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LaeA and VeA coordinate secondary metabolism and differentiation in response to light signals in  Aspergillus  spp. Their orthologs, ChLae1 and ChVel1, were identified in the maize pathogen  Cochliobolus heterostrophus , known to produce a wealth of secondary metabolites, including the host selective toxin, T-toxin. Produced by race T, T-toxin promotes high virulence to maize carrying Texas male sterile cytoplasm (T-cms). T-toxin production is significantly increased in the dark in wild type (WT), whereas  Chvel1  and  Chlae1  mutant toxin levels are much reduced in the dark compared to WT. Correspondingly, expression of T-toxin biosynthetic genes ( Tox1 ) is up-regulated in the dark in WT, while dark-induced expression is much reduced/minimal in  Chvel1  and  Chlae1  mutants. Toxin production and  Tox1  gene expression are increased in  ChVEL1  overexpression (OE) strains grown in the dark and in  ChLAE1  strains grown in either light or dark, compared to WT. These observations establish ChLae1 and ChVel1 as the first factors known to regulate host selective toxin production. Virulence of  Chlae1  and  Chvel1  mutants and OE strains is altered on both T-cms and normal cytoplasm maize, indicating that both T-toxin mediated super virulence and basic pathogenic ability are affected. Deletion of  ChLAE1  or  ChVEL1  reduces tolerance to H 2 O 2 . Expression of  CAT3 , one of the three catalase genes, is reduced in the  Chvel1  mutant.  Chlae1  and  Chvel1  mutants also show decreased aerial hyphal growth, increased asexual sporulation and female sterility.  ChLAE1  OE strains are female sterile, while  ChVEL1  OE strains are more fertile than WT. ChLae1 and ChVel1 repress expression of 1,8-dihydroxynaphthalene (DHN) melanin biosynthesis genes, and, accordingly, melanization is enhanced in  Chlae1  and  Chvel1  mutants, and reduced in OE strains. Thus, ChLae1 and ChVel1 positively regulate T-toxin biosynthesis, pathogenicity and super virulence, oxidative stress responses, sexual development, and aerial hyphal growth, and negatively control melanin biosynthesis and asexual differentiation.

ChLae1 and ChVel1 Regulate T-toxin Production, Virulence, Oxidative Stress Response, and Development of the Maize Pathogen Cochliobolus heterostrophus