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Fig. 4 | BMC Biology

Fig. 4

From: Evolution of pathogenicity-associated genes in Rhizoctonia solani AG1-IA by genome duplication and transposon-mediated gene function alterations

Fig. 4

Loss and gain of domain in paralog gene pairs modulate the pathogenesis of R. solani AG1-IA. qRT-PCR-based expression analysis (2−ΔΔCt) of A paralog pair (Rs_06191; with glycosyl hydrolase domain and Rs_10629; lacking the domain) and B Paralog pair (Rs_09094; with GMC oxidoreductase domain and Rs_11334; lacking the domain) upon R. solani infection in rice, at different time points. The fold change in the gene expression was estimated with respect to 0 dpi, using 18S rRNA of R. solani for normalization. C Disease symptoms, D disease index (% RVSC) and E pathogen load in rice tillers infected with gene-silenced (dsRNA-treated) and buffer-treated (control) R. solani mycelia, at 3 dpi. F Disease symptoms, G disease index and H pathogen load in tomato leaves infected with gene silenced (dsRNA-treated) and buffer-treated (control) R. solani mycelia, at 3 dpi. The Rs_GT34-silenced and buffer-treated R. solani were used as a negative control. The pathogen load (2−ΔCt) was estimated as an abundance of 18S rRNA of R. solani, upon normalization with rice 18S or tomato actin gene. The graph shows the mean values ± standard error of three biological replicates. “**”indicates significant difference at p ≤ 0.01, and “*” indicates significant difference at p ≤ 0.05. GMC oxidoreductase, glucose–methanol–choline oxidoreductases. Scale bar: 1 cm

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