Answer:
- Alteration of an enzyme involved in folic acid synthesis
- A change in the structure of 23S rRNA
- The terminal D-alanine of pentapeptide mutates to D-serine
Step-by-step explanation:
Antibiotic resistance is the phenomenon by which microorganisms naturally have, acquire, or develop the ability to defeat the drugs designed to eliminate them. For example, trimethoprim is able to bind with the enzyme dihydrofolate reductase (DHFR) in order to inhibit the folic acid synthesis pathway. Sulfonamides (sulfa drugs) competitively inhibit the incorporation of para-aminobenzoic acid (​PABA) into folic acid and thus also prevent the synthesis of folic acid. Ribosomes are organelles where proteins are synthesized. The 23S rRNA is a component of the large subunit (50S) of bacteria and archaea ribosomes. In consequence, it is expected that a modification in the structure of 23S rRNA alters protein synthesis. Finally, vancomycin acts by binding the terminal D-Ala-D-Ala residues of the polymeric lipid-PP-disaccharide-pentapeptides and thus inhibits cell wall synthesis in Gram-positive bacteria. In consequence, it is expected that a mutation at the terminal D-alanine that modifies this sequence alters the vancomycin binding site and thus also confers antibiotic resistance.