Design as heuristic?

 Emily Reeves: How to Study Biology with Systems Engineering Principles

Andrew McDiarmid

Traditional methods in biology have proven insufficient for understanding and accurately predicting complex biological systems. Why? The great majority of biologists are trained to study life from the bottom up, as the result of unguided evolutionary processes. It turns out there are better ways to observe, question, hypothesize, experiment, and analyze a complex system. On a new episode of ID the Future, I welcome biochemist and metabolic nutritionist Dr. Emily Reeves to the podcast to discuss her co-authored paper on how biologists can apply principles from systems engineering to biology to better approach the study of complex living systems. 

As Dr. Reeves explains, the need for a new methodology in biology is motivated by two key observations. First, biological systems appear to be designed. Zoom into any complex system in biology, such as the bacterial flagellar motor, the light harvesting complex of Photosystem I, or ATP synthase, and you’ll find exquisite nanotechnology that is better engineered than its human-engineered counterpart. Second, biological systems have already been demonstrated to have much in common with human engineered systems. Biological systems are hierarchical, integrated, modular, optimized, and robust. These are all characteristics of top-down designed systems. “Therefore,” explains Dr. Reeves, “the tools that engineers use to makes these systems can be adapted to better understand biology.”

In addition to explaining how the new methodology operates, Dr. Reeves shows how it can be applied to various systems and phenomena to produce fruitful scientific research. As a case study, she describes how to use the methodology to better understand the commonly studied process of glycolysis. She also highlights the implications of this approach for understanding phenomena such as the Warburg effect, a proposal that seeks to explain the metabolic requirements of cell proliferation in many types of cancer. Dr. Reeves notes that a systems engineering approach to the Warburg effect suggests a different reason, one that has not yet been widely studied or reported in the scientific literature. Download the podcast or listen to it here.

More primeval engineering vs. Darwin

 Missiles and Jackhammers: How Plants Spread Themselves Far and Wide

Andrew McDiarmid

On a new episode of ID the Future, I welcome science reporter David Coppedge to explore some fascinating examples of intelligent design in the plant world. Plants look so helpless tied to the soil, but they and fungi alike have perfected technologies for spreading themselves far and wide. Coppedge describes how various mechanisms, including cavitation and turgor pressure, enable these organisms to launch their spores effectively, turning them into short-range, medium-range, and even long-range missiles that travel great distances relative to their size in order to further life. The conversation also touches on the engineering principles behind plant root systems, and how studying these natural designs can inspire advancements in human technology through biomimetics.

You’ll learn about the fungi Deightoniella, for example, and how they use explosive bubble formation in their stalks to launch spores like tiny rockets as far as 15 times their own length. That might only be a few millimeters, but it’s enough to escape the boundary layer of still air on the leaf surface where they grow. Then there are ferns, which also use cavitation to create a miniature slingshot to shoot spores out at some of the fastest speeds in biology. And let’s not forget the mighty little fungus known as Pilobolus (pictured above), which uses turgor pressure like a mini squirt gun to shoot spores as far as six feet away!

Coppedge also discusses plant root systems, likening root tips to jackhammers and root hairs to stabilizers that allow plants to push through formidable barriers in search of nutrients and water. Coppedge explains how these plant systems exhibit irreducible complexity in their design and function. He also points out that by studying nature’s solutions to engineering problems, we can improve human engineering, an example of intelligent design in action. Download the podcast or listen to it here

Darwinism designs Darwinism?

 The Convoluted Concept of Evolving Evolvability

David Coppedge

Try to wrap your mind around the concept that evolvability evolves by natural selection. On second thought, don’t. It’s not conducive to mental health.

Valuing charity, I try to approach new evolutionary papers with dispassionate tolerance, seeking understanding before forming an opinion about them one way or another. This one was a particular challenge. It’s like trying to imagine a Mobius strip wrapping a Klein bottle in hyperspace. What on earth is meant by natural selection favoring the evolution of evolvability? Is this even a potentially useful notion for understanding how the world works?

