What question did this study set out to answer?

Identify the genetic basis of resistance to the toxic analogue aspartic hydroxamate and characterize the regulatory mechanisms governing asparaginase activity in Aspergillus nidulans.

February 1, 1977Journal of General Microbiology

Aspartic Hydroxamate Resistance and Asparaginase Regulation in the Fungus Aspergillus nidulans

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Authors

CDConstantin Drainas JKJ. R. Kinghorn JPJoe Pateman

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Overview

Genetic analysis reveals that recessive ahrA mutations eliminate asparaginase activity in Aspergillus nidulans, indicating that ammonium repression controls enzyme derepression.

Key Points

Identify the genetic basis of resistance to the toxic analogue aspartic hydroxamate and characterize the regulatory mechanisms governing asparaginase activity in Aspergillus nidulans.
Isolated 11 aspartic hydroxamate-resistant mutants and conducted genetic linkage mapping.
Assayed asparaginase enzyme kinetics and Michaelis constants (Km) by quantifying aspartic hydroxamate formation across diverse nitrogen growth conditions.
All 11 resistant mutations mapped to the recessive ahrA locus on linkage group VIII, resulting in low or undetectable asparaginase activity.
Asparaginase exhibited Km values of 0.6 mM for asparagine and 8.3 mM for hydroxylamine, with repression observed on ammonium or glutamine.
Peak asparaginase activity occurred after transferring ammonium-grown cells to nitrogen-free medium for 3 hours, a derepression process requiring de novo protein synthesis.

Cite This Study

Drainas et al. (1977) studied this question.

synapsesocial.com/papers/6a8a404b5edafe343d930c4f https://doi.org/10.1099/00221287-98-2-493

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February 1, 1977Journal of General Microbiology

Aspartic Hydroxamate Resistance and Asparaginase Regulation in the Fungus Aspergillus nidulans

View Full Paper

Ask AI

Bookmark

Authors

CDConstantin Drainas JKJ. R. Kinghorn JPJoe Pateman

Discussion

Member takes

Overview

Genetic analysis reveals that recessive ahrA mutations eliminate asparaginase activity in Aspergillus nidulans, indicating that ammonium repression controls enzyme derepression.

Key Points

Identify the genetic basis of resistance to the toxic analogue aspartic hydroxamate and characterize the regulatory mechanisms governing asparaginase activity in Aspergillus nidulans.
Isolated 11 aspartic hydroxamate-resistant mutants and conducted genetic linkage mapping.
Assayed asparaginase enzyme kinetics and Michaelis constants (Km) by quantifying aspartic hydroxamate formation across diverse nitrogen growth conditions.
All 11 resistant mutations mapped to the recessive ahrA locus on linkage group VIII, resulting in low or undetectable asparaginase activity.
Asparaginase exhibited Km values of 0.6 mM for asparagine and 8.3 mM for hydroxylamine, with repression observed on ammonium or glutamine.
Peak asparaginase activity occurred after transferring ammonium-grown cells to nitrogen-free medium for 3 hours, a derepression process requiring de novo protein synthesis.

Cite This Study

Drainas et al. (1977) studied this question.

synapsesocial.com/papers/6a8a404b5edafe343d930c4f https://doi.org/10.1099/00221287-98-2-493

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