<prompt> Please answer with one of the option in the bracket. Write reasoning in between . Write answer in between .Q:An investigator studying fungal growth isolates organisms from an infant with diaper rash. The isolate is cultured and exposed to increasing concentrations of nystatin. Selected colonies continue to grow and replicate even at high concentrations of the drug. Which of the following is the most likely explanation for this finding?? A: Reduced ergosterol content in cell membrane, B: Inactivation of cytosine permease, C: Mutation of the β-glucan gene, D: Altered binding site of squalene epoxidase, E: Expression of dysfunctional cytochrome P-450 enzymes,  <response>: This is a question about antifungal resistance. Nystatin is a polyene antifungal that binds to ergosterol in the fungal cell membrane. The ability of the fungus to continue growing at high nystatin concentrations indicates it has developed resistance. Choice A about reduced ergosterol content is a common resistance mechanism, as this reduces nystatin binding. Choice B is incorrect since cytosine permease is involved in nucleotide synthesis, not antifungal resistance. Choice C is incorrect because beta-glucan is a cell wall component, not involved in nystatin binding. Choices D and E are incorrect because squalene epoxidase and cytochrome P450 are involved in ergosterol biosynthesis; changes in these enzymes would not explain nystatin resistance.A: Reduced ergosterol content in cell membrane 