Mentions of “evolvability” here at Evolution News can be found scattered through articles by several contributing authors, but none I searched for have treated it in detail. Now that two papers on evolvability have appeared in separate journals in February 2025, it’s a good time to examine the concept. 

The first paper, in PNAS, led by Luis Zaman from the University of Michigan, will not require much analysis, for two reasons: (1) The authors are consumed with Darwinism to the point of absurdity, and (2) Their justification is entirely built on a computer model running Avida. Even the title of the press release mentions evolution five times! “Evolution, evolution, evolution: How evolution got so good at evolving.” 

Now, a University of Michigan study shows that perhaps why evolution is so effective is that evolution is itself something that can evolve. The research is published in the Proceedings of the National Academy of Sciences.

“Life is really, really good at solving problems. If you look around, there’s so much diversity in life, and that all these things come from a common ancestor seems really surprising to me,” said Luis Zaman, an evolutionary biologist at U-M and lead author of the study. “Why is evolution so seemingly creative? It seems like maybe that ability is something that evolved itself.” 

Forms of the word “evolution” appear 38 times in this short press release, and 214 times in the paper. Such overuse of a word appears pathological, like an addiction. Worse, it contains no biological field work at all. Its conclusions are rationalized entirely by a computer model with imaginary organisms in silico that were designed to evolve or fail by natural selection. Live Science liked the paper, but because the Avida platform that supported this computer game has been debunked extensively by others at Evolution News (here, here, and here), it deserves no further serious consideration other than for the possible entertainment value, like watching clowns in a curved maze looking for a penny in the nonexistent corner.

Much Empiricism About Nothing

The second paper, published in Science, gets more into the weeds. Barnett, Meister, and Rainey titled their work “Experimental evolution of evolvability.” For a synopsis of the paper, see the Perspective by Edo Kussell (“Enabling evolvability to evolve”) in the same issue of Science, or see the press release from the Max Planck Institute for Evolutionary Biology featuring two of the authors, Michael Barnett and Paul Rainey.

A new study by researchers at the Max Planck Institute for Evolutionary Biology (MPI-EB) sheds fresh light on one of the most debated concepts in biology: evolvability. The work provides the first experimental evidence showing how natural selection can shape genetic systems to enhance future capacity for evolution, challenging traditional perspectives on evolutionary processes.

Right at the outset, we see them “challenging traditional perspectives on evolutionary processes,” leading one to proceed with caution as if handed a bottle of New Coke. Arguing that mutation and selection interact, they propose a concept called “lineage-level selection.” Here we go; just what the world needs now: not love, sweet love, but another type of natural selection. 

A caption to the opening diagram explains:

Central to this is lineage-level selection: bacterial lineages (connected nodes) were required to repeatedly evolve between two phenotypic states. Mutational transitions were initially unreliable, leading to lineage deathand replacement by more successful competitors. Final surviving lineages evolved mutation-prone sequencesin a key gene underpinning the phenotypes, enabling rapid transitions between states.

According to their concept, “natural selection optimises genetic systems for future adaptations.” Lineage selection locates the target of selection in the lineage rather than in the individual or population. In this view, your genealogy determines how natural selection will let you evolve.

Imaginary Foresight by Natural Selection

Dr. Marcos Eberlin wrote about Foresight as a sign of intelligence. In the theory of Barnett et al., however, foresight evolves (believe it or not). It’s not real foresight. It’s just imaginary foresight. They call it “evolutionary foresight.” Selection looks down through the halls of time and muses, “Which of my future lineages might win the competition for fitness?” It decides that the winner will be the most evolvable one. This is where the authors start playing mind games with your sanity. “This is not the selection you are looking for,” they say with a hypnotic gesture of the hands.

