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16. Beskrive hvordan translationen kan hæmmes i bakterier af antibiotika og i eukaryote celler af toxiner
Devlin, s.254-5
Stryer, s.838-9

Protein synthesis is central to the continuing of life and reproduction of cells. An organism can gain a biological advantage by interfering with the ability of its competitors to synthesize proteins, and many antibiotics and toxins function this way.  

In bacteria:

Many antibiotics work by inhibiting proteins synthesis. They exploit the difference between prokaryotic and eukaryotic ribosomes.

Several examples:

• Streptomycin – binds to the 30S subunit of prokaryotic ribosomes, interferes with the initiation process and causes misreading of mRNA (initiation)

• Tetracycline – Binds to the 30S subunit and inhibits binding of aminoacyl tRNA. (initiation)

• Puromycin - resembles an aminoacyl t-RNA and binds to the A site, acting as an acceptor in the peptidyltransferase reaction. However, it can not serve as a donor, so it terminates the translation prematurely, leading to the release of an incomplete and non-functional protein. Has effect on both pro- and eukaryotes. Not too good for our cells.  (elongation)

• Chloramphenicol – binds to the peptidyltransferase center in the 50S subunit and inhibits forming of a peptide bond. (elongation)

In eukaryotic cells:

Eukaryotic translation is inhibited by diphtheria toxin, a product of Corynebacterium diphtharieae, a bacterium that grows in the upper respiratory tract of the infected person. The toxin binds at the cell membrane and a subunit enter the cytoplasm, where it inactivates the EF2-elongerings factor which catalyses the translocation. The tRNA is not moved to the adjacent site so elongation is inhibited.

Ricin – N-glycosidase that cleaves a single adenine from the 60S subunit of the eukaryotic ribosome, which becomes completely deactivated by this minor damage. The ribosome can not assemble for translation.

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