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. Author manuscript; available in PMC: 2011 Aug 1.
Published in final edited form as: Mol Microbiol. 2010 Jun 1;77(3):587–604. doi: 10.1111/j.1365-2958.2010.07234.x

Fig. 5.

Fig. 5

Reduction of FTR1 copy number reduces R. oryzae virulence in the DKA mouse models. (A) Survival of DKA mice (n=6 for wild-type and 5 for pyrF null mutant) infected with R. oryzae wild-type (3.3 × 103) or pyrF null mutant (2.6 × 103). (B) A representative of the putative ftr1 null mutant demonstrated comparable growth to R. oryzae PyrF-complemented strain on YPD or CSM-URA media. (C) Survival of mice (n=13 per group from two experiments with similar results) infected i.v. with R. oryzae wild-type (average inoculum of 4.3 × 103 spores), R. oryzae PyrF-complemented strain (average inoculum of 4.2 × 103 spores) or with putative ftr1 null mutant (average inoculum of 3.2 × 103 spores). *, P<0.0005 compared to wild-type or PyrF-complemented strains. (D) Survival of mice (n= 9) infected intranasally with R. oryzae wild-type (4.3 × 103 spores), R. oryzae PyrF-complemented strain (5.1 × 103 spores) or putative ftr1 null mutant (5.3 × 103 spores). *, P=0.04 compared to wild-type or PyrF-complemented strains.

HHS Vulnerability Disclosure