Evolution by natural selection is a blind process, but living systems can appear to possess evolutionary foresight. Mechanistically, this is conceivable. Certain configurations of gene regulatory networks, developmental systems, chromosomal architectures, and mutational processes have apparent adaptive utility in future environments. Taking advantage of such future adaptive potential requires not only memory of evolutionary history but often an ability to regenerate previously achieved phenotypic states. In this work, we show how selection on lineages can incorporate prior evolutionary history into the genetic architecture of a single cell, such that mutation appears to anticipate future environmental change.

They lost me on the assertion that “evolutionary foresight” is mechanistically conceivable. That is certainly not your grandpa’s Darwinism. At that point, I looked into their Materials and Methods to see what scientific experiments they did to support this notion. Sure enough, they ran actual lab experiments for three years on real organisms, not just computer models. 

Madness in the Methodology

They carefully studied populations of the bacterium Pseudomonas fluorescens (pictured at the top) kept in “glass microcosms” (presumably flasks or test tubes) each with billions of cells. Some of the populations were able to manufacture cellulose (CEL+) and some were not (CEL–). When starved for oxygen, bacteria with the genes to make cellulose created cellulose mats on which individuals could get close to the air/liquid interface for access to oxygen. The presence of cellulose made by CEL+members, therefore, provided a fitness advantage (meaning, the ability to avoid dying). 

The team identified “hypermutable” loci with 10,000 times the mutation rate that they describe as similar to “contingency loci” in pathogenic bacteria. Having a contingency plan sounds like design, but they believe the ability for rapid mutation gives the bacterium “foresight” in the form of “evolutionary potential.” The press release explains,

“Our findings show that selection at the level of lineages can drive the evolution of traits that enhance evolutionary potential, offering a fascinating glimpse into how evolution can gain what appears to be ‘foresight’.” Michael Barnett, the study’s first author, added: “By demonstrating the evolution of a hyper-mutable locus, we show that adaptation is not just about surviving in the present but also about refining the ability to adapt in the future.”

The results challenge the long-held view that evolution operates without foresight. Instead, they reveal how natural selection can embed evolutionary history into genetic architecture, enabling organisms to “anticipate” environmental changes and accelerate their adaptation.

Several design words can be seen there: architecture, anticipation, embedding. Are these things that blind selectors do? In a response to the paper, David G. King, emeritus professor from Southern Illinois University, saw something different going on: neither random mutation nor directed mutagenesis:

For example, the insertions and deletions that characterize short tandem repeats (and also enable phenotypic switching in bacterial contingency genes) confer “tuning knob” or “rheostat” functionality on many, perhaps most eukaryotic genes. Without being biased in the direction of adaptation, repeat number mutability helps assure a relatively advantageous distribution [of] mutation effects.

If so, this would indicate a function for such hypermutable loci. They act like “mutational sponges” that diffuse the harmful effects of random mutations. King explains,

This is the domain of “mutation protocols” whereby an abundant supply of unbiased mutations entails a minimal probability of harm. Put simply, mutations produced “according to protocol” are constrained to avoid vast domains of DNA sequence space where deleterious results would be practically guaranteed.

Design is evident in concepts like a “tuning knob” or “rheostat” functionality. Another idea not discussed in the paper is the possibility that the populations of bacteria form “quasispecies” in which members of a population retain functional loci that can be shared by horizontal gene transfer. In both cases, genetic changes would not be random.

Conceptual Flaws

But since the authors wish to argue that natural selection (NS), which they admit is “a blind process,” somehow had foresight to “enhance evolutionary potential” (i.e., evolvability), their convoluted concept is subject to the critical scrutiny of NS by illustrious writers including John West (“a corrosive impact on society”), Neil Thomas (“a conceptually incoherent term”), Jonathan Wells (“cannot explain the arrival of the fittest”), and others. Have Barnett et al. twisted NS into a creative force beyond its means by its very nature as an unguided process? Here are a few considerations to keep in mind:

No origin of species: They started with one species and ended with the same species. 

