Monday, 9 May 2022

(As always the question is) Who will watch the watchers?

The Caesars of 1st century.

1st century ce

Augustus (31 bce–14 ce)
Tiberius (14–37 ce)
Caligula (37–41 ce)
Claudius (41–54 ce)
Nero (54–68 ce)
Galba (68–69 ce)
Otho (January–April 69 ce)
Aulus Vitellius (July–December 69 ce)
Vespasian (69–79 ce)
Titus (79–81 ce)
Domitian (81–96 ce)
Nerva (96–98 ce)

But who will save us from our friends?

Actual design: A science stopper?

Science Stopper? Intelligent Design as a Fruitful Scientific Paradigm

Casey Luskin

Editor’s note: We have been delighted to present a series by geologist Casey Luskin on “The Positive Case for Intelligent Design.” This is the 12^th and final entry in the series, a modified excerpt from the new book The Comprehensive Guide to Science and Faith: Exploring the Ultimate Questions About Life and the Cosmos. Find the full series here.

There’s a final common objection to intelligent design that the positive case for ID, outlined in this series, helps us to answer. In his Kitzmiller v. Dover testimony, biologist Kenneth Miller referred to intelligent design as a “science stopper.”¹ Similarly, in his book Only a Theory, Miller stated, “The hypothesis of design is compatible with any conceivable data, makes no testable predictions, and suggests no new avenues for research. As such, it’s a literal dead end…”²

Yet as we’ve already seen, ID makes a variety of testable and successful predictions. This allows ID to serve as a paradigm guiding scientific research to make new discoveries. The list below shows various fields where ID is helping science to generate knowledge. For each field, multiple ID-friendly scientific publications are cited as examples.

How ID Inspires the Progress of Science

Protein science: ID encourages scientists to do research to test for high levels of complex and specified information in biology in the form of the fine-tuning of protein sequences.³ This has practical implications not just for explaining biological origins, but also for engineering enzymes and anticipating and fighting the future evolution of diseases.
Physics and cosmology: ID has inspired scientists to seek and find instances of fine-tuning of the laws and constants of physics to allow for life, leading to new fine-tuning arguments such as the Galactic Habitable Zone. This has implications for proper cosmological models of the universe, hinting at proper avenues for successful “theories of everything” that must accommodate fine-tuning, and other implications for theoretical physics.⁴
Information theory: ID leads scientists to understand intelligence as a cause of biological complexity, capable of being scientifically studied, and to understand the types of information it generates.⁵
Pharmacology: ID directs both experimental and theoretical research to investigate the limitations of Darwinian evolution to produce traits that require multiple mutations in order to function. This has practical implications for fighting problems like antibiotic resistance or engineering bacteria.⁶
Evolutionary computation: ID produces theoretical research into the information-generative powers of Darwinian searches, leading to the discovery that the search abilities of Darwinian processes are limited, which has practical implications for the viability of using genetic algorithms to solve problems.⁷
Anatomy and physiology: ID predicts function for allegedly “vestigial” organs, structures, or systems whereas evolution has made many faulty predictions of nonfunction.⁸
Bioinformatics: ID has helped scientists develop proper measures of biological information, leading to concepts like complex and specified information or functional sequence complexity. This allows us to better quantify complexity and understand what features are, or are not, within the reach of Darwinian evolution.⁹
Molecular machines: ID encourages scientists to reverse-engineer molecular machines — like the bacterial flagellum — to understand their function like machines, and to understand how the machine-like properties of life allow biological systems to function.¹⁰
Cell biology: ID causes scientists to view cellular components as “designed structures rather than accidental by-products of neo-Darwinian evolution,” allowing scientists to propose testable hypotheses about cellular function and causes of cancer.¹¹
Systematics: ID helps scientists explain the cause of the widespread features of conflicting phylogenetic trees and “convergent evolution” by producing models where parts can be reused in non-treelike patterns.¹² ID has spawned ideas about life being front-loaded with information such that it is designed to evolve, and has led scientists to expect (and now find!) previously unanticipated “out-of-place” genes in various taxa.¹³
Paleontology: ID allows scientists to understand and predict patterns in the fossil record, showing explosions of biodiversity (as well as mass extinction) in the history of life.¹⁴
Genetics: ID has inspired scientists to investigate the computer-like properties of DNA and the genome in the hopes of better understanding genetics and the origin of biological systems.¹⁵ ID has also inspired scientists to seek function for noncoding junk-DNA, allowing us to understand development and cellular biology.¹⁶

