Polyamine-deficient Neurospora crassa mutants and synthesis of cadaverine

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Abstract
The polyamine path of N. crassa originates with the decarboxylation of ornithine to form putrescine (1,4-diaminobutane). Putrescine acquires 1 or 2 aminopropyl groups to form spermidine or spermine, respectively. An ornithine decarboxylase-deficient mutant was isolated and the mutation is allelic with 2 previously isolated polyamine-requiring mutants. The locus is named spe-1. The 3 spe-1 mutants form little or no polyamines and grow well on medium supplemented with putrescine, spermidine or spermine. Cadaverine (1,5-diaminopentane), a putrescine analog, supports very slow growth of spe-1 mutants. An arginase-deficient mutant (aga) can be deprived of ornithine by growth in the presence of arginine, because arginine feedback inhibits ornithine synthesis. Like spe-1 cultures, the ornithine-deprived aga culture failed to make the normal polyamines. Unlike spe-1 cultures, it had highly derepressed ornithine decarboxylase activity and contained cadaverine and aminopropylcadaverine (a spermidine analog), especially when lysine was added to cells. The ornithine-deprived aga culture was capable of indefinite growth. It is likely that the continued growth is due to the presence of cadaverine and its derivatives and that ornithine decarboxylase is responsible for cadaverine synthesis from lysine. An inefficient lysine decarboxylase activity (Km > 20 mM) was detectable in N. crassa. It varied in constant ratio with ornithine decarboxylase activity and was wholly absent in the spe-1 mutants.