Artificial selection: They acted like breeders, which is intelligent design, the opposite of NS.

Investigator interference: They forced the organisms to “evolve or perish” according to criteria they had set up in advance.

Unnatural assistance: When a population went “extinct” they transferred cells from a living population to keep it going (see the diagram in Kussell’s Perspective article).

Limited options: They forced the organisms to exhibit only one of two phenotypic states.

Personification: They applied terms like foresight, anticipation, and future adaptive potential to blind, mindless processes.

Magical thinking: Only in Darwin’s Fantasyland can NS be deemed capable of “refining the ability to adapt in the future.”

Obfuscation: Inventing concepts like “the evolution of evolvability” is no more conducive to understanding than speaking of “the phlogistification of phlogiston"

Conclusion: Keep Your Investment on Design

Try as they might to resurrect NS from the dead, Barnett et al. and Zaman et al. are stuck with blind, unguided processes with no foresight or desire to adapt. Scientists in Darwin’s day saw through his flawed attempt to present natural selection as analogous to artificial selection, as Robert Shedinger has exposed in Darwin’s Bluff.

Design scientists, by contrast, have the tools in their toolkit to explain adaptation. It takes foresight (real foresight by a designing intelligence, not imaginary “evolutionary” foresight) to engineer a machine for robustness against potential risks. More and more, scientists are finding that life comes equipped with built-in capabilities for adapting to environmental changes. This has been the focus of lively conferences on biological engineering over the past few years. The next Conference on Engineering in Living Systems (CELS), sponsored by Discovery Institute, is coming this summer in Seattle and promises to be a fertile occasion for enlightening discussions in Adventureland and Tomorrowland instead of Fantasyland.

It is irreducible complexity all the way down?

 Irreducible Complexity Nested Within Irreducible Complexity: The Case of Chromosome Condensation

Jonathan McLatchie

In previous articles, I have described the molecular marvel that is mitotic cell division, with a view towards imparting to readers a sense of the engineering prowess and, indeed, genius behind this phenomenal process. Here, I will zoom in on the process of chromosome condensation, which occurs during prophase. The compaction of chromatin to form the recognizable mitotic chromosome structures would serve little value until the evolution of the machinery for facilitating mitotic segregation. And yet, it is essential for mitotic division to proceed — that is, the process of chromosome condensation resides within an irreducibly complex system. As we shall see, however, the process of chromosome condensation itself exhibits irreducible complexity. Thus, this represents an example of irreducible complexity that is nested within a larger irreducibly complex apparatus. It is, therefore, difficult to envision such a process coming together through a blind process, without foresight of the target. This aspect of cell division is best explained by teleology – i.e., conscious design.

What Happens During Prophase? The Big Picture

During prophase, the replicated chromosomes (each consisting of two sister chromatids) condense and are recognizable under the microscope. This process of condensation reduces the length of a typical interphase chromosome by approximately ten-fold and gene expression shuts down. The two sister chromatids of each mitotic chromosome have been disentangled from one another and are joined at the centromere. This facilitates the later separation of the sister chromatids as they are segregated between the two daughter cells. The compaction also protects the fragile DNA molecules during this process. Each pair of sister chromatids are genetically identical to one another. Outside of the cell nucleus, the mitotic spindle (which is made up of microtubules) begins to form between the two centrosomes, which have already duplicated during S and G2 phases of the cell cycle. The mitotic spindle will be responsible later (during anaphase) for facilitating the separation of the two sister chromatids.

