Jonathan McLatchie

Proponents of intelligent design (ID) have long predicted that many of the features of living systems which are said to exhibit “sub-optimal” design will, in time, turn out to have a rationally engineered purpose. This is one of several areas where ID actively encourages a fruitful research agenda, in a manner in which neo-Darwinian evolution does not. One such area, and a field for which I have long held an inquisitive fascination for, is the subject of so-called “junk DNA,” and the non-coding stetches of RNA which are transcribed from them.

Skepticism of the “junk DNA” paradigm is not a phenomenon which is limited to proponents of ID. This popular view of the genome — while still resonating as the conventional view among neo-Darwinian thinkers — has also been challenged by John Mattick of the University of Queensland and Jim Shapiro of the University of Chicago.

Earlier this month, an article appeared in the journal Cell by a Spanish team. The article announced the discovery of the ability of long non-coding RNA, which are often encoded in DNA near genes known to be important to both stem cells and cancer, to serve as enhancer elements (which promote gene expression).

According to the paper’s Abstract:

A news article published yesterday on haaretz.com reported that the Israeli Education Minister has dismissed their chief scientist, Dr Gavriel Avital, over — wait for it — questioning particular elements of two theories, specifically those pertaining to Darwinian evolution and global warming.
The article reports,

Dr. Gavriel Avital has generated controversy in the past for his statements questioning the validity of Darwin’s theory of evolution. He has also challenged conventional theory on pollution’s effects on global warming. “Someone who holds the opinions of Avital cannot serve as chief scientist of the Education Ministry,” said a ministry official. [emphasis mine]

What was Dr Avital’s crime? Let’s hear it straight from the horse’s mouth:

[Ed. Note: The previously published version of this post referred to Francisco Ayala as “of the BioLogos Foundation.” While Dr. Ayala has been a guest blogger with BioLogos, he is not directly affiliated with the foundation.]

Late last year, the eminent Christian philosopher and proponent of intelligent design, William Lane Craig, crossed swords in debate with the avid apologist for Darwinian evolution, Francisco Ayala. The debate was chaired by philosopher of physics Bradley Monton of the University of Colorado, an ID sympathizer, though a convinced atheist himself. Monton is the author of the book, Seeking God in Science: An Atheist Defends Intelligent Design. A fascinating ID the Future interview with Professor Monton can be downloaded here.

Following Dr. Ayala’s opening statement, Dr. Craig commenced his presentation by carefully setting out the definition of ID as the study of legitimate design inferences. Craig stipulated that, were Ayala to attempt to refute the inference to design with respect to biological systems, he would need to do one of two things. Either Ayala would need to directly challenge the legitimacy of the explanatory filter (presumably by demonstrating that it incorporates false positives) or demonstrate that the systems featured in biology do not meet the criteria of the explanatory filter. Setting aside the discussions pertaining to the tenability of universal common ancestry, Craig set about to argue that Ayala’s attempts to disqualify ID on scientific grounds were doomed because he had failed to demonstrate, in his published work, that the dual forces of random mutation and natural selection, are causally sufficient to account for macroevolution. He also argued that Ayala’s more numerous attempts to disqualify ID on theological grounds are completely irrelevant to the process of drawing a design inference from biological phenomena, because none of the arguments for ID aspire to show that the designer possesses the qualities of omnibenevolence or omnipotence. After all, Craig argued, a design inference is still warranted with respect to a medieval torture rack, regardless of the malevolent purposes of the system’s design. Questions pertaining to the nature of the designer are for natural theology, not for the scientific research program of ID. This is what distinguishes the modern concept of ID from the Watchmaker argument of William Paley’s Natural Theology.

The Darwinian model of evolution holds that one of the key mechanisms of evolutionary innovation is the duplication of genes and the subsequent divergence of one of the duplicate copies to undertake a new functional role. Because a probability of a single gene stumbling upon a significantly different (yet functionally advantageous) sequence is so small, the idea is that, following a duplication of a gene, one copy is able to retain the original function, while the other is free to explore the vast sea of combinatorial possibilities in search of some novel function.

