The proteins VeA, VelB and LaeA of Aspergillus nidulans form a heterotrimeric complex (the velvet complex)
in the dark to coordinate sexual development and production of some secondary metabolites. VeA
and VelB of A. nidulans and Aspergillus fumigatus also are repressors of conidiation, but VeA of Aspergillus
flavus in studied strains acts positively on conidiation. In the present study, we show via yeast-two hybrid
assays that interactions among A. flavus VeA, VelB, and LaeA are conserved as in the A. nidulans velvet
complex. We found that FluG, which is required for conidiophore formation in A. nidulans but whose deletion
in A. flavus delays onset of conidiation, was probably an interacting partner of VelB. Deletion of velB
in A. flavus CA14 severely impaired conidiation in the dark although to a lesser extent than deletion of
veA. In both mutants fluG deletion resulted in further decreased conidiation even in the light. Deletion
of fluG in the DlaeA strain, however, did not affect conidiation. All mutant types were unable to produce
aflatoxin and sclerotia. Cross-complementation of the DvelB strain with gpdA::veA restored conidiation
but not aflatoxin production although aflR, the aflatoxin pathway regulatory gene, was expressed at a
normal level. Cross-complementation of the DveA strain with gpdA::velB failed to restore conidiation
and aflatoxin production. The DvelB strain complemented with or a wild type transformed by gpdA::velB
had elevated sclerotial production as the DfluG strain. Concerted interactions of A. flavus VeA and VelB
with LaeA are critical for conidiation and aflatoxin biosynthesis. VelB may have a dual role and likely
coordinates with FluG to modulate sclerotial production.
The proteins VeA, VelB and LaeA of Aspergillus nidulans form a heterotrimeric complex (the velvet complex)
in the dark to coordinate sexual development and production of some secondary metabolites. VeA
and VelB of A. nidulans and Aspergillus fumigatus also are repressors of conidiation, but VeA of Aspergillus
flavus in studied strains acts positively on conidiation. In the present study, we show via yeast-two hybrid
assays that interactions among A. flavus VeA, VelB, and LaeA are conserved as in the A. nidulans velvet
complex. We found that FluG, which is required for conidiophore formation in A. nidulans but whose deletion
in A. flavus delays onset of conidiation, was probably an interacting partner of VelB. Deletion of velB
in A. flavus CA14 severely impaired conidiation in the dark although to a lesser extent than deletion of
veA. In both mutants fluG deletion resulted in further decreased conidiation even in the light. Deletion
of fluG in the DlaeA strain, however, did not affect conidiation. All mutant types were unable to produce
aflatoxin and sclerotia. Cross-complementation of the DvelB strain with gpdA::veA restored conidiation
but not aflatoxin production although aflR, the aflatoxin pathway regulatory gene, was expressed at a
normal level. Cross-complementation of the DveA strain with gpdA::velB failed to restore conidiation
and aflatoxin production. The DvelB strain complemented with or a wild type transformed by gpdA::velB
had elevated sclerotial production as the DfluG strain. Concerted interactions of A. flavus VeA and VelB
with LaeA are critical for conidiation and aflatoxin biosynthesis. VelB may have a dual role and likely
coordinates with FluG to modulate sclerotial production.
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