Irreducible Complexity and a Strawman

I made a comment in a Telic Thoughts thread entitled Sad Smoke and Mirrors in which I quoted from Dembski's book No Free Lunch. Dembski refers to irreducibly complex systems- ones which would not develop "in one fell swoop." What struck me about the quote was that Dembski was not making the claim that IC systems could not come about by identifiable means. In fact he mentions non-Darwinian events he excludes from the insuperable obstacle to an IC system outcome. The significance being that a strawman is destroyed i.e. the one alleging that IDists claim an IC system could not be produced by known physical means.

Est Proteins and Telomeres

Keeping Cells Youthful: How Telomere-building Proteins Get Drawn Into The Fold is a Science Daily article providing information about findings made by researchers from the Salk Institute for Biological Studies. A protein aids in the elongation of chromosome ends (telomeres) and in so doing prolongs cellular function as reported in the journal Nature Structure and Molecular Biology. The integrity of telomeres is maintained by a complex of proteins, which from an origins vantage point, makes irreducible complexity a natural perspective.

What is it about telomeres that is associated with problematic cell function? As the article explains cell division tends to result in telomeres becoming progressively shorter. If the progression continues unchecked, affected cells eventually lose their capacity to divide. The solution to this dilemna is an enzyme known as telomerase whose function is to restore the needed length to telomeres following cell division. Telomerase is not a solo performer however. Another protein known as Est1 has been found to help to bring telomerase to telomeres in yeast cells.

Researchers discovered that a protein known as Est3 is similar to a protein found in mammals which is labeled TPP1. TPP1 binds to telomeres and protects them from cellular repair enzymes which might interpret the chromosome ends as damaged DNA. A protein fold common to Est3 and TPP1 facilitates their function.

Flagellar Pathways

I get ideas about blog topics from many sources for blog entries here and at Telic Thoughts. I'm particularly grateful to an individual named Clare for the news stories she provides. Here is a link to a paper about a familiar topic and a quote from it:

The Evolution of the Flagellar Assembly Pathway in Endosymbiotic Bacterial Genomes (Molecular Biology and Evolution 2008 25(9):2069-2076; doi:10.1093/molbev/msn153; authored by Christina Toft and Mario A. Fares)

Genome shrinkage is a common feature of most intracellular pathogens and symbionts. Reduction of genome sizes is among the best-characterized evolutionary ways of intracellular organisms to save and avoid maintaining expensive redundant biological processes. Endosymbiotic bacteria of insects are examples of biological economy taken to completion because their genomes are dramatically reduced. These bacteria are nonmotile, and their biochemical processes are intimately related to those of their host. Because of this relationship, many of the processes in these bacteria have been either lost or have suffered massive remodeling to adapt to the intracellular symbiotic lifestyle. An example of such changes is the flagellum structure that is essential for bacterial motility and infectivity. Our analysis indicates that genes responsible for flagellar assembly have been partially or totally lost in most intracellular symbionts of gamma-Proteobacteria. Comparative genomic analyses show that flagellar genes have been differentially lost in endosymbiotic bacteria of insects. Only proteins involved in protein export within the flagella assembly pathway (type III secretion system and the basal body) have been kept in most of the endosymbionts, whereas those involved in building the filament and hook of flagella have only in few instances been kept, indicating a change in the functional purpose of this pathway. In some endosymbionts, genes controlling protein-export switch and hook length have undergone functional divergence as shown through an analysis of their evolutionary dynamics. Based on our results, we suggest that genes of flagellum have diverged functionally as to specialize in the export of proteins from the bacterium to the host.

Tracing a Pathway to DNA

Yesterday's post on supercoiling identified a constraint inherent to the topological structure of DNA which supports a front loading perspective. It also makes a gradual evolutionary approach to DNA dubious based on properties of DNA. Imagination is a wonderful thing but unconstrained imagination, applied to the solution of scientific dilemnas, is not.

