Final answer:
Hypothesis D, that the mutant cells have impaired glucose metabolism, is a plausible hypothesis considering the importance of enzymes in converting galactose to glucose and the impact of such mutations as seen in diseases like galactosemia.
Step-by-step explanation:
In considering a hypothesis for why mutant cells fail to produce any enzymes required for galactose metabolism, one hypothesis could be that the mutant cells have impaired glucose metabolism. Hypothesis D is the most relevant to the context given the failure of mutant cells to produce galactose-metabolizing enzymes. The discovery by Francois Jacob and Jacques Monod of E. coli mutant strains that lacked enzymes like ß-galactosidase, ß-galactoside permease, or ß-galactoside transacetylase illustrates the critical roles these enzymes play. A mutation that affects one such enzyme, as seen in galactosemia, a genetic disease where the absence of an enzyme results in the inability to convert galactose to glucose, can lead to serious consequences. This illustrates the impact that mutants failing to make these enzymes could have on metabolism, particularly glucose metabolism, as galactose is a part of lactose that would normally be converted into glucose for energy production through glycolysis.