Phosphorylation of Histone H3

Phosphorylation of histone H3, by Aurora B kinase, has been shown to play an important role in the condensation of mitotic chromosomes — in particular, at residues Ser10 and Ser28 (for short, H3S10 and H3S28).1,2 This disrupts electrostatic interactions between the DNA and histones, loosening chromatin structure and making it more accessible for the condensin complexes to bind. Phosphorylation of H3S10 and H3S28 also promotes the binding of topoisomerase IIα and the chromosomal passenger complex (CPC). These phosphorylations of Histone 3 are essential for chromosome condensation and segregation. Without them, the result would be defective chromosome condensation and, consequently, impaired segregation of the genetic material. In fact, deregulation of these epigenetic histone markings has been linked to cancer.3Moreover, when Aurora B kinase is depleted using RNA interference, the localization of the CPC to centromeres is impaired, disrupting mitotic progression.4

Chromatin Condensation

Electron micrograph images reveal that each chromatid is arranged into loops of chromatin, which emanate from a central scaffolding. Condensins work to coil the two DNA molecules, using the energy from ATP hydrolysis.5 The result is the two sister chromatids associated with the mitotic chromosome.

Condensin proteins are made up of five constituent parts.6 Among those are the SMC (Structural Maintenance of Chromosomes) proteins, SMC2 and SMC4 (which have ATPase activity). The SMC proteins have coiled-coil domains (i.e., long, flexible arms that fold back on themselves-creating a V-shaped structure), a hinge domain (facilitating the dimerization of the two SMC proteins), and head domains (possessing ATP-binding and ATPase sites, which energizes condensing activity). There are also three non-SMC subunits, which associate with specific regions of DNA and assist in regulating the activity of the condensins.

Condensin complexes load onto the chromatin in a stepwise manner, directed by the non-SMC subunits, which create loops in the DNA (energized by their ATPase activity). These loops are subsequently condensed into mitotic chromosomes. The condensin proteins are critical for cell division to occur. In their absence, the consequence would be chromosomal disorganization, as well as great difficulty in achieving proper segregation during mitosis. This is borne out by condensin knockout studies. For example, one paper reported that “CAP-D3 (condensin II) knockout results in masses of chromatin-containing anaphase bridges. CAP-H (condensin I)-knockout anaphases have a more subtle defect, with chromatids showing fine chromatin fibres that are associated with failure of cytokinesis and cell death.”7 The authors conclude that “condensin II alone can support mitotic chromosome rigidity, whereas condensin I is clearly not able to do so.” Though having both condensin I and II is apparently unnecessary, it is surely the case that having at least condensin II is essential for successful condensation to achieve the mitotic chromosome.

The Chromosome Passenger Complex

The Chromosome Passenger Complex (CPC) is a complex involving four proteins, which are essential to ensuring proper chromosome condensation, alignment, and segregation. The four main components are Aurora B kinase, Survivin, Borealin, and INCENP.8,9

As mentioned previously, Aurora B kinase plays a crucial role in phosphorylating histone H3.10 Aurora B kinase also phosphorylates Heterochromatin Protein 1 (HP1), a protein that normally maintains chromatin in its relaxed interphase state. Inhibitory phosphorylation of this protein promotes chromosome condensation.11Aurora B kinase is also responsible for phosphorylating and activating subunits of condensin.12 When Aurora B is depleted, condensin activity is significantly impaired — for example, in Xenopus (clawed frogs, pictured at the top) egg extracts, removal of Aurora B has been shown to result in a 50 percent decrease in condensin I association with chromosomes.13

Survivin is responsible for targeting the CPC to chromatin by associating with histone modifications, and thereby assisting with the positioning of Aurora B kinase.14,15,16 Depletion of survivin has been shown to result in “significant reduction of endogenous phosphorylated histone H3 and mislocalization of Aurora-B.”17

The CPC is itself stabilized at chromosomes by Borealin, ensuring the continued activity of Aurora B kinase and the efficient recruitment of condensins.18 When Borealin is knocked-out by RNA interference, mitotic progression is delayed and the consequence is “kinetochore-spindle misattachments and an increase in bipolar spindles associated with ectopic asters.”19

The Inner Centromere Protein (INCENP) serves a scaffolding role, and activates Aurora B kinase so that it can phosphorylate substrates (in particular, histones, condensins, and Topoisomerase IIα).20

