I’ve long suggested that life is a form of carbon-based nanotechnology, as the more we learn about the cell, the more sophisticated it becomes. Doubt me? Take 30 minutes and listen to the following lecture by microbiologist Lucy Shapiro as she describes how various events in the cell cycle in the simplest of cells is carried out. Among other things, you’ll learn about the importance of location and organization inside bacteria, you’ll learn that the bacterial chromosome is laid out in space in an organized fashion, you’ll see the ingenious method the cell uses to target the site where it splits into two, and see how epigenetics is used to control the whole process. Or at the very least, you’ll feel a little bit smarter for investing that half-hour of your life. 😉
Previously, I took issue with John Avise’s abrupt description of alternative splicing as having “some advantage,” as alternative splicing may play a crucial role in the evolution of metazoans by shielding sequence from selection, allowing minor variants to emerge and grow before being put to the full test of selection. It’s such shielding that might be required to expand a more complex state. One way to think of alternative splicing is as an evolutionary capacitor. I’ll let the Masel group describe what that means:
Let me add one more comment concerning Avise’s PNAS paper. In the last entry, I focused on his argument that introns counts as evidence against intelligent design. We saw the whole argument fails if we envision design working through evolution. But I want to you to notice something else. In the paragraph preceding the discussion of introns, Avise wrote:
Approximately 1% of all known genes in the human genome encode molecular products that our cells employ to build spliceosomes and conduct splicing operations on premRNA. All this rigmarole has some advantages (e.g., opportunities for alternative splicing during ontogeny and exon shuffling during evolution, both of which can generate functional protein diversity), but such benefits do not come without major fitness costs.
Note that Avise describes alternative splicing as something that confers “some advantage.” Some advantage. As if alternative splicing is just a minor factor in evolution.
Now let’s contrast this to the abstract from a paper by Stephanie Boue, Ivica Letunic, and Peer Bork (Alternative splicing and evolution. BioEssays 2003 25:1031–1034):
Alternative splicing is a critical post-transcriptional event leading to an increase in the transcriptome diversity. Recent bioinformatics studies revealed a high frequency of alternative splicing. Although the extent of AS conservation among mammals is still being discussed, it has been argued that major forms of alternatively spliced transcripts are much better conserved than minor forms.(1) It suggests that alternative splicing plays a major role in genome evolution allowing new exons to evolve with less constraint.
“A major role in genome evolution” sounds a tad more than “some advantage “ to me. In fact, consider the conclusion of Boue et al.:
So what is the consequence of Avise’s false dichotomy? The bulk of his paper is a detailed exploration of the “outlandish features of the human genome that defy notions of ID by a caring cognitive agent.” While this is an argument that works against design that is coupled to special creation, it fails against design that is coupled to evolution. To see this, let’s pick one of the outlandish features that Avise explores – introns. I chose this example simply because I have already written about it.
Avise’s core argument is as follows:
There are good reasons to think that cells might be better off without introns, in an ideal world.
Let me now add to this argument with the following point:
There are good reasons to think that evolution might be worse off without introns.
In other words, if introns are an “outlandish features of the human genome,” we might also point out that without this outlandish feature, there is no evidence to think that evolution would have cobbled together a human, or human-like, genome.
Recall that I have used the teleological perspective of front-loading to propose a testable hypothesis about introns – they have facilitated the emergence of metazoan-type complexity – that is supported by evidence (here, here, here, and here) and has been successfully defended. (If you have not read these essays, then what follows below will not make much sense to you).
If the design objective is to nudge the emergence of metazoan-type complexity, and not to ensure that cells would be “better off,” then we can see that Avise’s core argument has collapsed.
Nevertheless, let’s have a look at Avise’s reasons.
Biologist John Avise recently published a paper about intelligent design in the journal PNAS entitled, “Footprints of nonsentient design inside the human genome.” Avise poses an argument against ID:
my focus in this paper is on a relatively neglected category of argument against ID and in favor of evolution: the argument from imperfection, as applied to the human genome in this case.
The problem here is that Avise never defines or describes perfection. So how are we to determine if imperfection exists? What’s more, Avise never makes the case that intelligent designs must necessarily be perfect designs. Given these two simple facts – failure to define perfection and failure to show that design entails perfection – Avise’s stated focus fails.
But the situation becomes much more interesting if we simply discard the focus “on imperfection” and consider what Avise is trying to communicate. I think this portion of the abstract makes his argument more clear:
Yet, many complex biological traits are gratuitously complicated, function poorly, and debilitate their bearers.
It’s not that some system or feature is “imperfect” that is relevant. It’s that the system or feature is “gratuitously complicated, function poorly, and debilitate their bearers.” For any system that is indeed gratuitously complicated, functions poorly, and debilitates their bearers, is not something I would consider to be intelligently designed. This is even more true if the poor function and constant breakdowns are a consequence of a complexity that is gratuitous. If I had reviewed Avise’s paper, I would have suggested he drop the whole “imperfection” argument and focus on first establishing the gratuitous nature of biotic complexity and then tracing poor performance to this very gratuity. I think that is the argument Avise is making, but it gets lost in all the harping about imperfections.
