Why was not RNA completely replaced by DNA when the RNA world evolved into a DNA and protein world?

If DNA just has a slightly different chemical composition from RNA, why can't DNA act as a catalyst and why hasn't it replaced RNA? Here, I am talking in terms of evolution, shouldn't evolution just replace all the RNA with DNA?

A related question is Why do some bad traits evolve, and good ones don't? Basically a strong selection pressure is necessary to filter out a trait.

Having said that, there is no strong argument in support of transcription being disadvantageous.

RNA has unique properties that makes it suitable for certain functions. RNA can adopt different secondary/tertiary structures that an equivalent ssDNA cannot. One of the reasons is that GU wobble pairs are stable in RNAs but not in DNA thereby allowing structural flexibility to the former. See

RNA also has a high turnover because of different RNAses. If there was DNA instead of RNA for carrying temporary messages and there were equivalent DNAses to increase the turnover of the "mDNAs", then the genomic DNA would also become susceptible to degradation by these DNAses, which would cause genomic instability. You can argue that protein synthesis could directly begin on DNA as a template instead of mRNA. I guess that it would crowd the DNA and clash with replication. Even transcription machinery clashes with the replication machinery; this is called Transcription Replication Conflict which leads to genomic instability. A hypothetical situation in which there are multiple ribosomes on a DNA, is likely to have higher chances of the conflicts with replication than transcription-replication conflicts, thereby causing higher degree of genomic instability. I am assuming so because a large number of ribosomes need to simultaneously be progressing through the gene in order to produce sufficient amount of corresponding protein (like in case of polysomes).

Another possibility is based on the RNA world hypothesis. If it is really true that RNA preceded DNA as a functional as well as a hereditary molecule then it is difficult to get rid of all RNAs that easily. Even if most of the functions of the archaic RNAs were taken over by DNA and proteins, they are still performing some vital functions. To replace RNA from these roles, an alternative should exist which performs much better than the RNAs.

These are just guesses. An absolute reason can not easily be attributed to many biological observations. This is because we do not know the actual evolutionary trajectory of how things happened. However, what is important to keep in mind is that evolution does to proceed towards some kind of global optimum. Evolution does not "aim" for perfection.

The argument in this question is based on the false premises that a slight difference between two macromolecular structures is an unimportant difference, and that any importance or lack of it for that difference will have the same weight for different functions.

The slight differences between DNA and RNA gave DNA certain advantages as genetic material - for example it is less subject to alkaline hydrolysis and therefore can make longer stable genomes. It will only replace DNA if its chemistry does the job better - for other functions of RNA, this is not generally so.

RNA was largely replaced as a catalyst - but by protein, not DNA, something one can rationalize chemically because there were a wider variety of groups for catalysis etc. in the 20 amino acid side-chains of proteins.

RNA was retained for functions in which either its extra sugar hydroyl group or acid lability conveys and advantage over DNA (e.g. mRNA), or replacement by DNA would seem to convey no advantage (e.g. ribosomes). I am not an expert on catalytic RNA, but I understand that the 2'-OH is involved in the acid-base catalysis.

In conclusion, if you talk about biological molecules, you need to think about how their chemistry affects their function. If you have no chemistry, go away and learn some or restrict yourself to some non-molecular area of biology.


I have an answer to a related question here: Why don't different organisms have nucleic acid genomes containing different bases and sugar?

What Is The RNA World Hypothesis?

What is the best way to explain the RNA World hypothesis? originally appeared on Quora: the place to gain and share knowledge, empowering people to learn from others and better understand the world.

Answer by Drew Smith, Studied catalytic RNA and developed aptamers for therapeutics and diagnostic applications, on Quora:

The RNA World hypothesis resolves the chicken-and-egg conundrum posed by the structure of growth shared by all living organisms. DNA encodes RNA, which directs the synthesis of proteins. Proteins do the biochemical work of capturing energy. This energy is directed into the synthesis of new copies of DNA, resulting in the growth of new cells and organisms.

Proteins require DNA to store information, but DNA also requires protein to do biochemical work. Neither DNA nor protein can support life alone. It’s a complex system, far too complex to have appeared spontaneously at life’s origin. Something simpler must have preceded it.

Tom Cech and Art Zaug’s discovery that RNA could do biochemical work [1], in addition to its known ability to store information, was an electrifying revelation. RNA could be both a chicken and an egg. The origin of self-replicating systems became an addressable scientific problem, not an embarrassing mystery.