Topoisomerase IIα

Topoisomerase IIα is crucial for successful mitotic division. In its absence, the typical result is chromosomal mis-segregation, aneuploidy, and cell death. In particular, Topoisomerase IIα is essential for resolving chromosomal catenations. Catenation refers to the physical intertwining of the sister chromatids following DNA replication (resulting from the DNA becoming topologically linked during copying). Failure to disentangle the sister chromatids can result in their improper separation during anaphase, the consequence of which is mis-segregation and aneuploidy. Catenation can also result in the chromatids being subject to tensile stress during the process of mitosis — this can result in chromosomal breakage. When Topoisomerase IIα has been experimentally deleted prior to mitosis, the effect is a failure of chromatin condensation, and exit of the cell from mitosis without chromosome segregation having occurred.21 In addition, it was found that “removal of TOP2A from cells arrested in prometaphase or metaphase cause dramatic loss of compacted mitotic chromosome structure,” indicating that Topoisomerase IIα is “crucial for maintenance of mitotic chromosomes.”22

How does Topoisomerase IIα resolve catenation to allow mitosis to proceed successfully?23,24,25 First, it recognizes and binds to catenated regions where the sister chromatids are entangled. Two DNA-binding domains recognize two DNA segments — i.e., the G and T segments (Gate and Transport Segments respectively). The G-segment is on the DNA duplex that will be cleaved, while the T-segment is on the duplex that will be passed through the break. Using the energy from ATP hydrolysis, Topoisomerase IIα induces a conformational change that places the G-segment within its active site. Both strands of the G-segment are then cleaved, and the T-segment is passed through the break. The result of this process is the untangling of the interlinked chromatids. Topoisomerase IIα then relegates the broken G-segment, and the enzyme is released from DNA (energized by another round of ATP hydrolysis), and the enzyme is reset.

The function of Topoisomerase enzymes is, of course, not limited to resolving catenation in preparation for mitosis — they are also important for alleviating supercoils during DNA replication. However, following genome duplication, some catenation remains, especially in centromeric and heterochromatic regions — this must be fully resolved in advance of mitosis (otherwise, it will hinder proper chromosome segregation). To ensure that this happens, Topoisomerase IIα is phosphorylated by Cyclin-dependent kinase (Cdk) 1 and Aurora B kinase, enhancing its activity in late G2/M phase for the task of catenation-resolution that is needed for chromosome condensation.26,27

There is even a checkpoint in late G2 that determines that catenation has been completely resolved.28 If topological stress is detected, Ataxia Telangiectasia and Rad3-Related kinase (ATR) are recruited to chromatin. This phosphorylates Checkpoint kinase 1 (Chk1), which in turn phosphorylates Cdc25C, a phosphatase that activates Cdk1. This results in the inhibition of Cdc25C, preventing activation of Cdk1, thereby delaying entry of the cell into mitosis. In fact, experimental knockout of ATR in mice has been shown to result in early embryonic lethality due to massive apoptosis and mitotic defects, demonstrating the essential role of ATR in mitotic fidelity.29,30 A similar study also revealed that Chk1 deletion in mice results in embryonic lethality.31

Intelligent Design

The process of chromosomal condensation is absolutely essential to successful mitotic cell division — that is to say, it is a part of a larger irreducibly complex system. Moreover, the highly condensed mitotic chromosome structures (with sister chromatids joined at the centromere) do not serve a purpose apart from in the context of mitosis. And yet, as we have seen, various components are themselves indispensable for effective chromosome condensation. Thus, we have an example of an irreducibly complex apparatus that is nested within a larger irreducibly complex system. It is highly implausible that such a wonder of engineering arose by means of an unguided evolutionary process. It is, in my judgment, far better explained on the hypo

Notes

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Wilkins BJ, Rall NA, Ostwal Y, Kruitwagen T, Hiragami-Hamada K, Winkler M, Barral Y, Fischle W, Neumann H. A cascade of histone modifications induces chromatin condensation in mitosis. Science. 2014 Jan 3;343(6166):77-80. doi: 10.1126/science.1244508. PMID: 24385627.

