Science Literature

The DNA code is made up of codons (3-letter words) derived from 64 different arrangements of bases linking the two DNA strands. Yet these 64 combinations code for only 20 amino acids and a stop signal (as set out here). Thus, different codons are able to produce the same amino acid. The phenomenon is described as the genetic code having "redundancy". In the early years of molecular biology, this redundancy was perceived as an evolutionary accident, unworthy of detailed research but fortunate because it meant that any damaging effects of point mutations were cushioned. However, the evidence has been accumulating that "redundancy" is a misleading word.

"Scientists have known about this redundancy for 50 years, but in recent years, as more and more genomes from creatures as diverse as domestic dogs to wild rice have been decoded, scientists have come to appreciate that not all redundant codons are equal. Many organisms have a clear preference for one type of codon over another, even though the end result is the same. This begged the question the new research answered: if redundant codons do the same thing, why would nature prefer one to the other?" (Source here)

The ribosome in action in protein translation, assembling (and then completing) a protein step by step [=algorithmically] based on the sequence of three-letter codons in the mRNA tape and using tRNA's as amino acid "taxis" and position-arm tool-tips, implementing a key part of a von Neumann-type self replicator (Source here)

New research into protein synthesis in bacteria has shone new light on these issues. "A hidden and never before recognized layer of information in the genetic code has been uncovered by a team of scientists" using a technique called ribosome profiling. This tool allows gene activity inside living cells to be monitored, including the speed with which proteins are made.

"Ribosome profiling takes account of gene activity by pilfering from a cell all the molecular machines known as ribosomes. Typical bacterial cells are filled with hundreds of thousands of these ribosomes, and human cells have even more. They play a key role in life by translating genetic messages into proteins. Isolating them and pulling out all their genetic material allows scientists to see what proteins a cell is making and where they are in the process. Weissman and Li were able to use this technique to measure the rate of protein synthesis by looking statistically at all the genes being expressed in a bacterial cell." (Source here)

Ribosomes bind to mRNA strands and produce protein products. To do this, they have to "read" the sequence of bases and translate them into the sequence of amino acids that make up the protein. The starting point is an AUG codon. However, AUG sequences can appear elsewhere along the mRNA strand so a mechanism is needed to establish whether the AUG codon is the starting point or just a part of the coding sequence. Prokaryotes make extensive use of the Shine-Dalgarno sequence (SD sequence) within the mRNA located near the start codon. The SD sequence forms a strong bond with an anti-Shine-Dalgarno sequence in the ribosome. Consequently, once the SD-aSD bond is formed, the ribosome can readily locate the correct starting point for synthesising the protein.

The key point emerging from the new research is that "redundancy" affecting SD sequences were found to affect the rate of translation.

"By measuring the rate of protein production in bacteria, the team discovered that slight genetic alterations could have a dramatic effect. This was true even for seemingly insignificant genetic changes known as "silent mutations," which swap out a single DNA letter without changing the ultimate gene product. To their surprise, the scientists found these changes can slow the protein production process to one-tenth of its normal speed or less. [. . .] [T]he speed change is caused by information contained in what are known as redundant codons - small pieces of DNA that form part of the genetic code. They were called "redundant" because they were previously thought to contain duplicative rather than unique instructions. This new discovery challenges half a century of fundamental assumptions in biology." (Source here)

What has been discovered is that the genetic code not only has information about the sequence of amino acids, but also about the rate at which the translational machinery carries out its work. The information is about process as well as content.

"What the scientists hypothesize is that the pausing exists as part of a regulatory mechanism that ensures proper checks - so that cells don't produce proteins at the wrong time or in the wrong abundance." (Source here)

The implications of this work go far beyond bacteria. Redundancy is the wrong word! What we have here is another level of information that needs to be part of ongoing research. Are these better understood as regulatory variants? Cornelius Hunter has drawn attention to the erroneous presumption of evolutionists:

"For evolutionists this redundancy was just another biological kludge revealing nature's dysteleology. Their natural expectation was that mutations that produced no change in the amino acid sequence - the so-called synonymous mutations - would be worthless and discarded by evolution. The massive change required by evolution would come about by altering the amino acid sequences of proteins, and so the gene comparisons between species would mostly reveal mutations that did produce different amino acids - the so-called nonsynonymous mutations. It was yet another in a long line of failed expectations. In fact gene comparisons between different species [. . .] revealed that non synonymous sites are disproportionately more conserved than synonymous sites, sometimes by as much as an order of magnitude or more." (Source here)

Another blog post has raised questions about the way molecular data has been used to defend common descent. With this new understanding of the functionality of "redundant" codons, the argument must be re-visited.

"The observation that silent synonymous base-pair substitutions can be of functional relevance to gene expression may undercut an argument made often in support of common descent - that is, the argument that, in genes shared between different taxa, a higher frequency of shared synonymous (assumed to be functionally insignificant) substitutions, than would be predicted under the assumption of neutral evolution, necessarily implies common ancestry." (Source here)

If evolutionary theorists have erred in presuming the variants are meaningless apart from tracing evolutionary lineages, what paradigm could help us move forward? The answer is a paradigm that presumes functionality and keeps searching for functionality within the architecture of living cells. The Design paradigm is capable of doing this - what is needed is less polemic from those who are hostile to design and a greater appreciation that biology as a discipline suffers when design issues are not addressed fairly and openly in scientific discourse.

The anti-Shine-Dalgarno sequence drives translational pausing and codon choice in bacteria
Gene-Wei Li, Eugene Oh and Jonathan S. Weissman
Nature, 484, 538-541, (26 April 2012) | doi:10.1038/nature10965

Protein synthesis by ribosomes takes place on a linear substrate but at non-uniform speeds. Transient pausing of ribosomes can affect a variety of co-translational processes, including protein targeting and folding. These pauses are influenced by the sequence of the messenger RNA. Thus, redundancy in the genetic code allows the same protein to be translated at different rates. However, our knowledge of both the position and the mechanism of translational pausing in vivo is highly limited. Here we present a genome-wide analysis of translational pausing in bacteria by ribosome profiling - deep sequencing of ribosome-protected mRNA fragments. This approach enables the high-resolution measurement of ribosome density profiles along most transcripts at unperturbed, endogenous expression levels. Unexpectedly, we found that codons decoded by rare transfer RNAs do not lead to slow translation under nutrient-rich conditions. Instead, Shine-Dalgarno-(SD)-like features within coding sequences cause pervasive translational pausing. Using an orthogonal ribosome possessing an altered anti-SD sequence, we show that pausing is due to hybridization between the mRNA and 16S ribosomal RNA of the translating ribosome. In protein-coding sequences, internal SD sequences are disfavoured, which leads to biased usage, avoiding codons and codon pairs that resemble canonical SD sites. Our results indicate that internal SD-like sequences are a major determinant of translation rates and a global driving force for the coding of bacterial genomes.

See also:

New Layer of Genetic Information Helps Determine How Fast Proteins Are Produced, ScienceDaily (28 March 2012)

A New Study Adds Further Depth to the Information Story, by Jonathan M. (Evolution News & Views, 30 March 2012)

Hunter, C. Here's What That New UCSF Paper Says in Plain English (And Why Evolution Needs Another Do-Over) (Darwin's God, 31 March 2012)

Hunter, C. Here is a Completely Different Way of Doing Science, (Darwin's God, 1st April 2012)