From The Design Matrix:
A core element of the non-teleological perspective of evolution is that mutations are random with regard to fitness. This means that mutations are not inherently forward- or outward-looking. Instead, a mutation simply occurs in a random fashion (a genuine mistake) and whether or not it benefits the organism depends on contingency, for as far as we know, evolution does not create targeted mutations to solve specific problems.
What you have instead are a large number of cells each mutating their genomes at random. The population of cells is effectively playing the lottery. The one genome that happens to mutate the “right” spot wins the prize, as this genome is at a selective advantage in comparison and will then spread its progeny throughout the population. The problem is that the lottery winners, over time, cannot be predicted and such winners may explore trajectories that not only were not intended by a designer, but may actually hinder the ability to design across time using reproduction. All of this unintended evolution can thus be considered noise.If a designer is trying to use reproduction to perpetuate a design far into the future, how does one control for all the noise that Darwinian evolution will produce along the way? What would prevent this noise from drowning out the signal of design? How can a designer solve these problems?
Let me now provide a couple of clues to support the hypothesis that introns facilitated the evolution of multicellular life.
First, as a general rule, introns are far more common in multicellular genomes than single-celled genomes. Consider the human genome. It has 21, 746 genes and only 1,760 are without introns. Compare this to the genome of baker’s yeast. It has about 6200 genes and only about 250 have introns. In other words, while 92% of human genes have introns, only about 4% of the single-celled yeast genes have introns. What’s more, only about dozen yeast genes have more than one intron, while the typical human gene has around ten introns.
Posted in introns
By following the lead of Richard Dawkins, we realize that random variations coupled with natural selection can function as a designer-mimic – the blind watchmaker. But as I have noted earlier, all designers are constrained (and thus, in a way, guided) by their design material.
When we survey the living world today, it would be unjustified to assume that the blind watchmaker could craft a world of similarly complex and integrated creatures without proteins for the simple reason that the living world today is a protein-dependent reality. Without the use of proteins as design material, it is not clear what the designer-mimic could actually design.
But what if we moved up the ladder of complexity and considered the two basic cell designs – prokaryotic and eukaryotic.
Posted in evolution
Since I will be discussing introns, let me begin with a few points of clarification.
First, I will be focusing on introns found in protein-coding genes. In other words, these are the introns that interrupt sequence that code for amino acids and are removed by spliceosomes in order to form the mature mRNA. There are other introns that may have front-loaded the existence of these protein-coding introns, but that is another topic for another day. For now, when I refer to ‘introns,’ I am referring to introns found in protein-coding genes
Posted in introns
Over at his blog, Steve Matheson has been reviewing Stephen Meyer’s book, Signature in the Cell. Matheson quotes Meyer:
..the original DNA text in eukaryotic organisms has long sections of text called “introns” that do not (typically) encode proteins. Although these introns were once thought to be nonfunctional “junk DNA,” they are now known to play many important functional roles in the cell.
Here’s a short explanation for why Meyer’s statement is ludicrous. The human genome contains at least 190,000 introns (though it’s been recently estimated to contain almost 210,000). Together those introns comprise almost 1/4 of the human genome. One fourth. That’s 768 million base pairs. And biologists have identified “important functional roles” for a handful of them. How many? Oh, probably a dozen, but let’s be really generous. Let’s say that a hundred introns in the human genome are known to have “important functional roles.” Oh fine, let’s make it a thousand. Well, guys, that leaves at least 189,000 introns without function, and gosh, they’re snipped out of the transcripts and discarded before the darn things even leave the nucleus.
I would agree with Matheson that it is highly unlikely that a couple hundred thousand introns each have an “important functional role” “in the cell.” But I’d like to take the topic of introns and steer it into a much more interesting teleological direction.
Let me propose a hypothesis that flows naturally from the hypothesis of front-loading evolution: introns facilitated the evolution of metazoan life.
To this end, I have created the ‘introns’ tag and will be periodically exploring this hypothesis from several angles over the next few weeks/months.
Let’s build on the convergence between vertebrates and cephalopods. This time, let me quote some excerpts from the following article: Squid vascular endothelial growth factor receptor: a shared molecular signature in the convergent evolution of closed circulatory systems by Masa-aki Yoshida, Shuichi Shigeno, Kazuhiko Tsuneki, and Hidetaka Furuyaa (in EVOLUTION & DEVELOPMENT 12:1, 25–33 (2010)).
First, the researchers lay the groundwork for the convergence of these two systems:
Metazoan animals have evolved an incredible diversity of hearts and heart-like structures. The most elaborate case in invertebrates is observed in coleoid cephalopods: they exhibit an elaborate closed circulatory system (Schipp 1987; Budelmann et al. 1997). Their heart possesses a kind of advanced output structure similar to that of the human heart, which differs largely from molluscan typical nonendothelium primitive chambered hearts (see Kling and Schipp 1987; Schipp 1987). Neither morphological nor molecular data give strong support to a close phylogenetic relationship between vertebrates and cephalopods, suggesting that the closed circulatory systems and complicated hearts were formed independently in each lineage, and have converged during their evolution.