As you know, I do agree with Avise that such “bad design” counts as evidence against intelligent design. Otherwise, why label a design as being “intelligent?” But I also believe in a fair- and open-minded approach to these issues. Thus, I would follow through with Avise’s logic to the next step.
I have previously raised four criteia that can be used, as a whole, to assess a design inference – Analogy, Discontinuity, Rationality, and Foresight. Over the years, I have placed most emphasis on Foresight, gradually fleshing out the hypothesis of front-loaded evolution. And while I remain quite encouraged by the increasing plausibility of front-loading, the criterion of Rationality has lately begun to attract more of my attention.
Several years ago, Howard Van Till reviewed Dembski’s book, No Free Lunch. Van Till hit on something that I mentioned in my book:
One of the expectations from the hypothesis of front-loading evolution is that cells would play a significant role in their own evolution, as this would constitute an intrinsic factor to evolution that would be more strongly connected to the original design event. To this end, consider just how smart cells can be:
Scientists studying how bacteria under stress collectively weigh and initiate different survival strategies say they have gained new insights into how humans make strategic decisions that affect their health, wealth and the fate of others in society.
“We have developed for the first time a system level model of a large gene network to decipher the underlying principles of the bacteria game theory and how an internal network of genes and proteins is used to calculate risks in this complicated situation,” he said.
This has applications to human society because many people encounter similar dilemmas during their own lives. For example, should people ignore side effects and vaccinate against a new potentially lethal virus or should they not vaccinate and take the risk of being infected with the possible consequences? If the majority of the population is going to get vaccinated, then it is better for each individual not to get vaccinated. However, if most people will not be vaccinated then it is better to be vaccinated.
“What each bacterium is doing is the equivalent if each individual on earth was able receive the exact information about the rate of spread of this new virus, the exact information about the intensions, to be vaccinated or not, by each person on the planet, and in addition the exact information about the health risks of side effects or being infected,” said Ben Jacob. “A decision is then made in the context of this vast amount of information.”
“We have shown how the bacteria do this complex calculation according to well-defined principles,” added Onuchic. “We learned a simple rule: Anyone who needs to make a decision under pressure in life, especially if it is a possible death decision, will take its time. She or he will review the trends of change, will render all possible chances and risks, and only then react.”
And speaking of humans, consider this research:
In my previous essay about proteins-as-design-material, I noted:
This all raises some interesting questions. For example, without proteins, and their manufacturing process, what becomes of the blind watchmaker? Without proteins, and the latent functions contained within, might not the blind watchmaker exist as the impotent, crippled, blind watchmaker with no one to notice its existence? If so, how much credit does the blind watchmaker really deserve?
The vast and immense Tree of Life is a protein-dependent output. Point to some evidence of evolution and I’ll point to the proteins that underlie it. Without proteins, would there be a Tree of Life 3.5 billion years after the RNA world took root? How do we know? If we believe so, would the Tree be as immense and vast as it is today? A life form composed of nucleic acids, carbohydrates, and lipids would suffice for the purposes of the blind watchmaker. But could the blind watchmaker turn this material into something that is analogous to an Ash tree filled with squirrels, beetles, and birds?
First up, a new clue about the origin of angiosperms:
To Charles Darwin it was an ‘abominable mystery’ and it is a question which has continued to vex evolutionists to this day: when did flowering plants evolve and how did they come to dominate plant life on earth? A new study in Ecology Letters reveals the evolutionary trigger which led to early flowering plants gaining a major competitive advantage over rival species, leading to their subsequent boom and abundance.
The study, by Dr Tim Brodribb and Dr Taylor Field of the University of Tasmania and University of Tennessee, used plant physiology to reveal how flowering plants, including crops, were able to dominate land by evolving more efficient hydraulics, or ‘leaf plumbing’, to increase rates of photosynthesis.
“Flowering plants are the most abundant and ecologically successful group of plants on earth,” said Brodribb. “One reason for this dominance is the relatively high photosynthetic capacity of their leaves, but when and how this increased photosynthetic capacity evolved has been a mystery.”
Using measurements of leaf vein density and a linked hydraulic-photosynthesis model, Brodribb and Field reconstructed the evolution of leaf hydraulic capacity in seed plants. Their results revealed that an evolutionary transformation in the plumbing of angiosperm leaves pushed photosynthetic capacity to new heights.
It will be interesting to track down the molecular machinery involved in the development of this “leaf plumbing,” as front-loading would lead us to expect that it existed prior to the development of angiosperms.
Next up, another example of the way cells facilitate their own evolution: