Abstract
We investigated the role of the siderophore rhodotorulic acid (RA) accumulation in the host–pathogen interaction of Microbotryum violaceum and Silene latifolia. While the wild-type M. violaceum accumulated RA in the culture medium in response to iron stress, the monogenic mutant 45 of M. violaceum did not accumulate detectable amounts of RA under limiting iron supply. Genetic analysis showed the mutant 45 locus to be 3.8 cM from the centromere, endorsing the pericentric gene clustering of M. violaceum. Crosses of mutant and wild-type strains demonstrated that the lack of siderophore accumulation in mutant 45 did not preclude pathogenesis, hence fungal reproduction.
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