1. Chloramphenicol • Prevents the normal joining of mRNA with ribosomes Inhibits the reaction that leads to the formation of bonds between amino acids 2. Streptomycin Causes misreading of the genetic code in mRNA 3. Puromycin Binds with the amino acid tyrosine and substitutes for the tRNA-tyrosine complex on ribosomes Prevents the further addition of amino acids to a polypeptide when tyrosine is required 4. Actinomycin • Binds to DNA nucleotides Inhibits the linking of nucleotides in mRNA or DNA 5. Tetracycline • Prevents binding of tRNA to the first codon in a mRNA molecule 6. Mechlorethamine Binds to guanine in cytosine-guanine base pairs Some antibiotics do not prevent the synthesis of protein by bacterial cells but do cause the cells to produce abnormal proteins. Two such antibiotics are numbered...
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Several antibiotics target the components of bacterial protein synthesis. Three of these antibiotics, along with their mechanism of action, are listed below. For each antibiotic, explain how it disrupts protein synthesis: Be specific. Pactamycin prevents the recognition of the Shine-Dalgarno sequence. Ribotoxin damages the EF-G binding site on the ribosome so that EF-G can no longer associate with the ribosome. Pulvomycin prevents the association of EF-Tu with tRNA.
Madhur L.
Antibiotics have different mechanisms of action. An antibiotic called transcription inhibitor, such as Puromycin, can be used to block translation. Another antibiotic called determinenoiy Actinomycin blocks the synthesis of regulatory molecules, such as proteins. You observe a lack of protein synthesis when you inject tissue with one of the above antibiotics. Which antibiotic (actinomycin and puromycin) was used in the above experiment? How can you explain the above result?
Adi S.
Erythromycin: acts by inhibition of protein synthesis by binding to the 23S ribosomal RNA molecule in the 50S subunit of ribosomes in susceptible bacterial organisms. Penicillin: kills bacteria by binding the beta-lactam ring to DD-transpeptidase, inhibiting its cross-linking activity and preventing the formation of new cell walls. A bacterial cell without a cell wall is vulnerable to outside water and molecular pressures, causing the cell to die quickly. Kanamycin: Kanamycin works by binding to the bacterial 30S ribosomal subunit, causing mRNA misreading and preventing the bacterium from synthesizing proteins required for growth. Chloramphenicol: Chloramphenicol is an antibacterial with broad activity against gram-positive, gram-negative, and Rickettsia bacteria. It works by interfering with bacterial protein synthesis by binding to ribosomes. Novobiocin: inhibition of the GyrB subunit of the bacterial DNA gyrase enzyme, which is involved in energy transfer. Tetracycline: binds reversibly to the 30S ribosomal subunit in a position that prevents aminoacyl-tRNA from binding to the acceptor site on the mRNA-ribosome complex. Streptomycin: interferes with the function of ribosomes in bacterial cells, the complex molecular machines that create proteins by linking amino acids together. Neomycin: Through irreversible binding to the 30S ribosomal subunit of susceptible bacteria, it inhibits bacterial protein synthesis. Question: Which antibiotics seem to have the broadest spectrum of activity and why?
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