SUMMARY: Eleven mutants resistant to a toxic analogue of asparagine, aspartic hydroxamate, have been isolated; they are allelic and map at the locus. These mutations result in low or non-detectable asparaginase activity. mutations are recessive for asparaginase activity and aspartic hydroxamate resistance. The locus is in linkage group VIII and is loosely linked with and Asparaginase activity was measured the by formation of aspartic hydroxamate from asparagine and hydroxylamine. The values of asparaginase for asparagine and hydroxylamine are 0.6 and 8.3 mM respectively. Minimum asparaginase activity is present in cells grown on ammonium or glutamine. Maximum asparaginase activity is present in wild-type cells grown on ammonium and then held in nitrogen-free medium for 3 h. Derepression from this ammonium repression requires protein synthesis. A number of different types of ammonium-repressed and of ammonium-derepressed mutants have abnormal regulation of asparaginase activity.


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