Summary: Uptake of CH NH (methylammonium) was measured as a probe of NH transport in intact cells and derivatives impaired in the Ntr regulatory system. The results suggest that expression of the high affinity CH NH transport system () requires polypeptide synthesis, () is activated the and regulatory products under nitrogen limitation, and () is repressed under nitrogen excess by the product. Cells deficient in glutamate synthase activity by virtue of their harbouring the mutation were unable to activate synthesis of CHNH transport. This could explain the inability of cells carrying mutations to grow on low concentrations of NH .


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