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Conidia of A. niger aggregated into clumps, and then germinated to form masses of mycelia (pellets) when grown in agitated, submerged, liquid cultures. Cyclic AMP and 5′-GMP promoted the aggregation of conidia, while adenosine, AMP, ADP, dibutyryl cyclic AMP, cyclic GMP, guanosine, GDP, GTP and theophylline were ineffective. ATP and 2′, 3′-cyclic AMP elicited a weak response. Conidia in the center of clumps did not germinate. The increase in “adhesiveness” of conidia by cyclic AMP and GMP may have implications in the regulation of germination, as well as the eventual growth and development of hyphae.

Aspergillus niger was found to possess adenyl cyclase, one or more cyclic adenosine 3′,5′-monophosphate (cAMP) binding proteins, and two apparently distinct cAMP phosphodiesterases, one intracellular (I-PDE) and the other extracellular (E-PDE). All these activities except E-PDE were located in the soluble fractions of the cells. The I-PDE was partially purified by protamine sulfate treatment, ammonium sulfate precipitation, ethanol precipitation, and DEAE-cellulose chromatography. The I-PDE had a pH optimum of 7.5, was activated by magnesium ions, and was inhibited by EDTA. The Km for cAMP was 2.5 mM, and for cyclic guanosine 3′,5′-monophosphate (cGMP), 0.5 mM. The E-PDE had a pH optimum of 3.5 and was inactive at pH 7.5. The Km for cAMP was 18 μM. Preliminary evidence was obtained that the activity of the E-PDE may be regulated by endogenous inhibitor.

Aspergillus niger accumulated citric acid in the medium under certain conditions. Cyclic AMP concentrations of the order of 10−6M and higher caused an increase in the rate of citrate synthesis. Adenosine, ATP, and cyclic GMP at 10−3M also stimulated, but were ineffective at 10−4M. 5′-AMP had no effect while 5′-GMP and guanosine inhibited slightly. ADP showed a 42% inhibition. Theophylline enhanced the cyclic AMP effect. It is proposed that citric acid accumulation by Aspergillus niger may result from abnormal cyclic AMP metabolism.