Selenate-resistant (SelR) mutants of Botrytis cinerea were selected by
plating conidia or mycelial plugs onto minimal medium amended with se
lenate and taurine. Ultraviolet irradiation of conidia to give 5% surv
ival increased mutant yield twenty-fold. Mutants could be divided into
three classes based on growth in the presence of selenate or chromate
and on response to taurine in minimal media. Nitrate non-utilizing (N
it) mutants, generated as spontaneous sectors on minimal media amended
with chlorate, behaved as nif1 mutants in growth tests (i.e. putative
ly defective in nitrate reductase apoenzyme). When nit1 mutants were p
aired on medium with nitrate as sole nitrogen source some pairings com
plemented, behaviour attributed to intragenic complementation. Selecte
d crosses of SelR and nit1 mutants with wild-type strains gave 1:1 seg
regation of both phenotypes and no evidence of linkage to either Mbc1
(benzimidazole resistance) or Daf 1 (dicarboximide resistance) markers
; loose linkage was confirmed between Mbc1 and Daf 1. Strains showing
the SelR phenotype may result from mutations in different genes; the g
enotypic symbol Sel 1 is allocated to one of these mutations. Four-poi
nt crosses involving the markers at Sel1, nit1, Mbc1 and Daf1 generate
d progeny with all 16 genotypes. Both Sel1R and nit1 mutants were stab
le following subculture and retained pathogenicity in a bean seedling
assay. Complementation was demonstrated between SelR and nit1 mutants
selected from the same parent.