The flux to arginine was determined in growing mycelium of carrying the mutation, by measuring the exponential growth rate and the arginine content of the free pool and that in protein. Derepression of the enzymes in the pathway by a factor of about three resulted in a 14% increase in the flux. Using a mutant (), which affected the cross-pathway control, the pathway enzymes were found to have about threefold lower activities. This resulted in a 16% decrease in the measured flux. The effect of arginine acting as a feedback inhibitor of acetylglutamate kinase was estimated in an mutant by varying the steady-state arginine concentration using histidine as a competitive inhibitor of the citrulline uptake. It is concluded that the feedback loop is mainly responsible for the small response of the flux to the large coordinate changes in the pathway enzymes. The results are discussed in terms of control analysis of metabolic systems.