Their cardiovascular system is considerably similar to vertebrates in several respects such as high oxygen binding capacity, high concentrations of proteins, and short circulation time (Schipp 1987). Each vessel in the cephalopod is constructed similarly to vertebrate vessels, with an endothelial lining on a basement membrane (Budelmann et al. 1997), although the cephalopod blood vessel lining does not have the cellular junction typical among vertebrate species. Most invertebrates have no endothelium in their vascular walls so the cephalopods are unusual in that they are invertebrates with vertebrate type blood vessels. As the other molluscs have open vascular system, the peculiar blood vessel configuration in the cephalopods is in all probability secondarily developed similarly to the vertebrate among chordates (Ruppert and Carle 1983).
Then, they find something really cool.
Most people are familiar with the human circulatory system, its heart, and its network of blood vessels (you should have learned it in health class!). It represents an example of a closed circulatory system, described as follows:
The blood always remains inside the blood vessels and never comes in direct contact with the cells. The materials enter and exit the blood vessels through the walls. The blood flows in the blood vessels under high pressure such that it reaches all the parts of the body in good time. The blood vessels are branched into fine capillaries which are actually involved in the exchange of materials.
But did you ever hear of an open circulatory system? Here is a nice description:
In higher animals, there are two primary types of circulatory systems — open and closed. Arthropods and mollusks have an open circulatory system. In this type of system, there is neither a true heart or capillaries as are found in humans. Instead of a heart there are blood vessels that act as pumps to force the blood along. Instead of capillaries, blood vessels join directly with open sinuses. “Blood,” actually a combination of blood and interstitial fluid called ‘hemolymph’, is forced from the blood vessels into large sinuses, where it actually baths the internal organs. Other vessels receive blood forced from these sinuses and conduct it back to the pumping vessels. It helps to imagine a bucket with two hoses coming out of it, these hoses connected to a squeeze bulb. As the bulb is squeezed, it forces the water along to the bucket. One hose will be shooting water into the bucket, the other is sucking water out of the bucket. Needless to say, this is a very inefficient system. Insects can get by with this type system because they have numerous openings in their bodies (spiracles) that allow the “blood” to come into contact with air.
And here is a picture to help you better visualize it:
So why bring this up?
We’ve just seen that many preadaptations for the evolution of neurons were in place. Calcium toolkit for secretion of neurotransmitters? Check. Post-synaptic scaffold? Check. Circuitry for neurogenesis? Check. But what about the neurotransmitters themselves?
Now, in principle, just about any molecule could serve as a neurotransmitter, as you simply need something that specifically binds to a receptor that triggers the opening of an ion channel. In fact, some amino acids, like glutamate, can moonlight as neurotransmitters.
Nevertheless, I decided to check up on two important neurotransmitters – acetylcholine and epinephrine. These neurotransmitters play key roles in your autonomic nervous system, the ancient system that maintains homeostasis through the regulation of all your body’s organs. What’s more, acetylcholine is the neurotransmitter used to stimulate muscle contraction.
The hypothesis of front-loading neurons would lead us to expect that these neurotransmitters exist in organisms that do no possess neurons. And sure enough, they do.
A neuron is a very fascinating cell. It is a cell that is specialized to detect changes in the environment, translate that environmental information into the language of membrane potential changes (electrical signals), and engage in long-distance communication by transmitting such electric signals to distant targets in a body. The key to this transmission is the synapse, where the axon of one neuron uses exocytosis to release neurotransmitters that can diffuse and bind to receptors on the dendrite of an adjacent neuron.
In essence, the synapse is a ‘decision point’ for determining whether or not the signal will proceed. It is the synapse which confers immense plasticity and potential for control to the whole circuit.
Over at the First Things blog, a standard “ID vs. Evolution” fight broke out involving some major players. Unfortunately, I arrived late (as usual), but I decided to add my two cents to the kerfuffle anyway:
Over the years I have discovered a primary reason there is so much heated argument about this issue is that people employ numerous personal definitions for the concepts “intelligent design,” “evolution,” and “science.” Thus, I appreciate that Stephen Barr spells out his definition of ID: “The ID claim is that certain biological phenomena lie outside the ordinary course of nature.” If that is ID, then I would disagree. But ID can also mean something more modest, where one simply infers some form of intelligent influence on biological phenomenon, including evolution itself. For example, life itself could have been designed to shape subsequent evolution, thereby imparting some form of direction to evolution. This form of ID would not require evolution to fail or evolutionary mechanisms to be inadequate. On the contrary (!), this form of ID would more likely marvel at the success of evolution and try to develop a deeper understanding of why evolution succeeded.
I also added:
a clever designer could actually recruit and exploit the processes of random mutations and natural selection to carry out some purpose. After all, a common belief shared by both the ID people and their critics is that random mutations and natural selection are antithetical to purpose. I think that common belief is simply an assumption (or reflex response) that has become entrenched for historical and cultural reasons.
design and evolution are not mutually exclusive. There may be ways to make intelligent use of randomness and natural selection such that they can carry out an objective. For example, scientists already make use of randomness when designing new proteins.
In response, someone proposed the following questions to me:
Can you (at least) provide a useful essential hint of how “intelligent use of randomness and natural selection … can carry out an objective”? What would INTELLIGENT mean, in such context?
This person hit on something very important.
Posted in design