The catalytic properties of RNA were added to several other clues regarding primitive life:

  • RNA is central to the protein synthesis process. Indeed, the ribosome, the site of protein synthesis, is mostly RNA and it is the RNA portion that links amino acids together into proteins [2].
  • RNA-like nucleotides are still present in the enzymes that catalyze many fundamental biochemical reactions [3], suggesting that protein enzymes gradually took over from RNA enzymes.
  • The building blocks of DNA are made from RNA precursors, indicating that RNA preceded DNA.

But attempts to create self-replicating RNA worlds under plausible early-Earth conditions have pretty much failed. The fundamental problem is the RNA is not very stable in water. It requires a constant input of energy in order for synthesis rates to outpace degradation rates.

Nick Lane used this observation (along with many others) to postulate that the RNA World was an intermediate stage of biotic evolution. He proposes that a primitive form of energy metabolism appeared in alkaline hydrothermal vents. RNA precursors captured this energy and began the process of Darwinian evolution that resulted in life as we know it today [4]. I’ve written a bit more about this here: Drew Smith's answer to Which hypothesis has the most evidence for the origin of life: Metabolism or RNA self-replication?

The RNA World probably was not at the origin of life. But it almost certainly existed, and was a critical step in the jump-starting of Darwinian evolution and thus the appearance of complex life forms. It is possible that life could have evolved without the existence of self-coding and self-replicating molecules, but it may not have proceeded nearly as fast or as far, and could well have failed altogether.

This question originally appeared on Quora - the place to gain and share knowledge, empowering people to learn from others and better understand the world. You can follow Quora on Twitter, Facebook, and Google+. More questions:

As a Solution to the Origin of Life, RNA World Model Comes Under Attack

According to a recent article at New Scientist, “Why ‘RNA world’ theory on origin of life may be wrong after all,” the RNA world model of the origin of life is under attack:

Life has a chicken-and-egg problem: enzymes are needed to make nucleic acids — the genetic material — but to build them you need the genetic information contained in nucleic acids. So most researchers assume that the earliest life, long before the evolution of cells, consisted of RNA molecules. These contain genetic information but can also fold into complex shapes, so could serve as enzymes to help make more RNA in their own image — enabling Darwinian evolution on a molecular level.

At some point, the idea goes, this RNA world ended when life outsourced enzymatic functions to proteins, which are more versatile. The key step in this switch was the evolution of the ribosome, a structure that builds protein molecules from genetic blueprints held in RNA.

But such a transition would require abandoning the enzymatic functions of RNA and reinventing them in proteins. “That is not a simple model,” says Loren Williams, a biochemist at the Georgia Institute of Technology in Atlanta.

That’s a reasonable point at the end of the quote: If a self-replicating system has all of the enzymatic functions it needs from RNAs (something that hasn’t been demonstrated), then rebuilding that system using an entirely different type of molecule (proteins) would be an extremely difficult task and highly unlikely. Yet this is essentially precisely what the classical RNA world model requires.

But there are many other criticisms of the RNA world model. A 2012 paper in Biology Direct by biochemist Harold S Bernhardt keenly titled, “The RNA world hypothesis: the worst theory of the early evolution of life (except for all the others),” notes that “the following objections have been raised to the RNA world hypothesis”:

(i) RNA is too complex a molecule to have arisen prebiotically (ii) RNA is inherently unstable (iii) catalysis is a relatively rare property of long RNA sequences only and (iv) the catalytic repertoire of RNA is too limited.

Now the author himself accepts the view that the RNA world is the best materialistic model for the origin of life. But he’s very frank about its problems. For example, regarding the objection that “RNA is too complex a molecule to have arisen prebiotically,” he writes:

RNA is an extremely complex molecule, with four different nitrogen-containing heterocycles hanging off a back-bone of alternating phosphate and D-ribose groups joined by 3′,5′ linkages. Although there are a number of problems with its prebiotic synthesis, there are a few indications that these may not be insurmountable. Following on from the earlier work of Sanchez and Orgel, Powner, Sutherland and colleagues have published a pathway for the synthesis of pyrimidine nucleotides utilizing plausibly prebiotic precursor molecules, albeit with the necessity of their timed delivery (this requirement for timed delivery has been criticized by Benner and colleagues, although most origin of life models invoke a succession of changing conditions, dealing as they do with the evolution of chemical systems over time what is critical is the plausibility of the changes).

