Increased virulence of Δ<i>amr1</i> mutants on individual host plants (<i>Brassica oleracea</i>).

<p>A. Lesions on <i>B. oleracea</i> 5 days after inoculation with ∼2,000 conidia of the wild type, a Δ<i>amr1</i> mutant, and three complemented mutants with two types of constructs. B. Lesions produced by ∼440 and ∼400 conidia respectively of the wild type (left) and a Δ<i>amr1</i> mutant (right). C. Lesions produced by ∼330 and ∼300 conidia respectively of the wild-type (left) and a Δ<i>amr1</i> mutant (right). The three images in panels A–C are replicate experiments with the same pattern of inoculation. Note that the size of lesions caused by the mutant is similar on all leaves, while lesions caused by the wild type are smaller on young leaves than on old leaves. Δ<i>amr1-1</i> and Δ<i>amr1-4</i> produced similar results. D. Pathogenicity assay results for three mutants (Δ<i>amr1-1</i>, Δ<i>amr1-4</i>, and Δ<i>amr1-5</i>) compared to the wild type. E. Pathogenicity assay results with average lesion diameter (mm) and standard deviation. Abbreviations: wt = wild-type <i>A. brassicicola</i>; Δ<i>amr1 = Amr1</i> deletion mutant; compl = mutant complemented with a native allele of the <i>Amr1</i> gene (Δ<i>amr1:Amr1</i>); cons = mutant complemented with chimeric constructs of the <i>TrpC</i> promoter and a native allele of the <i>Amr1</i> coding region (Δ<i>amr1:TrpCp-Amr1</i>).