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3. Describe the difference between prokaryotic ribosomes and eukaryotic ribosome

ID: 253562 • Letter: 3

Question

3. Describe the difference between prokaryotic ribosomes and eukaryotic ribosomes. How does this difference allow us to safely target prokaryotic ribosomes? 4. Explain the mechanism of action for the aminoglycoside drugs. What is their target and how does this kill bacterial cells? 5. Explain the mechanism of action for the quinolone drugs. What is their target and how does this kill bacterial cells? What is the SOS response system in E. coli? the SOS response system? bacterial cells? 6. What is the role of the Rec A and Lexa proteins in What role does the SOS response system play in quinolone treated IF Page 1 of2 Focus Show All

Explanation / Answer

3.Eukaryotes have larger size ribosome. Their ribosome is made of two subunits, a large 60S and a small 40S. Both of these subunits formed a 80S rib osome. The weight of eukaryotic ribosome is 4200Kd. Whereas, in prokaryotes the ribosome is 70S with a molecular mass of 2700Kd. It is made of two subunit, 50S and 30S.

When addressing a bacterial infection, drugs can be used due to the difference in the ribosome between prokaryotes and eukaryotes. Drugs which are effective against bacteria can be formulated in such a way that they can preferentially bind with smaller subunit of bacterial ribosomes to inhibit the protein translation.

4. Aminoglycosides are mostly affective against gram negative bacteria. These drugs are made of amino-modified glycoside. In general, these drugs use 30S subunit of ribosome as target. After the drug binds to 30S subunit, it can not read the genetic code properly, as a result protein synthesis gets interrupted.

5. Quinolone group of drugs inhbit the bacterial growth by blocking DNA replication. DNA gyrase is essential for DNA supercoiling during replication. Quinolone can bind with DNA-gyrase which inhibit the replication process.

6. When DNA is damaged in E.coli, SOS response becomes activates. There are two genes, LexA and RecA which are the mainly regulates SOS response. When DNA get excessively damage, there is no replication occurs, which produces lots of single stranded gaps. In this situation RecA protein will bind to these single stranded part. In normal situation LexA acts as repressor which represses the SOS genes and also repress the function of RecA. But, in response to DNA damage, when RecA gets activated, it interact with LexA and cleaves it. Once LexA is degraded, SOS genes becomes active which initiate several DNA repair pathway.

Now, think of quinolone mode of action, it can bind with DNA gyrase. As a result DNA gyrase can not bind with DNA anymore and as a result several double stranded broken DNA accumulates. These accumulation generates SOS response in E.coli.

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