We covered the research of Powner and Sutherland here and here, pointing out that it was carefully designed to yield the desired results and noting how the goal-directed nature of the experiment undermines claims of the model’s plausibility under unguided natural conditions. Hence the criticism that it has an unlikely “requirement for timed delivery.”

Bernhardt then moves on to another criticism:

RNA is often considered too unstable to have accumulated in the prebiotic environment. RNA is particularly labile at moderate to high temperatures, and thus a number of groups have proposed the RNA world may have evolved on ice, possibly in the eutectic phase (a liquid phase within the ice solid).

But there’s a major problem with the “cold” origin of life hypothesis: at low temperatures, reactions become so slow that nothing interesting ever happens. That’s going to be a problem for many types of organic chemistry necessary for the origin of life. This is an especially significant problem when one considers that life appeared on earth very rapidly after conditions became favorable:

  • “…we have now what we believe is strong evidence for life on Earth 3,800 thousand million years [ago]. This brings the theory for the Origin of Life on Earth down to a very narrow range … we are now thinking, in geochemical terms, of instant life…” (C. Ponnamperuma, Evolution from Space 1981.)
  • “[W]e are left with very little time between the development of suitable conditions for life on the earth’s surface and the origin of life. Life is not a complex accident that required immense time to convert the vastly improbable into the nearly certain. Instead, life, for all its intricacy, probably arose rapidly about as soon as it could.” (Stephen Jay Gould, “An Early Start,” Natural History, February, 1978.)

A cold origin of life makes it much more difficult for life to arise under such a short timescale. Moreover, the notion that the early earth was cold rather than hot flies in the face of everything geologists have ever said about the conditions on the early earth.

Next, Bernhardt notes that “Catalysis is a relatively rare property of long RNA sequences only,” and he offers a nice discussion of the gross improbability of randomly producing a long, self-replicating RNA molecule:

The RNA world hypothesis has been criticized because of the belief that long RNA sequences are needed for catalytic activity, and for the enormous numbers of andomized sequences required to isolate catalytic and binding functions using in vitro selection. For example, the best ribozyme replicase created so far — able to replicate an impressive 95-nucleotide stretch of RNA — is

190 nucleotides in length, far too long a sequence to have arisen through any conceivable process of random assembly. And typically 10,000,000,000,000-1,000,000,000,000,000 randomized RNA molecules are required as a starting point for the isolation of ribozymic and/or binding activity in in vitro selection experiments, completely divorced from the probable prebiotic situation. As Charles Carter, in a published review of our recent paper in Biology Direct, puts it:

“I, for one, have never subscribed to this view of the origin of life, and I am by no means alone. The RNA world hypothesis is driven almost entirely by the flow of data from very high technology combinatorial libraries, whose relationship to the prebiotic world is anything but worthy of “unanimous support”. There are several serious problems associated with it, and I view it as little more than a popular fantasy” (reviewer’s report in [5]).

10 14 – 10 16 is an awful lot of RNA molecules.

Don’t miss what’s being said here: the argument directly parallels ID proponents who observe that it’s extremely unlikely for an RNA molecule with just the right nucleotide sequence needed for self-replication to arise by chance. In other words, he’s making the information sequence challenge to the origin of life.

Now Bernhardt proposes that perhaps the first self-replicating RNA was much shorter, reducing the probabilistic obstacles to randomly generating the right nucleotide sequence. But the evidence that this is actually possible is non-existent. Indeed, one of the reviewers, Eugene Koonin, points out that such a self-replicating RNA — whether long or short — has yet to be demonstrated:

I basically agree with Bernhardt. The RNA World scenario is bad as a scientific hypothesis: it is hardly falsifiable and is extremely difficult to verify due to a great number of holes in the most important parts. To wit, no one has achieved bona fide self-replication of RNA which is the cornerstone of the RNA World.

Finally, Bernhardt explains a fourth problem with the RNA world model, namely “The catalytic repertoire of RNA is too limited”:

It has been suggested that the probable metabolic requirements of an RNA world would have exceeded the catalytic capacity of RNA. The majority of naturally occurring ribozymes catalyze phosphoryl transfer reactions — the making and breaking of RNA phosphodiester bonds. Although the most efficient of these ribozymes catalyze the reaction at a comparable rate to protein enzymes — and in vitro selection has isolated ribozymes with a far wider range of catalytic abilities — the estimate of proteins being one million times fitter than RNA as catalysts seems reasonable, presumably due to proteins being composed of 22 chemically rather different amino acids as opposed to the 4 very similar nucleotides of RNA.

