1887

Abstract

SUMMARY: A pyrimidine-requiring mutant of Neurospora was found to grow on minimal medium when the proportion of CO in the gas-phase (air) was increased to 30% (v/v); arginine prevented growth in 30% CO, but did not prevent growth when pyrimidines were present. An arginine-requiring mutant also grew on minimal medium in the presence of 30% CO. The response of this mutant to CO was annulled by pyrimidines. It is proposed that these mutants have defects in carbamoyl phosphate synthesis. Wild-type Neurospora may have two pathways for making carbamoyl phosphate from CO, one pathway subject to feed-back inhibition or repression by arginine, the other pathway subject to feed-back inhibition or repression by pyrimidines. The pyrimidine mutant may lack an enzyme which produces carbamoyl phosphate for pyrimidine synthesis, and the arginine mutant may lack an enzyme which produces carbamoyl phosphate for arginine synthesis. Thus each mutant may have only one effective mechanism for carbamoyl phosphate synthesis. It is suggested that 30% CO causes increased synthesis of carbamoyl phosphate by the remaining pathway in each mutant, thereby providing sufficient carbamoyl phosphate to overcome the nutritional deficiency. The inhibition of the pyrimidine mutant by arginine, and the inhibition of the arginine mutant by pyrimidines, are explained as feed-back inhibition or repression of the remaining pathway for carbamoyl phosphate synthesis.

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/content/journal/micro/10.1099/00221287-34-1-131
1964-01-01
2021-10-23
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