A selection perspective of pathways to DNA should be guided by considerations that go beyond supercoiling. Enzymes enabling deoxyribose metabolism have obvious selection value. But that does not explain their origin. Enzymes are needed prior to the biosynthesis of deoxyribose. Yet what selection value would they confer prior to the point in time when DNA was a repository for genomic information?

Which brings me to a more substantial point. DNA enables cellular functions because it comes loaded with genetic information, mechanisms that enable gene expression and a genetic code already in place. These would have to be accounted for by any viable origins theory. Fitting theory within a selection framework is confounded by the very nature of genes and mechanisms needed to allow for their expression. Step by step approaches are not suggested by the biological systems discussed.

A designer faced with the task of incorporating DNA within a cellular environment would front load genetic information and the means of accessing and expressing it. It would be good design. Yet we are to expect unidentified forces on nature to have accomplished the same. But of what biological use is a gradual encoding process when minimally functional genomes number in the dozens of genes? How do transcription and translation functions gradually evolve? If the structures discussed were anything but biological, a front loaded origin would seem obvious based on the nature of the structures themselves.

Fear of designer implications ought not guide rational considerations of origin matters. That includes irreducibly complex DNA.

Irreducible Complexity and Functional Intermediates

William Brookfield wrote a comment at Telic Thoughts, within a thread discussing irreducible complexity, which I think merits some attention. The quote:

It seem to me that if a (mouse) trap is functioning within a biological system not — as a "trap" — but as "a blunt instrument" then NS will be selecting for the optimum "blunt instrument" and RM will just be scrambling in no specific direction (randomly). The result is that the function of this "(Mouse) trap" has no causal anticedent and its appearance by RM&NS or any other such material agents must be taken on faith. It seems to me that NS optimizes for existing function not future function and that these are two divergent directions.

Attempts to refute intelligent design inferences, drawn from Behe's irreducible complexity, are based to a great extent on homology arguments and the cooption concept. Brookfield correctly points out that functional discontinuity is associated with a selection perspective. Although he does not explicitly state it, the discontinuity is linked to cooption and homology based explanations. The explanations lack the detail needed to establish a functional trail. Precusor function is evident when the coopted entity is identified and the function of the relevant IC system is also clear. However, intermediate functions are unclear. If precursor and IC functions are disparate then the lack of clarity becomes problematic for theoretical applications. How predictive are theoretical models lacking identifiable functional intermediates?

Potential Windfall from Nuclear Tinkering

A Science Daily article titled Location Matters, Even For Genes notes how a change in the location of a gene can affect gene expression. Specifically, moving an active gene from a cell nucleus interior to its periphery appears to inavtivate the gene. The related paper on which the story is based was published in the journal Nature. The significance to this lies in a potential to silence genes by preventing the transcription of them. This would occur when such genes are attached to the inner part of the nuclear membrane. This could become a form of treatment for medical maladies through manipulation of gene regulation. Such maladies could include cancer whose development has been, at times, associated with the malfunction of gene regulation.

Is there any significance for Intelligent design? Quite possibly. Enhanced capacities to regulate gene expression may prove useful in assessing ID concepts like irreducible complexity and front loading. Tinkering with cellular mechanisms can be a means of ascertaining the fitness value of constituent parts of a biological function. It could also indicate a hitherto unrealized hierarchical structure to biological development useful to a front loading perspective.

Casey Luskin on Irreducible Complexity

At Telic Thoughts I posted this blog entry centered around an article by Casey Luskin which appeared here. Casey Luskin posted this comment. The following part of it deals with irreducible complexity. Note the reference to empirical evidence cited namely, Scott Minnich's genetic knockout experiments. (The quote appears in blue.)

Raevmo wrote: "Luskin simply asserts IC without any logical arguments or empirical evidence. Overall, Luskin's piece has nothing new to offer."

I reply: These are neither accurate nor fair accusations. This was intended to be a review of the NAS's document, not a presentation of new research. If you have criticisms, then criticize based upon the intent of the document.

