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Pleiotropy and epistasis within and between signaling pathways defines the genetic architecture of fungal virulence

Fig 6

SSK1, SSK2, and RIC8 gene models.

Exons are shown as large grey rectangles, while the introns, 5’ UTR, and 3’ UTR are shown as grey, horizontal lines. The positions of the predicted start and stop codons are annotated along the bottom of the gene bodies and the positions of genetic differences between 431α and XL280a are marked by black, vertical lines. Within the second exon of SSK1, an insertion of a single nucleotide, present in the 431α parental strain is predicted to cause a frame shift that leads to a downstream early stop-gain. Within the second and third exons of SSK2, two SNPs are annotated that lead to non-synonymous changes previously identified by Bahn et al. [143]. Within the second-to-last exon of RIC8, a SNP is present in the XL280a parental strain that is predicted to cause a premature stop. The local, predicted translations of the regions near these non-synonymous, genetic variants and associated amino acids are annotated in colored rectangles.

Fig 6