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DLS DLS
wrote...
Posts: 30
Rep: 8 0
8 years ago Edited: 8 years ago, DLS
You are studying Proteins 1 and 2 in E. coli.  A mutation causes a premature STOP codon and leads to a truncated version of Protein 1.  The mutation also down-regulates translation of Protein 2. Genes for Protein 1 and 2 are in tandem and transcribed as a polycistronic mRNA.  Give a mechanism for how the STOP codon in gene 1 down-regulates translation of gene 2.

trp operon operates through attenuation by design, but the Q says a mutation occurred.

Attenuation is ANY mechanism that down-regulates a downstream gene, right?
So, this isn't  necessarily the trp operon (because we're talking about a mutation), yet it's still an example of attenuation?
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wrote...
Educator
8 years ago
Yes, I believe you are correct.

Attenuation (in genetics) is a proposed mechanism of control in some bacterial operons which results in premature termination of transcription and which is based on the fact that, in bacteria, transcription and translation proceed simultaneously.
DLS Author
wrote...
8 years ago Edited: 8 years ago, DLS
Thank you.  Does the premature stop codon cause a hairpin structure like in trp operon attenuation? I'm thinking "no".
wrote...
Educator
8 years ago
To be honest, I have no idea if it is the stop codon that causes the hairpin loop to form Undecided

Sorry
DLS Author
wrote...
8 years ago Edited: 8 years ago, DLS
Related topic...

A mutant mammalian gene has a premature stop codon in exon 1 but a Western blot shows no truncated protein. A plasmid is cloned from the wild-type gene and the mutant gene's premature stop codon is inserted at the same position. After transfecting the mutant plasmid into the mutant gene, the Western blot now shows the truncated protein. Why?

My guess...
Confused because the premature stop codon is in exon1.
wrote...
Educator
8 years ago
I have no idea, bro. If you happen to figure it out, please shed some light because I'm throwing blanks.
wrote...
8 years ago
Referring to your question about the mammalian gene--
I'm not sure if this is correct, but it would seem logical that if the protein is not truncated then the stop codon must have been removed during splicing. You don't know how many exons and introns this gene has, right? Maybe with this form of the protein, exon 1 is normally spliced out so the stop codon is not present in the mRNA and the transcribed protein is normal length.

If the gene is in a plasmid, however, maybe the spliceosome does not work properly. Exon 1 would now be present and the stop codon would be in the mRNA and halt transcription resulting in a truncated protein. Usually when we clone DNA into a plasmid we use a cDNA copy made from the mRNA so it contains no introns and does not need to be spliced.

Let me know what you think of this idea. I would like to know the answer myself.
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