Moreover, I gave arguments from Frank B. Salisbury and Øyvind Albert Voie that contend that the cell and DNA-enzyme system are irreducibly complex. Additionally, my response to the NAS observes that "proponents of intelligent design have done experimental tests on the bacterial flagellum showing it is irreducibly complex" and I then cited Scott Minnich's genetic knockout experiments presented at the Kitzmiller trial which show the flagellum is IC. So Raevmo's charges hold no water.

A Tall Tale

Casey Luskin authored Wolf-Ekkehard Lönnig Rebuts Latest Tall Tale of Giraffe Evolution at Evolution News & Views. Quoting from the blog entry (in blue):

Darwinists sometimes think that they can account for the evolutionary origin of a complex biological feature simply by citing some kind of experimental or theoretical evidence showing that the complex feature would have provided a selective advantage to its owner. However, such Darwinists forget that, as many have recounted, natural selection only accounts for the survival of the fittest, not the arrival of the fittest. Evidence that a given feature—when fully formed—provides some selective advantage does not demonstrate that the feature can be evolved in a step-wise, mutation-by-mutation fashion.

In fact it is a working assumption that functional advantage explains the origin of a given feature. Functional advantage addresses a causal process from a sifting point of view. It does not explain a generating process or a sequence of events. In fact the actual sequence of genomic events is vaguely presented. Although we cannot actually observe a process involving changes over geologic eons, we should demand a theoretical description with more details than has been forthcoming The cited evidence for change over time lies at the molecular level. But if we look at genes connected with the giraffe neck we find little indicating how a sequence of incremental events unfolded.

Here is an amply illustrated paper by Wolf-Ekkehard Lönnig which discusses details ommitted by the overly simplistic evolutionary accounts which are all too prevalent.

A Model for Basic Eukaryotic Functions

A PLOS Biology research article titled Mutation of RNA Pol III Subunit rpc2/polr3b Leads to Deficiency of Subunit Rpc11 and Disrupts Zebrafish Digestive Development, which is authored by Nelson S. Yee, Weilong Gong, Ying Huang, Kristin Lorent, Amy C. Dolan, Richard J. Maraia and Michael Pack, cited data obtained through use of the zebrafish as a model for POL III function analysis. POL III is an RNA polymerase subunit. RNA polymerases are very large multi-subunit protein complexes. Three types of subunits found in eukaryotes are:

RNA polymerase I (Pol I). It transcribes the rRNA genes for the precursor of the 28S, 18S, and 5.8S molecules (and is the busiest of the RNA polymerases).

RNA polymerase II (Pol II; also known as RNAP II). It transcribes protein-encoding genes into mRNA (and also the snRNA genes).

RNA polymerase III (Pol III). It transcribes the 5S rRNA genes and all the tRNA genes.

The following is the summary of the authors of Mutation of RNA Pol III Subunit rpc2/polr3b Leads to Deficiency of Subunit Rpc11 and Disrupts Zebrafish Digestive Development (in blue):

The transmission of genetic information from DNA to messenger RNA to protein depends on the function of a large number of small noncoding RNA molecules. The genes encoding these RNAs are transcribed by RNA polymerase III (Pol III), a 17-subunit protein complex whose structure is closely related to that of RNA polymerases I and II. Here, we report the effect of a mutation in a gene encoding one Pol III subunit, Polr3b, which disrupts proliferation and growth of tissue progenitor cells in the zebrafish digestive system. Analyses of a nearly identical mutation in the yeast S. pombe gene encoding Polr3b, also known as Rpc2, suggested that the zebrafish mutation disrupted the mutant Polr3b protein's interaction with another Pol III subunit, Polr3k, also known as Rpc11. Overexpression of the gene encoding Polr3k in the Polr3b mutants partially rescued (reversed) the mutant phenotype. These findings extend our knowledge of the mechanism of Pol III function, which appears to have been highly conserved during eukaryotic evolution. Furthermore, these data also suggest that assembly of the 17-subunit Pol III enzyme is a dynamic process, since Polr3k overexpression can partially rescue the mutant phenotype. Understanding how Pol III is assembled has implications for human disease, since Pol III activity is markedly increased in most cancers.