While Bernhardt discusses the various kinds of reactions that RNA can catalyze, he admits “RNAs are, in most cases, worse catalysts than proteins.” That sounds like Bernhardt just conceded the validity of the criticism that he described against the RNA world. Somehow, however, he manages to spin the inferiority of RNA catalysis, turning it into not a knock against the RNA world, but an argument for it: “This [the inferior catalytic abilities of RNA] implies that their [RNA’s] presence in modern biological systems can best be explained by their being remnants of an earlier stage of evolution, which were too embedded in biological systems to allow replacement easily.”

So RNA is used by living organisms — despite its inferior catalytic abilities — only because evolution wasn’t able to replace it? But aren’t we constantly told how proteins can evolve to accommodate virtually any need of an organism? Doesn’t this suggest severe limits to the evolvability of proteins? Now it seems that limits to evolution have become an argument for evolution.

This tortured logic brings us back to the criticism raised in the recent New Scientist article: the RNA world model is unlikely to be correct because it requires that proteins (with superior chemistry-catalyzing abilities) somehow swooped in and replaced what RNA was doing. That seems very unlikely. But Bernhardt again tries to spin this dilemma into an argument for the RNA world — that difficulties replacing RNA with protein point to the fact that RNA was once a precursor of life. However, if it’s so hard to replace RNA with proteins, how do we know that it happened in all the other cases required by the RNA world model?

It seems that whether proteins did or did not replace RNA, we’re being told that in either case that’s evidence for the RNA world. No wonder Eugene Koonin called the model “unfalsifiable.”

So why does anyone prefer the RNA world model, given all its problems? Koonin provides the answer in his reviewer’s comments at the end of Bernhardt’s article — it’s because he requires some materialistic model, and other materialistic models clearly won’t explain the origin of replication:

[T]he RNA World appears to be an outright logical inevitability. ‘Something’ had to start efficiently replicating to kick off evolution, and proteins do not have this ability.

Koonin’s argument thus goes like this: We know that unguided evolution is true, so some evolutionary model must be correct. If other unguided models of life’s origins won’t work, then the RNA world must be correct, because “something” had to happen to get life started.

But what if the RNA world itself has many problems and so it isn’t a viable solution? That’s not an option Koonin seems willing to consider. He’s right that “something” has to get life started. But there is a third way that Koonin hasn’t considered. That third way — the “something” he won’t consider — is the only known cause that can generate the kind of highly complex and specified digital sequences required at the origin of life: intelligent design.

A major difference between DNA and RNA could explain why one is the go-to blueprint for life

A new study could finally explain why our cells rely on DNA, and not its molecular relative RNA, to store and pass on genetic data. The findings show that RNA breaks apart when it tries to incorporate changes — such as chemical damage to the molecule — while DNA can twist and bend its shape to allow for changes.

The most important thing for any living thing on Earth is to pass on its genes to offspring. Life everywhere feeds, fights and flees all in the hopes that it can eventually bring about more life in its image. But all that effort would be for nothing if genetic information couldn’t be safely stored for when it’s needed. Two molecules are responsible for carrying this information — RNA, which is a simpler single-strand molecule, and DNA which is a more complex double-strand molecule.

But up to now no one really knew why most cells favor DNA to store this genetic data over RNA. But a new study lead by Hashim Al-Hashimi from the Duke University School of Medicine might have found the answer: DNA can accommodate damage in its structure which would cause RNA to break down.

“For something as fundamental as the double helix, it is amazing that we are discovering these basic properties so late in the game,” said lead researcher .

“We need to continue to zoom in to obtain a deeper understanding regarding these basic molecules of life.”

You’re probably familiar with the double-helix model of DNA. When they first proposed it in 1953, Watson and Crick predicted how the base pairs ( A&T. C&G ) bind to form up the whole. Two strands of DNA line up and link by bonding these pairs, and end up looking kind of like a ladder with the bonds being the rungs.

So these bonds were called Watson-Crick base pairs. But researchers struggled to find evidence that the pairs were binding in the way Watson and Crick predicted. Then in 1959, biochemist Karst Hoogsteen took a picture of an A–T base pair, finding a more skewed geometry than expected, with one base rotated 180 degrees relative to the other — and these were called Hoogsteen pairs. In more recent times, researchers have observed both Watson-Crick and Hoogsteen base pairs in images of DNA.