Avenues of Discovery

Critics wrongly charge that ID is just a negative argument against evolution, that ID makes no predictions, that it is a “god of the gaps” argument from ignorance, or that appealing to an intelligent cause means “giving up” or “stopping science.” As this series has shown, these charges are misguided.

Ironically, when critics claim that research is not permitted to detect design because that would stop science, it is they who hold science back by preventing scientists from investigating the scientific theory of intelligent design. When researchers are allowed to infer intelligent agency as the best explanation for information-rich structures in nature, this opens up many avenues of discovery that are bearing good fruit in the scientific community.

Notes

Kenneth R. Miller, Kitzmiller v. Dover, Day 2 AM Testimony (September 27, 2005).
Kenneth R. Miller, Only a Theory: Evolution and the Battle for America’s Soul (New York: Viking Penguin, 2008), 87.
Axe, “Extreme Functional Sensitivity to Conservative Amino Acid Changes on Enzyme Exteriors”; Axe, “Estimating the Prevalence of Protein Sequences Adopting Functional Enzyme Folds”; Behe and Snoke, “Simulating Evolution by Gene Duplication of Protein Features That Require Multiple Amino Acid Residues”; Axe, “The Case Against a Darwinian Origin of Protein Folds”; Gauger and Axe, “The Evolutionary Accessibility of New Enzyme Functions: A Case Study from the Biotin Pathway”; Reeves et al., “Enzyme Families-Shared Evolutionary History or Shared Design? A Study of the GABA-Aminotransferase Family”; Thorvaldsen and Hössjer, “Using statistical methods to model the fine-tuning of molecular machines and systems.”
Guillermo Gonzalez and Donald Brownlee, “The Galactic Habitable Zone: Galactic Chemical Evolution,” Icarus 152 (2001), 185-200; Guillermo Gonzalez, Donald Brownlee, and Peter D. Ward, “Refuges for Life in a Hostile Universe,” Scientific American (2001), 62-67; Guillermo Gonzalez and Jay Wesley Richards, The Privileged Planet: How Our Place in the Cosmos Is Designed for Discovery (Washington, DC, Regnery, 2004); Guillermo Gonzalez, “Setting the Stage for Habitable Planets,” Life 4 (2014), 34-65; D. Halsmer, J. Asper, N. Roman, and T. Todd, “The Coherence of an Engineered World,” International Journal of Design & Nature and Ecodynamics 4 (2009), 47-65.
William A. Dembski, The Design Inference; William A. Dembski and Robert J. Marks II, “Bernoulli’s Principle of Insufficient Reason and Conservation of Information in Computer Search,” Proceedings of the 2009 IEEE International Conference on Systems, Man, and Cybernetics(October 2009), 2647-2652; William A. Dembski and Robert J. Marks II, “The Search for a Search: Measuring the Information Cost of Higher Level Search,” Journal of Advanced Computational Intelligence and Intelligent Informatics 14 (2010), 475-486; Øyvind Albert Voie, “Biological function and the genetic code are interdependent,” Chaos, Solitons and Fractals 28 (2006), 1000-1004; McIntosh, “Information and Entropy —Top-Down or Bottom-Up Development in Living Systems?”
Behe and Snoke, “Simulating evolution by gene duplication of protein features that require multiple amino acid residues”; Ann K. Gauger, Stephanie Ebnet, Pamela F. Fahey, and Ralph Seelke, “Reductive Evolution Can Prevent Populations from Taking Simple Adaptive Paths to High Fitness,” BIO-Complexity 2010 (2).
