The Antibiotic That Stops Protein Synthesis
A researcher treats a culture of bacteria with an antibiotic that binds to the bacterial ribosome. She observes that protein synthesis stops almost immediately, but DNA replication and transcription continue for a short time. She then adds a second compound that blocks the initiation of translation. A control culture without antibiotic continues to grow. The researcher wants to know whether the antibiotic affects the elongation or the initiation step of translation, and whether it could also affect mitochondrial protein synthesis in human cells. She notes that the antibiotic does not enter human cells efficiently but does enter bacteria.
1. How can the researcher distinguish whether the antibiotic blocks initiation or elongation of translation?
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If the antibiotic blocks initiation, no new ribosomes can assemble on mRNA, so the appearance of newly synthesized peptides would stop, and polysomes would decrease while free ribosomal subunits accumulate. If it blocks elongation, initiation can still occur and ribosomes would stall on mRNA, so polysomes would persist or increase and short incomplete peptides might accumulate. The researcher can test this by adding the antibiotic after translation has already started: if elongation is blocked, existing polysomes stall and no full-length protein appears; if initiation is blocked, existing polysomes run off and no new initiation complexes form. Comparing polysome profiles and the size of labeled peptide products would distinguish the two mechanisms.
2. The researcher claims the antibiotic is safe for human cells because it 'does not enter human cells efficiently.' Evaluate this claim.
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The claim is only partly reassuring. The antibiotic targets the bacterial ribosome, and human cytoplasmic ribosomes differ, so it may not inhibit cytosolic translation. However, human mitochondria contain ribosomes that resemble bacterial ribosomes, and many antibiotics that target bacterial ribosomes also inhibit mitochondrial protein synthesis. If even a small amount enters human cells, mitochondrial translation could be affected, impairing oxidative phosphorylation and causing side effects. The claim that poor entry makes it safe is incomplete: safety requires evidence that mitochondrial ribosomes are not inhibited at achievable intracellular concentrations, not just that entry is inefficient. The researcher should test mitochondrial protein synthesis directly.