Note that the function of the genetic code is dependent on the transcription function of RNA polymerase III (Pol III). In addition the structure of Pol III, a 17 subunit protein, is similar to RNA polymerases I and II. The translation function is made possible by Pol III. The first paragraph of the introduction is instructive. Quoting (in blue):

RNA Polymerase III (Pol III) is a 17-subunit complex that is responsible for the transcription of small noncoding RNAs such as transfer RNAs (tRNAs), 5S ribosomal RNA (rRNA), U6 small nuclear RNA (snRNA), 7SL RNA, and others in eukaryotes [1,2]. The two largest subunits, Rpc1 (160 kDa) and Rpc2 (130 kDa), are highly homologous to their counterparts in Pol I and Pol II, and together provide a large surface area for interaction with many of the other subunits [2]. Structural analyses of Pol III complexes [3,4], together with two-hybrid analysis [5], have identified multiple subunit interactions (reviewed in [1]). These, together with biochemical and genetic analyses, have led to a model that attributes some of the unique functions of Pol III, including its high processivity, efficient transcription termination and recycling activity, RNA 3′ cleavage activity, and interaction with diverse promoters, to specific individual subunits.

The model links unique and specified Pol III functions, including a capacity to interact with diverse promotors, to individual subunits. Quoting from the next paragraph (in blue):

Mutational analyses in yeast clearly show that an intact Pol III system is essential for cell growth. The effects of reduced Pol III function are predicted to be broad, including protein synthesis necessary for cell-cycle progression (tRNAs), ribosome biogenesis (5S rRNA), mRNA splicing (U6 snRNA), and membrane targeting of newly translated proteins (7SL RNA). Pol III transcription is tightly regulated during the cell cycle [6] and in response to cellular stress [7]. Recent studies in human cells have also highlighted the roles of oncogenes and tumor suppressors such as Rb [8,9], p53 [9–11], and cMyc [9,12] in controlling the interactions between the transcription factors that bring the Pol III complex to the promoters of its target genes (reviewed in [13,14]). Other proteins, such as Maf1 [15–18] and the oncogenic kinase CK2 [19–20], can regulate Pol III function through direct interactions with the Pol III complex. Thus, eukaryotic cells have evolved multiple independent mechanisms for regulating Pol III activity.

It would have been interesting if Michael Behe had focused on biosynthesis as an example of irreducible complexity. I would have enjoyed reading the responses of critics. A depiction of pathways to the evolution of "multiple independent mechanisms for regulating Pol III activity" would have been most interesting. So would a gradual, incremental model for cell-cycle progression.

Crystal Arguments

The following exchange occurred in the comment section of a blog entry posted by Mike Gene. Part of the exchange is reproduced here for the purpose of commentary as it entails a flawed argument frequently employed against intelligent design. There are variations of crystal arguments which are arguments by analogy seeking to explain how biological complexity could be generated from laws of nature. The biological complexity referred to is that of an initial genome. My comments appear in green while those of the other commenter are in red. The follow-up commentary is in blue.

Bradford: The ateleologist would proceed to argue that the dice were fixed as a consequence of some natural force of nature. Perhaps the ends were eroded or the faces were indented in six places on each side by some mechanism.

Most scientists understand that humans act with purpose, and that dice are human manufactured devices that should be "fair", but are often tampered with to gain advantage over adversaries. Think Bradford! It is your knowledge of humans and dice that allows you to consider cheating to account for skewed distributions.

A more appropriate example might be water forming ice. Perhaps it is Jack Frost who carefully weaves beautiful and intricate crystals on the windowpane, or perhaps there is some underlying property of water. Making that scientific determination requires forming and testing valid hypotheses.

