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Redundancy of the genetic code enables translational pausing

  1. Sep 28, 2014 #1
    Thoughts on this?

    The codon redundancy (“degeneracy”) found in protein-coding regions of mRNA also prescribes Translational Pausing (TP). When coupled with the appropriate interpreters, multiple meanings and functions are programmed into the same sequence of configurable switch-settings. This additional layer of Ontological Prescriptive Information (PIo) purposely slows or speeds up the translation-decoding process within the ribosome. Variable translation rates help prescribe functional folding of the nascent protein. Redundancy of the codon to amino acid mapping, therefore, is anything but superfluous or degenerate.(continues)
  2. jcsd
  3. Sep 29, 2014 #2


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    I don't have the molecular background to offer a critique. If valid, It's not surprising to me, given the emphasis on systems biology and emergence in the last couple decades. Context is important in biogy!
  4. Sep 30, 2014 #3


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    Although translational pausing induced by rare codons is an intriguing idea that makes a lot of sense, there is not a whole lot of data actually showing that this is an important mechanism controlling protein synthesis and folding. For example, when Li et al. used a technique called ribosome profiling to detect ribosome pausing in bacteria, they did not see the ribosome pausing at rare codons (Li et al. 2012. The anti-Shine–Dalgarno sequence drives translational pausing and codon choice in bacteria. Nature 484: 538. http://dx.doi.org/10.1038/nature10965 [Broken]). Furthermore, while it was believed that rare codons at the N-terminus of genes affects expression of the protein, it was later shown that the apparent codon bias is a result of a bias against RNA secondary structure (Goodman et al. 2013. Causes and effects of N-terminal codon bias in bacterial genes. Science 342: 475 doi:10.1126/science.1241934).

    There are a few published examples where codon choice appears to affect protein folding (for example, Kimchi-Sarfaty et al. 2007. A "silent" polymorphism in the MDR1 gene changes substrate specificity. Science 315:525 doi:10.1126/science.1135308), but its not clear whether changing the codon might also change the secondary structure of the RNA or affect the RNA-binding proteins that might also play a role in controlling translational pausing and protein folding. There definitely is still a lot that needs to be worked out in this area.
    Last edited by a moderator: May 7, 2017
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