Redundancy of the genetic code enables translational pausing

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SUMMARY

The redundancy of the genetic code, specifically the codon degeneracy in protein-coding regions of mRNA, plays a crucial role in translational pausing (TP). This phenomenon, when combined with appropriate interpreters, allows for multiple meanings and functions to be encoded within the same sequence, thereby influencing the translation-decoding process in the ribosome. Research, including studies by Li et al. (2012) and Goodman et al. (2013), indicates that while translational pausing is a significant mechanism in protein synthesis, the relationship between rare codons and protein folding remains complex and not fully understood. Further investigation is necessary to clarify the impact of codon choice on RNA secondary structure and the role of RNA-binding proteins in this process.

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  • Understanding of codon redundancy and degeneracy in genetic coding
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  • Review the findings of Kimchi-Sarfaty et al. (2007) regarding silent polymorphisms and their effects on substrate specificity
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Researchers in molecular biology, geneticists, and biochemists interested in the mechanisms of protein synthesis, translational regulation, and the implications of codon usage on protein functionality.

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http://journal.frontiersin.org/Journal/10.3389/fgene.2014.00140/full

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)
 
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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!
 
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 ). 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.
 
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As child, before I got my first X-ray, I used to fantasize that I might have a mirror image anatomy - my heart on the right, my appendix on the right. Why not? (Caveat: I'm not talking about sci-fi molecular-level mirroring. We're not talking starvation because I couldn't process certain proteins, etc.) I'm simpy tlakng about, when a normal zygote divides, it technically has two options which way to form. Oen would expcet a 50:50 split. But we all have our heart on the left and our...

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