It is widely believed that a duplicate gene has no phenotypic cost or advantage associated with it – that is, it is selectively neutral. In such a state, it is thought that the gene is free to mutate, independent of selection constraints or pressure. When a previously protein-coding gene incurs deleterious mutations such that it no longer codes for a useful polypeptide, the gene is rendered a “pseudogene”.

One recent paper, which recently appeared in the open-access journal, PLoS Genetics, by Kuo and Ochman, entitled “The Extinction Dynamics of Bacterial Pseudogenes”, offers a potent challenge to this view. According to the paper’s abstract:

The mechanisms and processes of cellular information storage, processing and retrieval have always been a focus of ID argumentation and research. Indeed, it was the complexity and elegance of these systems which first captured my attention as a junior undergraduate as I became interested in the implications of information-rich systems in biology and the possible explicative powers of intelligent causation.

In recent years, there has been a dramatic surge in our appreciation of genomics and the processes of information flow in the cell. Papers continue to flood in, reporting on a plethora of recent discoveries which take genomic complexity to a whole new level, leading many academics to tentatively re-evaluate the causal sufficiency of Darwinian mechanisms, the dual forces of chance and necessity.

One recent paper, published in the journal, Nature, documents the discovery that human cells have the largescale capacity to copy, not only DNA, but also RNA molecules. According to the paper’s Abstract,

Small (<200 nucleotide) RNA (sRNA) profiling of human cells using various technologies demonstrates unexpected complexity of sRNAs with hundreds of thousands of sRNA species present. Genetic and in vitro studies show that these RNAs are not merely degradation products of longer transcripts but could indeed have a function. Furthermore, profiling of RNAs, including the sRNAs, can reveal not only novel transcripts, but also make clear predictions about the existence and properties of novel biochemical pathways operating in a cell. For example, sRNA profiling in human cells indicated the existence of an unknown capping mechanism operating on cleaved RNA, a biochemical component of which was later identified. Here we show that human cells contain a novel type of sRNA that has non-genomically encoded 5′ poly(U) tails. The presence of these RNAs at the termini of genes, specifically at the very 3′ ends of known mRNAs, strongly argues for the presence of a yet uncharacterized endogenous biochemical pathway in cells that can copy RNA. We show that this pathway can operate on multiple genes, with specific enrichment towards transcript-encoding components of the translational machinery. Finally, we show that genes are also flanked by sense, 3′ polyadenylated sRNAs that are likely to be capped.

An article appeared in The New York Times last week written by the popular geneticist, Sean B. Carroll, who is probably best known for his professional and popular work on the emerging science of evo devo. Carroll’s article attempts to refute the challenges posed by the Cambrian fossil record to evolutionary thought. Carroll writes,

The difficulty posed by the Cambrian Explosion was that in Darwin’s day (and for many years after), no fossils were known in the enormous, older rock formations below those of the Cambrian. This was an extremely unsettling fact for his theory of evolution because complex animals should have been preceded in the fossil record by simpler forms.
In “On the Origin of Species,” Darwin posited that “during these vast, yet quite unknown, periods of time, the world swarmed with living creatures.” But he admitted candidly, “To the question why we do not find records of these vast primordial periods, I can give no satisfactory answer.”

Advocates of intelligent design have long been skeptical of the claim that the majority of our genome is nonfunctional gibberish, a mere relic of our evolutionary past. Many of the key arguments for common ancestry are based around the supposition that certain loci of our genome are functionless. But the gaps in our knowledge of the genome (in which such supposition resides) are continually shrinking.

A recent paper published in Science by Kondo et al. reported on the discovery that some of the supposed “non-coding” regions of the RNA transcript actually actively encode for short peptides that regulate genes involved in Drosophila development.