Al-Hashimi and his team stumbled onto something five years ago that no one has ever observed before: DNA pairs that shift back and forth between Watson-Crick and Hoogsteen bonds. They found that DNA employs Hoogsteen bonds when there’s a protein bond to a DNA site – or the bases suffered chemical damage. Once the damage is fixed or the protein is released, the DNA goes back to Watson-Crick bonds. The discovery was big in itself, but now the team has shown that RNA doesn’t have the ability. This could explain why DNA forms the blueprint — it can absorb chemical changes and repair damage, RNA becomes too stiff and falls apart.

“In DNA this modification is a form of damage, and it can readily be absorbed by flipping the base and forming a Hoogsteen base pair. In contrast, the same modification severely disrupts the double helical structure of RNA,” said one of the team, Huiqing Zhou.

“The finding will likely rewrite textbook coverage of the difference between the two purveyors of genetic information, DNA and RNA,” said a Duke University press release.

DNA (left) can form Hoogsteen bonding to incorporate damaged base-pairs, while RNA (right) falls apart in the same case.
Image credits Huiqing Zhou.

The team figured this out by using RNA and DNA molecules to create double-helices, then observed how their base pairs form bonds using advanced imaging techniques. At any one time, around 1 percent of DNA bases were shifting into Hoogsteen pairs, they found. The RNA strands however didn’t do the same.

They tested RNA double-helices under a host of conditions, but couldn’t determine them to naturally form Hoogsteen pairs. When they forced the molecules to form such pairs, the RNA strands fell apart completely. This happens because RNA double-helices are more tightly packed than DNA, and can’t change direction without hitting something or shifting atoms around, which makes the structure critically unstable.

“There is an amazing complexity built into these simple beautiful structures, whole new layers or dimensions that we have been blinded to because we didn’t have the tools to see them, until now,” said Al-Hashimi.

Further research is needed to determine if DNA’s flexibility compared to RNA is what lead to it becoming the go-to molecule for storing genetic data, but if confirmed, it could help us understand why life on Earth evolved into what we see today.

The full paper, “Scientists have just uncovered a major difference between DNA and RNA” has been published in the journal Nature Structural & Molecular Biology.

Why is uracil present in RNA but not DNA?

One major problem with using uracil as a base is that cytosine can be deaminated, which converts it into uracil. This is not a rare reaction it happens around 100 times per cell, per day. This is no major problem when using thymine, as the cell can easily recognize that the uracil doesn't belong there and can repair it by substituting it by a cytosine again.

There is an enzyme, uracil DNA glycosylase, that does exactly that it excises uracil bases from double-stranded DNA. It can safely do that as uracil is not supposed to be present in the DNA and has to be the result of a base modification.

Now, if we would use uracil in DNA it would not be so easy to decide how to repair that error. It would prevent the usage of this important repair pathway.

The inability to repair such damage doesn't matter for RNA as the mRNA is comparatively short-lived and any potential errors don't lead to any lasting damage. It matters a lot for DNA as the errors are continued through every replication. Now, this explains why there is an advantage to using thymine in DNA, it doesn't explain why RNA uses uracil. Iɽ guess it just evolved that way and there was no significant drawback that could be selected against, but there might be a better reason (more difficult biosynthesis of thymine, maybe?).

You'll find a bit more information on that in "Molecular Biology of the Cell" from Bruce Alberts et al. in the chapter about DNA repair (from page 267 on in the 4th edition).

Testing the hypothesis

The following two proposed RNA world activities are compatible with an acidic milieu, and are open to experimental testing. While not proving the hypothesis, demonstration of the feasibility of either or both of these mechanisms (and the acidic conditions required) would give added weight to our proposal of an RNA world evolving at acidic pH (see Figure 2 for a possible chronology of the proposed mechanisms).