William A. Dembski and Robert J. Marks II, “Conservation of Information in Search: Measuring the Cost of Success,” IEEE Transactions on Systems, Man, and Cybernetics-Part A: Systems and Humans 39 (September 2009), 1051-1061; Winston Ewert, William A. Dembski, and Robert J. Marks II, “Evolutionary Synthesis of Nand Logic: Dissecting a Digital Organism,” Proceedings of the 2009 IEEE International Conference on Systems, Man, and Cybernetics (October 2009); Dembski and Marks, “Bernoulli’s Principle of Insufficient Reason and Conservation of Information in Computer Search”; Winston Ewert, George Montanez, William Dembski and Robert J. Marks II, “Efficient Per Query Information Extraction from a Hamming Oracle,” 42nd South Eastern Symposium on System Theory (March 2010), 290-297; Douglas D. Axe, Brendan W. Dixon, and Philip Lu, “Stylus: A System for Evolutionary Experimentation Based on a Protein/Proteome Model with Non-Arbitrary Functional Constraints,” Plos One 3 (June 2008), e2246.
Jonathan Wells, “Using Intelligent Design Theory to Guide Scientific Research”; William Dembski and Jonathan Wells, The Design of Life: Discovering Signs of Intelligence in Living Systems (Dallas, TX: Foundation for Thought and Ethics, 2008).
Meyer, “The origin of biological information and the higher taxonomic categories”; Kirk K. Durston, David K.Y. Chiu, David L. Abel, Jack T. Trevors, “Measuring the functional sequence complexity of proteins,” Theoretical Biology and Medical Modelling 4 (2007), 47; David K.Y. Chiu and Thomas W.H. Lui, “Integrated Use of Multiple Interdependent Patterns for Biomolecular Sequence Analysis,” International Journal of Fuzzy Systems4 (September 2002), 766-775.
Minnich and Meyer. “Genetic Analysis of Coordinate Flagellar and Type III Regulatory Circuits in Pathogenic Bacteria”; McIntosh, “Information and Entropy—Top-Down or Bottom-Up Development in Living Systems?”
Jonathan Wells, “Do Centrioles Generate a Polar Ejection Force?,” Rivista di Biologia / Biology Forum, 98 (2005), 71-96; Scott A. Minnich and Stephen C. Meyer, “Genetic analysis of coordinate flagellar and type III regulatory circuits in pathogenic bacteria,” Proceedings of the Second International Conference on Design & Nature Rhodes Greece (2004); Behe, Darwin’s Black Box; Lönnig, “Dynamic genomes, morphological stasis, and the origin of irreducible complexity.”
Lönnig, “Dynamic genomes, morphological stasis, and the origin of irreducible complexity”; Nelson and Jonathan Wells, “Homology in Biology”; Ewert, “The Dependency Graph of Life”; John A. Davison, “A Prescribed Evolutionary Hypothesis,” Rivista di Biologia/Biology Forum 98 (2005), 155-166; Ewert, “The Dependency Graph of Life.”
Sherman, “Universal Genome in the Origin of Metazoa: Thoughts About Evolution”; Albert D.G. de Roos, “Origins of introns based on the definition of exon modules and their conserved interfaces,” Bioinformatics 21 (2005), 2-9; Albert D.G. de Roos, “Conserved intron positions in ancient protein modules,” Biology Direct 2 (2007), 7; Albert D.G. de Roos, “The Origin of the Eukaryotic Cell Based on Conservation of Existing Interfaces,” Artificial Life 12 (2006), 513-523.
Meyer et al., “The Cambrian Explosion: Biology’s Big Bang”; Meyer, “The Cambrian Information Explosion”; Meyer, “The origin of biological information and the higher taxonomic categories”; Lönnig, “Dynamic genomes, morphological stasis, and the origin of irreducible complexity.”
Richard v. Sternberg, “DNA Codes and Information: Formal Structures and Relational Causes,” Acta Biotheoretica 56 (September 2008), 205-232; Voie, “Biological function and the genetic code are interdependent”; David L. Abel and Jack T. Trevors, “Self-organization vs. self-ordering events in life-origin models,” Physics of Life Reviews 3 (2006), 211-228.
Richard v. Sternberg, “On the Roles of Repetitive DNA Elements in the Context of a Unified Genomic– Epigenetic System”; Jonathan Wells, “Using Intelligent Design Theory to Guide Scientific Research”; Josiah D. Seaman and John C. Sanford, “Skittle: A 2-Dimensional Genome Visualization Tool,” BMC Informatics 10 (2009), 451.