Komar D, Juszczynski P. Rebelled epigenome: histone H3S10 phosphorylation and H3S10 kinases in cancer biology and therapy. Clin Epigenetics. 2020 Oct 14;12(1):147. doi: 10.1186/s13148-020-00941-2. PMID: 33054831; PMCID: PMC7556946.

Honda R, Körner R, Nigg EA. Exploring the functional interactions between Aurora B, INCENP, and survivin in mitosis. Mol Biol Cell. 2003 Aug;14(8):3325-41. doi: 10.1091/mbc.e02-11-0769. Epub 2003 May 29. PMID: 12925766; PMCID: PMC181570.

Paul MR, Hochwagen A, Ercan S. Condensin action and compaction. Curr Genet. 2019 Apr;65(2):407-415. doi: 10.1007/s00294-018-0899-4. Epub 2018 Oct 25. PMID: 30361853; PMCID: PMC6421088.

Hirano T. Condensin-Based Chromosome Organization from Bacteria to Vertebrates. Cell. 2016 Feb 25;164(5):847-57. doi: 10.1016/j.cell.2016.01.033. PMID: 26919425.

Green LC, Kalitsis P, Chang TM, Cipetic M, Kim JH, Marshall O, Turnbull L, Whitchurch CB, Vagnarelli P, Samejima K, Earnshaw WC, Choo KH, Hudson DF. Contrasting roles of condensin I and condensin II in mitotic chromosome formation. J Cell Sci. 2012 Mar 15;125(Pt 6):1591-604. doi: 10.1242/jcs.097790. Epub 2012 Feb 17. PMID: 22344259; PMCID: PMC3336382..Carmena M, Wheelock M, Funabiki H, Earnshaw WC. The chromosomal passenger complex (CPC): from easy rider to the godfather of mitosis. Nat Rev Mol Cell Biol. 2012 Dec;13(12):789-803. doi: 10.1038/nrm3474. PMID: 23175282; PMCID: PMC3729939.

Tan L, Kapoor TM. Examining the dynamics of chromosomal passenger complex (CPC)-dependent phosphorylation during cell division. Proc Natl Acad Sci U S A. 2011 Oct 4;108(40):16675-80. doi: 10.1073/pnas.1106748108. Epub 2011 Sep 26. PMID: 21949386; PMCID: PMC3189036.

10.Hirota T, Lipp JJ, Toh BH, Peters JM. Histone H3 serine 10 phosphorylation by Aurora B causes HP1 dissociation from heterochromatin. Nature. 2005 Dec 22;438(7071):1176-80. doi: 10.1038/nature04254. Epub 2005 Oct 12. PMID: 16222244.

Williams MM, Mathison AJ, Christensen T, Greipp PT, Knutson DL, Klee EW, Zimmermann MT, Iovanna J, Lomberk GA, Urrutia RA. Aurora kinase B-phosphorylated HP1α functions in chromosomal instability. Cell Cycle. 2019 Jun;18(12):1407-1421. doi: 10.1080/15384101.2019.1618126. Epub 2019 May 26. PMID: 31130069; PMCID: PMC6592258.

Lipp JJ, Hirota T, Poser I, Peters JM. Aurora B controls the association of condensin I but not condensin II with mitotic chromosomes. J Cell Sci. 2007 Apr 1;120(Pt 7):1245-55. doi: 10.1242/jcs.03425. Epub 2007 Mar 13. PMID: 17356064.

Takemoto A, Murayama A, Katano M, Urano T, Furukawa K, Yokoyama S, Yanagisawa J, Hanaoka F, Kimura K. Analysis of the role of Aurora B on the chromosomal targeting of condensin I. Nucleic Acids Res. 2007;35(7):2403-12. doi: 10.1093/nar/gkm157. Epub 2007 Mar 28. PMID: 17392339; PMCID: PMC1874644.