A possible scheme for non-enzymatic template-directed RNA replication at pH 4-5

Prior to the emergence of an RNA replicase, non-enzymatic replication of shorter sequences of RNA may have occurred. It has proven difficult to find a pair of complementary oligonucleotides each of which will act as an efficient template for the other, allowing repeated amplification of the two sequences [34]. Work in this area has focused on C-rich sequences such as the RNA oligonucleotide CCGCC [35] and DNA oligonucleotide (CCCG)3CC [36], which make particularly good templates (this work has used the activated RNA nucleotide analogues 5'-phosphoro (2-methyl)-imidazolides, which - unlike standard RNA nucleotides - undergo efficient and regiospecific template-directed incorporation into a copy strand). At neutral pH however, C-rich sequences produce G-rich copies that tend to form higher-order structures that inhibit further replication [34]. Non-standard base pair interactions that can occur at acidic pH suggest a possible solution to this dilemma. As shown in Figure 5a, Escherichia coli (E. coli) tRNA Gly(GCC) forms dimers through its quasi-self complementary GCC anticodon, but only at pH 4-5 [37]. Romby and colleagues proposed that, at this acidic pH, the GCC anticodon is able to self-pair through the sharing of a proton between the two central cytosines, forming a C-C(+) hemi-protonated base pair. It would therefore appear possible that, as illustrated in Figure 5b, hemi-protonated linear GCC repeat sequences could serve as templates to produce identical copies at pH 4-5. If so, this might have provided a mechanism for successful non-enzymatic replication at the dawn of the RNA world, as both template and copy strands are similarly (equally) C-rich. DNA sequences consisting of GCC repeats form hairpins even at neutral pH [38], and these should be stabilized in acidic conditions by protonated C-C(+) base pairs (RNA hairpins probably played an important role in the early evolution of the RNA world due to their resistance to thermal and chemical degradation). Similarly, formation of protonated C-A(+) base pairs at acidic pH [39–43] suggests that RNA sequences consisting of GCC repeats might also template GAC repeat sequences or mixed GCC/GAC sequences under these conditions.

A possible scheme for non-enzymatic RNA replication at pH 4-5. (a) tRNA Gly(GCC) forms dimers through its GCC anticodon due to hemi-protonation of the central cytosine at pH 4-5 [37](b) At pH 4-5, C-rich (GCC) n sequences might produce C-rich duplicates by non-enzymatic replication. Base pairs involving hemi-protonated cytosines are indicated by (+).

A mechanism for specific aminoacylation of RNA hairpins and ancestral tRNA

With an RNA world at acidic pH, a possible mechanism for the specific aminoacylation of tRNA (and its hairpin precursor [19, 20]) can be suggested. Modern protein aminoacyl-tRNA synthetases achieve specificity through recognition of particular sequences of nucleotides in the tRNA aminoacyl stem adjacent to the 3' CCA terminus where the amino acid is attached, which has been termed the RNA operational code [44]. Di Giulio has proposed that tRNA arose by the duplication and ligation of a hairpin approximately half the length of the contemporary tRNA molecule [19]. Due to the symmetry of base pair interactions, the RNA operational code in tRNA would also have been present in the precursor hairpin, and conserved in the transition from hairpin to tRNA [20]. Prior to the evolution of coded protein synthesis in the RNA world, aminoacylation would have been catalyzed by ribozymes. Recognition of the RNA operational code nucleotides by modern protein synthetases is through the interaction of these nucleotides with specific amino acid residues. Recognition by a ribozymal synthetase could have instead been through either (i) tertiary interactions, (ii) base pairing between ribozymal nucleotides and nucleotides of the operational RNA code following strand-separation of the tRNA/hairpin aminoacyl stem, or (iii) formation of a base pair-specific triple-helix interaction with the tRNA/hairpin aminoacyl stem, which includes the RNA operational code nucleotides. Such a pyrimidine triple helix - pyrimidine-purine-pyrimidine, with the Watson-Crick helix in italics - only forms at acidic pH, with the third polypyrimidine strand forming parallel Hoogsteen interactions with the polypurine strand within the major groove of the Watson-Crick double helix ([45] see also [46]). Thermal dissociation studies have shown that, in DNA triple helixes at least, a single purine-pyrimidine swap in the Watson-Crick double helix can be accommodated within the triple helix, albeit with a slight decrease in stability for the resulting triple helix [47]. The RNA sequence analysed in [45] forms a triple helix with 7 base triples at pH 4.3, whereas the DNA triple helices containing single mismatches form stable structures at pH 5.6 [47]. Michael Yarus and colleagues have produced a 24-nucleotide self-aminoacylating ribozyme possessing only three conserved nucleotides [18] and this was subsequently truncated to a mere 5-nucleotide ribozyme able to aminoacylate a 4-nucleotide RNA substrate in trans [48]. This reaction suggests a possible mechanism for the specific recognition of the aminoacyl stem of tRNA or its hairpin without the requirement for strand-separation: as illustrated in Figure 6, a polypyrimidine stretch of the aminoacylating ribozyme could specifically recognize the operational RNA code nucleotides in the tRNA/hairpin aminoacyl stem through base-pair specific interaction with the purine-rich 5' strand at pH 4-5. Supporting this possibility, the analogous (5') strand of the aminoacyl stem of E. coli tRNA Gly(GCC) (we have previously proposed tRNA Gly was the first tRNA to evolve [20]) contains the strikingly purine-rich sequence GCGGGAA [49] a number of other tRNAs have a similarly purine-rich 5' strand [49]. Different purine-rich sequences embedded in the aminoacyl stems of hairpins/tRNAs could have been recognized by complementary polypyrimidine sequence 'tails' of ribozymes able to catalyse the attachment of different amino acids. These purine-rich sequences may have been the forerunners of the operational RNA code, recognized today by protein aminoacyl-tRNA synthetases.

