Three mutations impairing penicillin production in Aspergillus nidulans, npeB, npeC and npeD, have been located on linkage groups III, IV and II, respectively, and positioned relative to other loci on these chromosomes.

No abstract

A number of mutants impaired in penicillin production have previously been isolated from Penicillium chrysogenum and Aspergillus nidulans. During cofermentation of osmotically fragile mycelia derived from these strains, in the presence of inhibitors of cell wall regeneration, intergeneric cosynthesis has been demonstrated between mutants which are probably impaired in different parts of th penicillin biosynthetic pathway.

A mixed culture of Aspergillus nidulans (GH79) and Aspergillusflavus (CMI 91019B) produced two antibiotics, designated VI and VII, which were not elaborated when either fungus was grown alone. Chemical and spectroscopic analysis of VI, the major component, indicated that this compound was identical to hydroxyaspergillic acid. The minor component, VII, was produced in too low a yield for its identity to be established. However, partial characterization suggests that this antibiotic also belongs to the aspergillic acid group of mycotoxins.

Mycelia from four mutants of Aspergillus nidulans impaired in penicillin production at separate genetic loci were treated with an enzyme complex capable of lysine cell walls, then mixed in all possible paired combinations and grown in osmotically buffered penicillin production media, containing 2-deoxyglucose and an unrefined mixture of polyoxins to prevent cell wall regeneration. The culture filtrates were assayed after 6 d and significant penicillin yields were observed in four of the six possible combinations. None of these pairs produced penicillin when grown together as normal mycelium, suggesting that intermediates of the penicillin biosynthetic pathway unable to diffuse from untreated mycelium could do so from enzyme-treated mycelium when cell wall regeneration was inhibited. A general method is thus available for examining biochemical pathways with mutants accumulating intermediates unable to cross the cell wall barrier.