Our home world: The best seat in the house?

Guillermo Gonzalez on What’s Changed Since The Privileged Planet

Evolution News @DiscoveryCSC

On a classic episode of ID the Future, host Jay Richards and astronomer Guillermo Gonzalez, authors of The Privileged Planet: How Our Place in the Cosmos Is Designed for Discovery, discuss what’s changed in the years since the book first appeared. Download the podcast or listen to it here.

One big change they note: the number of exo-planets discovered has exploded, from 200 or so to several thousand. Gonzalez walks through this and other exciting recent advances in astronomy, and the two reflect on how these new discoveries bear upon the predictions and arguments they advanced in their book. Also in the conversation, Gonzalez speculates about what the James Webb Space Telescope may uncover after it comes online.

Primeval tech v. Darwinism:The big picture.

Devo vs. evo?

Cell Fate: Another Hurdle for Evolution

David Coppedge

When a stem cell divides, one daughter cell must maintain its stemness (i.e., ability to differentiate into any cell type) while the other specializes. Therein lies another truckload of requirements for coordinated action that, if it goes awry, can spell disaster for an animal or human. Watch this subject grow into a huge problem for evolutionary theory.

Researchers at University of California at Riverside investigated what happens when stem cells divide and specialize. UCR’s reporter Iqbal Pittawala describes how “genome organization influences cell fate.”

Understanding the molecular mechanisms that specify and maintain the identities of more than 200 cell types of the human body is arguably one of the most fundamental problems in molecular and cellular biology, with critical implications for the treatment of human diseases. Central to the cell fate decision process are stem cells residing within each tissue of the body. [Emphasis added.]

The two daughter cells face a massive organization problem. Even though they contain the same DNA code, they will take on separate roles in the cell. This means that the accessibility of genes between the two cells must radically differ.

Chromatin — a package of DNA wrapped around histone proteins — makes some genes accessible for transcription but hides others from the transcription factors (additional proteins) that switch on transcription. Begin to get a sense of how difficult this will be. There are tens of thousands of genes, and 200 cell types that utilize specific genes but not others. What process determines how chromatin will package the specialist daughter cell to make genes available if it will be a nerve cell as opposed to a muscle cell or heart cell? And how does the system keep the other daughter cell unaltered from the original stem cell?

A Challenge for a Librarian

Biochemist Sihem Cheloufi at UCR, together with colleague Jernej Murn, researched a protein complex involved in the process named “chromatin assembly factor 1” or CAF-1. As you read their description, think of the challenge a librarian faces with the card catalog for a large library.

“To help CAF-1 secure correct chromatin organization during cell division, a host of transcription factors are attracted to open regions in a DNA sequence-specific manner to serve as bookmarks and recruit transcription machinery to correct lineage-specific genes, ensuring their expression,” she said. “We wondered about the extent to which CAF-1 is required to maintain cell-specific chromatin organization during cell division.”

CAF-1 normally keeps genes tightly bound in chromatin so that they are inaccessible to transcription factors.

For a specific case, the biochemists looked at how blood stem cells divide and specialize into neutrophils — a type of white blood cell that acts as a first responder against an invasion by pathogens. They noticed that the levels of CAF-1 are finely balanced to prevent access by a particular transcription factor for that lineage named ELF1. (Note in passing that each cell type has its own suite of lineage-specific transcription factors.) Neutrophils artificially deprived of CAF-1 went awry and forgot their identity.

“By looking at chromatin organization, we found a whole slew of genomic sites that are aberrantly open and attract ELF1 as a result of CAF-1 loss,” Murn said. “Our study further points to a key role of ELF1 in defining the fate of several blood cell lineages.”