Indeed it is my knowledge of humans and dice that allows for a conclusion of cheating when skewed distributions are observed. It is important to note that accurate conclusions are pegged to correct assessments of contingencies inherent to the situation at hand. But would one infer that an intelligent designer was a necessary part of a hypothesis involved in the explanation of snowflake patterns or the beauty of frozen ice on a windowpane? No. But why not?

While the patterns themselves can be complex and beautiful they are made possible through a change in one variable- temperature. The temperature leads to an appearance that is a property of water under conditions that can be specified. Causality is determined. Given the properties of matter (in this case water) and the environmental conditions, snowflakes or ice will form; along with the complex patterns in the snowflakes or ice. Complexity is predictable and linked to the properties of matter and weather conditions. It is our scientific knowledge that allows us to make accurate predictions that complex patterns will arise.

Contrast this with nucleic acids; biochemicals organisms utilize to store information used to code for proteins and RNA and the related functions these encoded end products enable. Like water nucleic acids have chemical properties. Unlike water the chemical properties of nucleic acids do not reveal the conditions of a prebiotic environment that would lead to the unique sequencing patterns enabling the synthesis of functional proteins and RNA. But is that because we simply have not determined what those conditions are or do the chemical properties of nucleci acids and the nature of encoding systems signal that environmental conditions alone are insufficient to account for biologically functional nucleic acids?

It is the latter condition and it is our knowledge of chemistry, biology and encoding symbolism that allows for a correct inference of intelligent design. Like the example of dice and humans, it is our knowledge, not our ignorance, that makes possible an accurate conclusion. While determinism marks the physical process that results in crystalline formation a functional sequencing of nucleotides is contingent on an existing biological condition that confers selective value to the sequencing. That condition being an availability of amino acids corresponding to codons and of proteins to the nucleic acids containing the codons. This is irreducible complexity on a most basic biological level.

The biological utility of codons lies in their symbolic nature. The symbolism is as real as the amino acids composing proteins synthesized in accordance with the identity and order of the codons. It's contingency all the way and a contingency whose logic lies in the existence of a larger replicating biological system- the cell. Crystals provide evidence of the molecular properties of their constituent substance. Functional nucleic acids provide evidence of an already existing cell replete with the proteins they code for. That's a problem for those seeking to convey the idea that life was generated like crystals.

Transcription and DNA Repair

This linked news article, from the National Institutes of Health, Scientists Discover Role of Enzyme in DNA Repair, notes a mechanism involved in DNA repair and the transcription function. From the linked article (in green) (I added the link which helps to explain ataxia telangiectasia):

Scientists from the National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), National Cancer Institute (NCI), and Integrative Bioinformatics Inc. have made an important discovery about the role of an enzyme called ataxia telangiectasia mutated protein (ATM) in the body’s ability to repair damaged DNA. NIAMS and NCI are part of the National Institutes of Health (NIH).

When DNA within a cell is damaged, the cell’s protective mechanism must do one of two things: repair the defect or “commit suicide,” says Rafael Casellas, Ph.D., an investigator in NIAMS’ Molecular Immunology and Inflammation Branch and leading author of a new paper describing the discovery. But the way in which the cell performs these protective functions has been largely a mystery, says Casellas, whose research is beginning to unravel this mystery.

Casellas’ research focuses largely on certain genes that are deliberately broken and repaired as part of the immune response. Through a tightly controlled process of breaking and rejoining DNA segments, immune system cells called B lymphocytes are able to produce tens of millions of different types of antibodies to fight almost limitless types of invaders. This process of genetic recombination requires the activity of repair enzymes, which must be able to recognize and repair breaks in tightly wrapped and inaccessible DNA. During immunoglobulin gene recombination, DNA is rendered accessible by the process of transcription, which unzips double-stranded DNA as part of the conversion of genetic information into functional proteins.

