Table 1.
Six hypotheses to explain increased CYP-mediated resistance that are testable with RNA-seq and/or proteomic data.
Fig 1.
Genes and lncRNAs that were up- or down-regulated between two strains from the RNA-seq experiments.
A: Venn diagram of the number of genes and lncRNAs that are significantly up-regulated (log2 (FC) ≥ 1 & FDR ≤ 0.01) between two strains; B: Venn diagram of the number of genes and lncRNAs that are down-regulated (log2 (FC) ≤ -1 & FDR ≤ 0.01) between two strains; C: Heat map of the top 20 most differentially expressed genes (based on CKR vs. ROCK comparison, but all genes shown were also differentially expressed in SP relative to ROCK). Heat maps were generated using PHEATMAP (https://www.rdocumentation.org/packages/pheatmap/versions/1.0.12/topics/pheatmap).
Fig 2.
Venn diagram of homozygous single nucleotide polymorphisms (SNPs) called from transcriptomic data in ROCK, SP and CKR strains, relative to the susceptible Liverpool strain.
Fig 3.
The distribution of potentially resistance associated SNPs across three chromosomes within a 10 Mb window size.
The two resistance loci detected on chromosome 1 and chromosome 3 are shown by the orange and blue shaded areas, respectively. Red arrow indicates the coordinate of Vssc on chromosome 3.
Fig 4.
Proteins that were significantly up- or down-regulated between two strains.
A: Venn diagram of the numbers of proteins that are significantly up-regulated (p ≤ 0.05) between two strains; B: Venn diagram of the number of genes that are down-regulated (p ≤ 0.05) between two strains; C: Heat map of the top 20 most differentially expressed proteins (based on CKR vs. ROCK comparison, but all genes shown were also differentially expressed in SP relative to ROCK). Heat maps were generated using PHEATMAP (https://www.rdocumentation.org/packages/pheatmap/versions/1.0.12/topics/pheatmap).
Table 2.
Summary of CYPs that were overexpressed in transcriptomic and/or proteomic analyses.
Table 3.
Summary of non-CYP genes that were up- or down- regulated at both transcript and protein levels in the SP and CKR relative to ROCK.
Table 4.
Comparison of differences found in the RNA-seq and proteomics studies using an unrelated resistant strain, a congenic resistant strain, or both.
Fig 5.
Correlation between all detected proteins and transcripts.
A: Plot of the log2 (FC) between all detected proteins and transcripts (red line) for SP relative to ROCK (Pearson’s correlation of 0.32). B: Plot of the log2 (FC) between all detected proteins and transcripts for CKR relative to ROCK (Pearson’s correlation of 0.20). The dashed line represents a slope of 1.0.
Fig 6.
Correlation plots of the log2 (FC) between detected CYP proteins and transcripts (red line) for SP and CKR relative to ROCK.
A: Correlation plot of the log2 (FC) between detected CYP proteins and transcripts for SP relative to ROCK. B: Correlation plot of the log2 (FC) between detected CYP proteins and transcripts for CKR relative to ROCK. The dashed line represents a slope of 1.0.
Table 5.
List of factors potentially responsible for CYP-mediated resistance in SP identified by RNA-seq and proteomic analyses.
The hypotheses are explained in Table 1. Genes were put into the final column if their position in the genome was consistent with the mapped resistance loci (40Mb-250Mb and 300Mb-310Mb in chromosome 1; 310Mb-320Mb and 330Mb-360Mb in chromosome 3, Fig 3). The VectorBase accession numbers for the CYPs are shown in S18 Table. .