Shattered assumptions, broken rules and overturned beliefs. The science media seems eager these days to emphasize science’s capacity to shift paradigms. And it was such a handful of descriptives that was used to convey the implications of a new study that redefines our view of genome architecture (1). At the heart of such excitement lay a tunicate organism called Oikopleura dioica that carries in its genetic armory “several peculiarities” (1). Weighing in with its 70 million base pairs of DNA Oikopleura is today venerated as the animal with the smallest known genome (1). But what stands out for biologists who have dedicated years to unpacking Oikopleura’s treasure box genome is the ‘odd ball’ physical location of many of its genes (1). The Scientist’s Megan Scudellari remarked that “Oikopleura’s genes appear to have been shuffled like a deck of cards” (1).
At the apex of this presumed shuffling is that all-elusive but much loved patch-all process called evolution. “UV rays and other mutagens” that bombard Oikopleura as it ekes out its existence just below the ocean surface are the suggested deck dealers of this particular shuffle (1). But apart from this rather misty association between cause and effect, there is precious little in the evolutionary inferences of this study to satisfy an appetite for robust scientific argumentation. To be fair, there are observable facts that we can latch onto and embrace as the products of rigorous science:
(i) Oikopleura’s genome is extremely small containing the same number of genes found in humans (18,000) but compacted into a genome that is 1/40th of the size (1). Genome compactness is reflected in small intergenic distances (53% are less than 1Kb)(2).
(ii) While the Oikopleura external phenotype is clearly in line with that observed in other tunicates, the intronic organization of its genome is vastly different (introns are very small peaking at 47 base pairs in length)(2).
(iii) Oikopleura is unique amongst the tunicates in having both male and female individuals (2).
(iv) Oikopleura exhibits high mutation rates and low dN/dS ratios per each 4-day long generation (dN and dS being the rate of substitutions in non-silent and silent sites respectively)(2).
But there is also fact-less guesswork. For example, since this new study found that many of Oikopleura’s introns display high sequence homology, the follow-on assertion put forth by the authors is that introns multiplied in the genome in a hap stance, “by chance” fashion and that genome architecture across the animal kingdom is therefore inherently plastic and unconnected to morphological/developmental complexity (1,2). Such a grossly overstated endpoint does not appear to be supported by anything close to a thorough examination of intron location and animal morphological variability.
Twenty years ago scientists began to understand the intimate role that introns play in gene regulation in higher order animals (3). We now know that intron splicing involves “the precise deletion of an intron from the primary transcript” so that exons on either end can be joined in readiness for protein translation (4). The choice of specific splice sites depends on the surrounding sequence and structure of the RNA (5). Three types of sequence- the 5’ splice site, the 3’ splice site and a branchpoint sequence- are almost invariably found in pre-mRNA introns of higher eukaryotes although these elements alone are insufficient to account for the specificity of the splicing reaction (5). Additional signals in abutting exons not only ensure that accurate splicing is maintained but also prevent exon ‘skipping’, which would of course adversely impact the functionality of the translated product (6).
In some cases more than one mRNA can be coded for by a “single stretch of DNA” as a result of different splicing pathways, different intron cleavage sites and selectively active promoters (3). The mouse salivary amylase gene is perhaps the archetypal example of the multi-variant role that introns play in gene regulation. In this instance alternative but nevertheless nucleotide-specific splice sites are used depending upon whether expression is required in salivary glands or the liver (3). Stephen Meyer writes: “like Russian dolls stored within Russian dolls, exons and introns encode multiple genetic messages within themselves and are themselves part of a larger genetic message” (7).
Genomic mapping has shown that “of 5589 introns mapped by interspecies protein alignments, 76% had positions unique to Oikopleura” (2). It is therefore assumed evolutionarily speaking that Oikopleura’s single major spliceosome made up of U1 snRNP and U2AF proteins, is capable of recognizing donor and acceptor sites in the genome and shuffling introns around accordingly (2). Such a proposed transposition and propagation seems to fly in the face of what we know about the contextual requirements of intron splicing as outlined above. For instance, if differing intron splicing pathways are active in distinct parts of an organism then we would expect their transposition to novel genome sites to be extremely disruptive to gene function within their new context.
Evolutionists’ intron-splicing magic is rife with factless guesswork. Even the briefest of considerations as is offered here makes that plain.
.Further Reading
- Megan Sculellari (2010) Who Needs Structure Anyway? The Scientist, 18th November, 2010, See http://www.the-scientist.com/news/display/57814/
- France Denoeud et al (2010) Plasticity of Animal Genome Architecture Unmasked by Rapid Evolution of a Pelagic Tunicate, Science, Vol 330, pp.1381-1385
- Benjamin Lewin (1990), Genes IV, Oxford Cell Press, pp.484-486
- Christopher Wills (1991) Exons, Introns & Talking Genes: The Science Behind The Human Genome Project, Oxford University Press, Oxford UK, p.112
- Adrian Kramer & Tom Maniatis (1990) RNA Splicing, in Transcription And Splicing, Eds B.D. Hames & D.M. Glover, IRL Press, Washington DC, pp.141-145
- Ibid. p.159
- Stephen Meyer (2009) Signature In The Cell: DNA And The Evidence For Intelligent Design, Harper Collins Publishers, New York, p.463