When DNA is transcribed and damaged DNA is present what happens? Effective repair entails shutting down transcription; specifically interfering with the function of RNA polymerase. Shutting down transcription is accomplished by specified proteins recruited to the site of the DNA damage. Three repair protein factors, ATM, Nbs1 and MDC1, are probably involved in the regulatory shut down function.

The Irreducible Complexity of Photosynthesis

An Uncommon Descent blog entry entitled 'Is Photosynthesis Irreducibly Complex?' references two articles (one from 'Nature' and another from 'Science Daily') and cites information from them. This is from the blog entry (my reactions in blue):

"After decades of research, biochemists now understand that this critical biological process depends on some very elaborate and rapid chemistry involving a series of enormously large and complex molecules a set of complex molecular systems all working together.

“We know that the process evolved in bacteria, probably before 2.5 billion years ago, but the history of photosynthesis’s development is very hard to trace,” said Blankenship."

Very elaborate chemistry indeed. No wonder the history of photosynthesis development is hard to trace. It's difficult to conceptualize, let alone trace, when explained by a paradigm of purposelessness and mindless direction. One reason for this is the interdependency of different cellular functions. For example, ATP is utilized during photosynthesis. So are by-products of metabolic pathways. If one assumes all related processes (including the Calvin Cycle) evolved prior to photosynthesis, chicken-egg dilemnas arise. They also present themselves if the opposite is assumed. The interdependency of basic universal pathways is strong evidence for design. So too are some points raised in the next comment.

This comment also appeared in that thread:

"There is no question about photosynthesis being IC. But it’s worse than that from an evolutionary perspective. There are 17 enzymes alone involved in the synthesis of chlorophyll. Are we to believe that all intermediates had selective value? Not when some of them form triplet states that have the same effect as free radicals like O2. In addition if chlorophyll evolved before antenna proteins, whose function is to bind chlorophyll, then chlorophyll would be toxic to cells. Yet the binding function explains the selective value of antenana proteins. Why would such proteins evolve prior to chlorophyll and if they did not how would cells survive chlorophyll until they did?"

That comment illustrates another problem for mainstream evolutionists. The evolution of parts can be toxic to the whole. Yet, the selective value of complementary systems is linked to the simultaneous existence of separate and distinct parts. The Darwinian answer is a generous dose of imagination consisting of homologous proteins and speculative "pathways." The purposeful arrangement of parts, suggested by the evidence, is philosophically anethema to mainstreamers.

T Cell Maturation

A Physorg article entitled Scientists identify new regulatory mechanism for critical protein signaling domain reveals the potential impact of a small molecule known as IP4 which is involved in the binding of particular proteins to membranes and in the maturation of T cells. From the linked article:

"In findings the authors called "unexpected and striking," the study found that a new regulating messenger IP4, a small soluble molecule, augments the binding of three different PH domain proteins to one of the most commonly recognized membrane lipids, PIP3. The study also showed that inhibiting production of IP4 can result in reduced protein binding to membranes and reduced activation of key signaling molecules in developing T cells, leading to a block of T cell maturation and to severe immunodeficiency in animal models."

Aside from advances in medical treatment that could result from the study, the development of the irreducibly complex signaling pathway connected with T cell maturation is of interest from an ID perspective. The enzyme ItpkB is needed to produce IP4 in mice. The normal development of T cells is disrupted when that enzyme is disabled. T cell development is regulated through signaling. Impaired signaling can lead to the death of T cells. Quoting again from the article:

"Itk is a key activator of another enzyme, PLC g1, in T- cells. PLC g1 is important for signaling in many cells, because it generates the secondary messenger molecules IP3 and DAG (diacylglycerol). We found that ItpkB deficient double positive cells have reduced PLCg1 activity and cannot make normal amounts of DAG. Without the IP4 or DAG messengers, which are essential for positive selection of T cells, these ItpkB-deficient T cells cannot develop into mature, functional cells."

Observe the linkage between biomolecules involved in the T cell maturation function. A study of the origin of pathways to this biochemical complex would be challenging.