Q.29 Rifampicin inhibits
I. Beta subunit of prokaryotic RNA polymerase
2. Beta subunit of prokaryotic DNA polymerase
3. All eukaryotic and prokaryotic polymerases
4. RNA dependent DNA polymerase
Rifampicin specifically inhibits the beta subunit of prokaryotic RNA polymerase, blocking bacterial transcription elongation without affecting eukaryotic enzymes.
Option Analysis
Rifampicin (rifampin) is a key antitubercular antibiotic that targets bacterial gene expression selectively.
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Option 1: Beta subunit of prokaryotic RNA polymerase – Correct. Rifampicin binds tightly to the β-subunit pocket in bacterial RNA polymerase (RNAP), sterically blocking RNA chain elongation after 2-3 nucleotides by occluding the DNA/RNA channel.
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Option 2: Beta subunit of prokaryotic DNA polymerase – Incorrect. DNA polymerase replicates DNA (not transcription); rifampicin has no activity against it—its specificity is for RNA synthesis enzymes.
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Option 3: All eukaryotic and prokaryotic polymerases – Incorrect. Eukaryotic RNAPs differ structurally (no conserved rif-binding pocket), making rifampicin selective for bacteria; mammalian polymerases are unaffected.
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Option 4: RNA dependent DNA polymerase – Incorrect. This refers to reverse transcriptase (e.g., in retroviruses); rifampicin does not inhibit it—some rifamycins do weakly, but standard rifampicin targets bacterial DNA-dependent RNAP.
Rifampicin inhibits the beta subunit of prokaryotic RNA polymerase, halting bacterial mRNA synthesis and treating TB/Mycobacterium infections. This SEO-optimized guide targets the key phrase “rifampicin inhibits,” breaking down the MCQ options for microbiology/pharmacology exam prep like GATE Life Sciences.
Mechanism of Rifampicin Inhibition
Rifampicin binds the β-subunit’s rif-pocket (near active site) in bacterial core RNAP, preventing phosphodiester bond formation beyond 2-3 nt during elongation (steric occlusion). Resistant mutants alter this pocket (e.g., Ser531Leu in rpoB gene). It’s bactericidal, used in TB regimens (e.g., RIF+INH).
Why Selective for Prokaryotes?
Eukaryotic RNAP I/II/III lack the precise β-pocket geometry; no cross-inhibition occurs at therapeutic doses. DNA pol (option 2) handles replication; reverse transcriptase (option 4) is viral-specific.
Enzyme Target Comparison
| Option | Enzyme Targeted | Rifampicin Effect | Relevance |
|---|---|---|---|
| Beta RNA pol (1) | Prokaryotic RNAP β-subunit | Strong inhibition | Correct, anti-TB |
| Beta DNA pol (2) | Prokaryotic DNA pol | None | Incorrect |
| All polymerases (3) | Euk/Prok all | Selective to bacteria only | Incorrect |
| RNA-dep DNA pol (4) | Reverse transcriptase | Minimal/none | Incorrect |
Focus on option 1 for exams—rifampicin exemplifies selective prokaryotic RNAP inhibition.