A possible mechanism for aminoacylation specificity in the RNA world. Specificity could have been through a triple helix interaction at acidic pH between the aminoacyl stem of a tRNA/precursor hairpin (shown here as the glycine tRNA sequence) (blue) and an aminoacylating ribozyme comprised of an active variant of the 5-nucleotide ribozyme from [48] fused to a 3' polypyrimidine 'tail' (red). See text for further comments and references. Xn = nucleotide linker sequence. Base triples involving protonated cytosines are indicated by (+).

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“Extra” Amino Acids

Even though life is overwhelmingly composed of the 20 amino acids, there are actually many different kinds of amino acids, well beyond the standard set of 20. Some of these “extra” amino acids are incorporated into proteins in our cells and are required for life. Selenocysteine and pyrrolysine are the two nonstandard amino acids and are incorporated into essential proteins, but at an extremely low frequency. While there are additional amino acids, the genetic code remains the same for nearly all of life. But because the genetic code is the same, scientists wondered whether that had any evolutionary significance for the origin of life. To address the uniformity of the genetic code, some molecular biologists have expanded the standard genetic code to incorporate novel amino acids, just to prove that they could. This team of molecular biologists recently introduced a new amino acid in the genetic code, using a novel amino acid from the laboratory to augment the genetic code.4 Not only have scientists successfully manipulated the genetic code, but there are also reports of incorporating nonnatural nucleotides besides the standard A, C, G, and T.5 Further magnifying the complexity of life, E. coli has 41 different tRNA genes for the 64 codons, and that sufficiently produces the 20 amino acids (i.e., 20 amino acids is less than the 64 possible codons).6 While there is an abundance of tRNA genes compared to the number of amino acids, the problem with fewer tRNA genes than the number of codons in the genetic code is something called redundancy built into the genetic code. The primary issue with the evolutionary model to explain the redundancy of the genetic code is that no selective pressure exists to clearly demonstrate how multiple copies of nearly identical genes can exist. Furthermore, evolution cannot randomly put together the nonrandom (and precise) code present in all of life. We are not blindly claiming that God created everything, but we are claiming that God created everything because we know that random processes never lead to order. Intelligence is required to provide not just the parts but the precise pairing as well. If some group of scientists has to tinker with God ’s original creation, they are not actually working with a random-chance combination of a genetic code appearing from nothing. Any evolutionist who makes a serious claim of expanding the genetic code needs to work in a universe that does not have any genetic code to start with. Having a genetic code in the first place is part of God ’s creation , and man is just working with part of what has already been made. There remains no new information provided. The fact that there is a core set of amino acids with a few additional is not sufficient proof that evolution happened, is happening, or ever will happen. These scientists have proven that we live in a world created by God as stated in Genesis.

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Author information


Department of Biology, Oberlin College and Conservatory, Oberlin, OH, 44074, USA

Blue Marble Space Institute of Science, Seattle, WA, 98154, USA

Aaron D. Goldman & Betul Kacar

Department of Molecular and Cellular Biology, University of Arizona, Tucson, AZ, 85721, USA

Lunar and Planetary Laboratory and Department of Astronomy, University of Arizona, Tucson, AZ, 85721, USA

Earth-Life Science Institute, Tokyo Institute of Technology, Meguro, Tokyo, 152-8550, Japan

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