Peeking into a Keyhole

Recalling the 200 cell types in the human body, how does CAF-1 organize chromatin for each type? How does it know what genes to make accessible for a kidney cell, an astrocyte in the brain, or a liver cell? The UCR work is peeking into a keyhole of a library with a big operation inside. They don’t yet know how CAF-1 “preserves the chromatin state at specific sites and whether this process works differently across different cell types.” Think of our librarian just starting to get a handle on the job of arranging books in one wing and then finding 200 more wings to manage. Maybe a different analogy will expose the magnitude of this challenge.

“Like a city, the genome has its landscape with specific landmarks,” Cheloufi said. “It would be interesting to know how precisely CAF-1 and other molecules sustain the genome’s ‘skyline.’ Solving this problem could also help us understand how the fate of cells could be manipulated in a predictive manner. Given the fundamental role of CAF-1 in packaging the genome during DNA replication, we expect it to act as a general gatekeeper of cellular identity. This would in principle apply to all dividing cells across numerous tissues, such as cells of the intestine, skin, bone marrow, and even the brain.”

Surely there is much, much more involved than one protein complex named CAF-1. Something needs to “know” how to keep one daughter cell’s chromatin unchanged to maintain the stem cell pool, while reorganizing the chromatin for the differentiating cell — assuming the system also “knows” what cell type that daughter cell must become out of 200 possibilities. This implies a complex signaling system for triggering the production of specific cell types, which must trigger the appropriate suite of protein complexes to package the chromatin for access by that cell type’s lineage-specific transcription factors. Differentiation proceeds down a stepwise transition through progenitor cell states until the specialized cell, such as a neutrophil, results. How many evolutionists have thought about this challenge?

Quality-Control Terms from Engineering

The research paper is published open access. It is Franklin et al., “Regulation of chromatin accessibility by the histone chaperone CAF-1 sustains lineage fidelity,” in Nature Communications. Perhaps the magnitude of the challenge caused the 21 authors to shy away from referring to evolution in the paper. Instead, they refer to “lineage integrity” or “lineage fidelity” a dozen times. Those are quality-control terms from engineering and systems design.

Cell fate commitment is driven by dynamic changes in chromatin architecture and activity of lineage-specific transcription factors (TFs). The chromatin assembly factor-1 (CAF-1) is a histone chaperone that regulates chromatin architecture by facilitating nucleosome assembly during DNA replication. Accumulating evidence supports a substantial role of CAF-1 in cell fate maintenance, but the mechanisms by which CAF-1 restricts lineage choice remain poorly understood. Here, we investigate how CAF-1 influences chromatin dynamics and TF activity during lineage differentiation. We show that CAF-1 suppression triggers rapid differentiation of myeloid stem and progenitor cells into a mixed lineage state. We find that CAF-1 sustains lineage fidelity by controlling chromatin accessibility at specific loci, and limiting the binding of ELF1 TF at newly-accessible diverging regulatory elements. Together, our findings decipher key traits of chromatin accessibility that sustain lineage integrity and point to a powerful strategy for dissecting transcriptional circuits central to cell fate commitment.

Expecting random mutations to somehow emerge then be “selected” by some blind, aimless, uncaring “agentless act” (as Neil Thomas has put it) to construct this complex system seems beyond rational consideration. Intelligent design scientists, though, could make testable predictions to guide further research. Knowing how comparable systems are made by intelligent engineers — that is, systems involving coordinated reorganization of information for multiple applications — they could expect to find new types of sensors, feedback circuits, quality-control checkpoints, or other functional modules at work. These might consist of proteins, protein complexes, small RNAs, sugars, ions, or combinations of them capable of storing or conveying information. (Note: even if automated, these are not “agentless acts.” The agency is one step removed from mind to program, but a mind with foresight was necessary for its origin.)

For example, an ID research team might look for a comparable system in industry that faces the same kind of challenge. They could identify the minimum number of job descriptions required to make the system work, then look for molecules performing those roles in the cellular analogue. Even if the match is imperfect, the ID approach can advance science, because what the researchers learn can feed back into biomimetic design, leading to improved applications in industry.

Poor Darwin. With his crude awareness of cells dividing that looked like bubbles separating, he had no idea what he would be in for in the 21st century.

meditations of aservantofJEHOVAH

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