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ARST HN, COVE DJ, 1970, MOLYBDATE METABOLISM IN ASPERGILLUS-NIDULANS .2. MUTATIONS AFFECTING PHOSPHATASE ACTIVITY OR GALACTOSE UTILIZATION, MOLECULAR AND GENERAL GENETICS, Vol: 108, Pages: 146-+, ISSN: 0026-8925
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Arst HN, MacDonald DW, Cove DJ, 1970, Molybdate metabolism in Aspergillus nidulans. I. Mutations affecting nitrate reductase and-or xanthine dehydrogenase., Mol Gen Genet, Vol: 108, Pages: 129-145, ISSN: 0026-8925
Arst HN, Cove DJ, 1970, Molybdate metabolism in Aspergillus nidulans. II. Mutations affecting phosphatase activity or galactose utilization., Mol Gen Genet, Vol: 108, Pages: 146-153, ISSN: 0026-8925
Elorza MV, Arst HN, Cove DJ, et al., 1969, Permeability properties of Aspergillus nidulans protoplasts., J Bacteriol, Vol: 99, Pages: 113-115, ISSN: 0021-9193
The regeneration of mycelial forms from protoplasts of mutant and wild-type strains of Aspergillus nidulans was followed microscopically under conditions with which the rate of regeneration depends upon a specific transport function. This method has shown that at least four uptake systems-one for divalent anions, two for purines, and one for sugars-remain functional after removal of the cell wall.
Arst HN, Cove DJ, 1969, Methylammonium resistance in Aspergillus nidulans., J Bacteriol, Vol: 98, Pages: 1284-1293, ISSN: 0021-9193
Mutants of Aspergillus nidulans resistant to methylammonium toxicity are simultaneously derepressed in the presence of ammonium for apparently all ammonium-repressible activities. Enzyme assays directly demonstrate derepression of nitrate, nitrite, and hydroxylamine reductases, xanthine dehydrogenase, urate oxidase, and allantoinase, whereas in vivo tests show that ammonium and methylammonium repression or inhibition (or both) is relieved in these mutants in pathways of nitrate assimilation, purine transport and degradation, and amino acid, amine, and amide catabolism. Ammonium and methylammonium uptake is apparently not defective in these mutants, for they grow normally on limiting levels of these ions as sole nitrogen source. There is no evidence that more than one gene can mutate to produce the methylammonium resistance (mea(R)) phenotype. Such mutations are semidominant in both heterocaryons and diploids. The ability of mea(R) mutations to effect derepression of activities specified by genes within another nucleus in a heterocaryon shows that the action of the mea product is not restricted to the nucleus. Three types of hypotheses might explain this generalized derepression. First, ammonium and methylammonium might not themselves be co-repressors but might require a metabolic conversion, blocked in these mutants, to become co-repressors. Secondly, the mea locus might specify an activity expressed in mea(R) but not wild-type (mea(S)) strains, which diminishes the concentration of ammonium and methylammonium participating in co-repression. Finally, ammonium repression might involve a macromolecular control element specified by the mea(R) locus and common to many or all ammonium-repressible systems. The existence of "regulation reversal mutations" at the mea(R) locus and the lack of uniformity and coordination with which different enzymatic activities respond to mutational derepression is most compatible with the last type of hypothesis.
Arst HN, 1968, Genetic analysis of the first steps of sulphate metabolism in Aspergillus nidulans., Nature, Vol: 219, Pages: 268-270, ISSN: 0028-0836
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