≥2-fold compared to the MHB control based on normalized CPM (numbers displayed in the heatmap matrix) for MHB Control, Time 0, 24 h (25°C) and 72 h(4°C). Square brackets display the type of stress response the gene is involved in (if known). The Histogram in the Colour key indicates the distribution of the data included in the heatmap.</p

Significant expression changes determined through BitSeq analysis of <i>C</i>. <i>jejuni</i> M1 chemotaxis components mapped in KEGG.

<p>Results are shown for Time 0, 25°C (24 h) and 4°C (72 h) in sterile distilled water.</p

Generation and transmission of interlineage recombinants in the SARS-CoV-2 pandemic

We present evidence for multiple independent origins of recombinant SARS-CoV-2 viruses sampled from late 2020 and early 2021 in the United Kingdom. Their genomes carry single-nucleotide polymorphisms and deletions that are characteristic of the B.1.1.7 variant of concern but lack the full complement of lineage-defining mutations. Instead, the remainder of their genomes share contiguous genetic variation with non-B.1.1.7 viruses circulating in the same geographic area at the same time as the recombinants. In four instances, there was evidence for onward transmission of a recombinant-origin virus, including one transmission cluster of 45 sequenced cases over the course of 2 months. The inferred genomic locations of recombination breakpoints suggest that every community-transmitted recombinant virus inherited its spike region from a B.1.1.7 parental virus, consistent with a transmission advantage for B.1.1.7's set of mutations.</p