Transcription: Therapeutics and Toxins o How does rifampicin inhibit transcripti
ID: 196634 • Letter: T
Question
Transcription: Therapeutics and Toxins
o How does rifampicin inhibit transcription?
o How does myxopyronin inhibit transcription? Be specific with regard to:
Conformational changes in RNAP what causes them Result of conformational changes in RNAP
o How does actinomycin D inhibit transcription? What about this mechanism of action allows it to: be used as a chemotherapeutic agent? inhibit both replication and transcription?
o Why is -amantin considered a toxin? What is its mechanism of action?
o What distinguishes an antibiotic from an antineoplastic from a toxin?
Explanation / Answer
How does rifampicin inhibit transcription?
Rifampicin inhibits transcription by deactivating the bacterial DNA-dependent RNA polymerase. Rifampicin binds to the beta subunit of RNA polymerase and through "steric occlusion", it prevents the elongation of the RNA transcript.
How does myxopyronin inhibit transcription? What causes them?
Myxopyronin inhibits transcription by binding allosterically to the "switch region" of RNAP and blocks initiation of transcription. RNAP is similar to crab's claw wherein the beta subunit must open to allow bacterial DNA into the catalytic region. The switch region in the beta subunit forms a hinge and acts as clamps. The myxopyronin specifically binds to the switch region and changes its conformation.
Results of conformation changes in RNAP
The conformational changes in RNAP prevent its interaction with the promoter DNA and block the initiation of transcription.
How does actinomycin D inhibit transcription?
Actinomycin D selectively binds to the DNA located in the transcription initiation complex and blocks the elongation of RNA transcript by RNAP.
What about this mechanism of action allows it to
a. be used as a chemotherapeutic agent?
Chemotherapy is mainly used for the treatment of cancer. Since actinomycin D has the ability to block transcription, uncontrolled growth by cancerous cells can be reduced using this drug.
b. inhibit both replication and transcription?
Primase (an RNA polymerase) is a key enzyme in DNA replication. Its activity is dependent on the availability of DNA and it forms short segments of RNA called Okazaki fragments in 5'-3' direction. Actinomycin D can bind to DNA and blocks the movement of primase. Hence inhibition of replication and transcription can both be achieved by actinomycin D.
Why is -amantin considered a toxin? What is its mechanism of action?
-amantin is a cyclic peptide commonly found in poisonous mushrooms. It can cause cytolysis of hepatocytes. It has higher affinity to RNA polymerase II. -amantin blocks the translocation of RNA and DNA by strongly binding to the bridge helix region of RNA polymerase II.
What distinguishes an antibiotic from an antineoplastic from a toxin?
Antibiotics are generally used to kill microorganisms.
Antineoplastic is an agent which is used to avoid the spreading of cancer
A toxin is an antigenic agent which can cause adverse effects on the living organism.
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