According to the Abstract,

A substantial proportion of eukaryotic transcripts are considered to be noncoding RNAs because they contain only short open reading frames (sORFs). Recent findings suggest, however, that some sORFs encode small bioactive peptides. Here, we show that peptides of 11 to 32 amino acids encoded by the polished rice (pri) sORF gene control epidermal differentiation in Drosophila by modifying the transcription factor Shavenbaby (Svb). Pri peptides trigger the amino-terminal truncation of the Svb protein, which converts Svb from a repressor to an activator. Our results demonstrate that during Drosophila embryogenesis, Pri sORF peptides provide a strict temporal control to the transcriptional program of epidermal morphogenesis.

Recently, Nick Lane, a biochemist and Provost’s Venture Research Fellow in the Department of Genetics, Evolution and Environment at University College London, published a new book, Life Ascending: The Ten Great Inventions of Evolution.

Nick Lane lays out ten biological phenomena for which he seeks to propose plausible evolutionary explanations. Among the phenomena discussed by Lane are the origin of life, DNA, photosynthesis, the complex cell, sex, movement, sight, hot blood, consciousness, and death. But does Darwinism have the goods? Or does Nick Lane offer us only a series of wishful speculations?

New Scientist offered the following praise for Lane’s work:

What makes this such a great read is that Lane, a biochemist by training, does not simply rehash the standard evolutionary tales – unlike many books published recently. Instead, he is familiar with all the latest research and has made up his own mind about who is right. The result is an original and awe-inspiring account. The first two chapters are the most coherent and convincing summaries of the dawn of life and of DNA that I have ever read.

The literature continues to flood in demonstrating that so-called ‘junk’ regions of the genome are not junk after all, but serve significant and important functions. One such recent paper reports evidence that retrotransposons may play significant roles in the cell. According to the abstract,

Retrotransposons including endogenous retroviruses and their solitary long terminal repeats (LTRs) compose >40% of the human genome. Many of them are located in intergenic regions far from genes. Whether these intergenic retrotransposons serve beneficial host functions is not known. Here we show that an LTR retrotransposon of ERV-9 human endogenous retrovirus located 40–70 kb upstream of the human fetal γ- and adult β-globin genes serves a long-range, host function. The ERV-9 LTR contains multiple CCAAT and GATA motifs and competitively recruits a high concentration of NF-Y and GATA-2 present in low abundance in adult erythroid cells to assemble an LTR/RNA polymerase II complex. The LTR complex transcribes intergenic RNAs unidirectionally through the intervening DNA to loop with and modulate transcription factor occupancies at the far downstream globin promoters, thereby modulating globin gene switching by a competitive mechanism.

Retrotransposons include the long interspersed nuclear elements (LINEs), short interspersed nuclear elements (SINEs), endogenous retroviruses (ERVs), and the solitary long terminal repeats (LTRs) of ERVs, and compose over 40% of the human genome. Retrotransposons possess enhancers and promoters which promote the expression of downstream polycistronic gene sequences. The cited paper seeks to determine whether the retrotransposons which are located in the intergenic (regions which intersperse genes, also known as ‘introns’) of the genome – which are often several hundred kilobases removed from the promoters – serve any beneficial function.

A few weeks ago, PZ Myers commented on so-called ‘Junk DNA’. Under the headline, ‘Junk DNA is still junk’, Myers wrote:

The ENCODE project made a big splash a couple of years ago — it is a huge project to not only ask what the sequence of a strand of human DNA was, but to analyzed and annotate and try to figure out what it was doing. One of the very surprising results was that in the sections of DNA analyzed, almost all of the DNA was transcribed into RNA, which sent the creationists and the popular press into unwarranted flutters of excitement that maybe all that junk DNA wasn’t junk at all, if enzymes were busy copying it into RNA. This was an erroneous assumption; as John Timmer pointed out, the genome is a noisy place, and coupled with the observations that the transcripts were not evolutionarily conserved, it suggested that these were non-functional transcripts.