Dipicolinic acid synthesis in
Penicillium citreoviride strain 3114 was inhibited by Ca
2+ ions, but not by Ba
2+, Cu
2+or Fe
2+. Among the metals tested, only Zn
2+ inhibited the synthesis of dipicolinic acid and promoted sporulation. None of these metals reversed the inhibition by Ca
2+ or Zn
2+. A mutant 27133
-dpa-ca selected for resistance to feedback inhibition by dipicolinic acid: Ca
2+ complex showed cross-resistance to inhibition by dipicolinic acid: Zn
2+. Both 3114 and
271 33-dpa-ca excreted a number of aliphatic and amino acids during secondary metabolism of dipicolinic acid. In the presence of 1000 ppm
of Ca
2+, accumulation of citric acid and α-aminoadipic acid was completely inhibited under conditions of inhibition of dipicolinic
acid in parent strain 3114 but not in the mutant. Citric acid with or without Ca
2+ did not inhibit the
de novo synthesis of dipicolinic acid in the strain 3114. In fact, citric acid in the presence of Ca
2+ improved significantly rate of dipicolinic acid synthesis. Apart from resistance to feed back inhibition by dipicolinic acid:
Ca
2+ complex, mutant differed from the parent in three other aspects
viz. (i) dipicolinic acid synthesis was not subject to catabolite repression by glucose, (ii) sporulation as well as dipicolinic
acid synthesis was dependent on the presence of Ca
2+ ions in the medium and (iii) Mg
2+ requirement for the mutant increased three fold. Higher requirement of the Mg
2+ could be partially relieved by Ca
2+ during secondary metabolism. The results support the inference that
de novo synthesis of dipicolinic acid is regulated through feedback inhibition by dipicolinic acid: Ca
2+complex.
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