15.Wheatley SP, Altieri DC. Survivin at a glance. J Cell Sci. 2019 Apr 4;132(7):jcs223826. doi: 10.1242/jcs.223826. PMID: 30948431; PMCID: PMC6467487.

Li F, Ling X. Survivin study: an update of “what is the next wave”? J Cell Physiol. 2006 Sep;208(3):476-86. doi: 10.1002/jcp.20634. PMID: 16557517; PMCID: PMC2821201.

Garg H, Suri P, Gupta JC, Talwar GP, Dubey S. Survivin: a unique target for tumor therapy. Cancer Cell Int. 2016 Jun 23;16:49. doi: 10.1186/s12935-016-0326-1. PMID: 27340370; PMCID: PMC4917988.

Chen J, Jin S, Tahir SK, Zhang H, Liu X, Sarthy AV, McGonigal TP, Liu Z, Rosenberg SH, Ng SC. Survivin enhances Aurora-B kinase activity and localizes Aurora-B in human cells. J Biol Chem. 2003 Jan 3;278(1):486-90. doi: 10.1074/jbc.M211119200. Epub 2002 Nov 4. PMID: 12419797.

Gassmann R, Carvalho A, Henzing AJ, Ruchaud S, Hudson DF, Honda R, Nigg EA, Gerloff DL, Earnshaw WC. Borealin: a novel chromosomal passenger required for stability of the bipolar mitotic spindle. J Cell Biol. 2004 Jul 19;166(2):179-91. doi: 10.1083/jcb.200404001. Epub 2004 Jul 12. PMID: 15249581; PMCID: PMC2172304.

Ibid.

Samejima K, Platani M, Wolny M, Ogawa H, Vargiu G, Knight PJ, Peckham M, Earnshaw WC. The Inner Centromere Protein (INCENP) Coil Is a Single α-Helix (SAH) Domain That Binds Directly to Microtubules and Is Important for Chromosome Passenger Complex (CPC) Localization and Function in Mitosis. J Biol Chem. 2015 Aug 28;290(35):21460-72. doi: 10.1074/jbc.M115.645317. Epub 2015 Jul 14. PMID: 26175154; PMCID: PMC4571873.

Nielsen CF, Zhang T, Barisic M, Kalitsis P, Hudson DF. Topoisomerase IIα is essential for maintenance of mitotic chromosome structure. Proc Natl Acad Sci U S A. 2020 Jun 2;117(22):12131-12142. doi: 10.1073/pnas.2001760117. Epub 2020 May 15. PMID: 32414923; PMCID: PMC7275761.

Ibid.

Roca J, Wang JC. DNA transport by a type II DNA topoisomerase: evidence in favor of a two-gate mechanism. Cell. 1994 May 20;77(4):609-16. doi: 10.1016/0092-8674(94)90222-4. PMID: 8187179.

Berger JM, Gamblin SJ, Harrison SC, Wang JC. Structure and mechanism of DNA topoisomerase II. Nature. 1996 Jan 18;379(6562):225-32. doi: 10.1038/379225a0. Erratum in: Nature 1996 Mar 14;380(6570):179. PMID: 8538787.

Champoux JJ. DNA topoisomerases: structure, function, and mechanism. Annu Rev Biochem. 2001;70:369-413. doi: 10.1146/annurev.biochem.70.1.369. PMID: 11395412.

Morrison C, Henzing AJ, Jensen ON, Osheroff N, Dodson H, Kandels-Lewis SE, Adams RR, Earnshaw WC. Proteomic analysis of human metaphase chromosomes reveals topoisomerase II alpha as an Aurora B substrate. Nucleic Acids Res. 2002 Dec 1;30(23):5318-27. doi: 10.1093/nar/gkf665. PMID: 12466558; PMCID: PMC137976.

Escargueil AE, Larsen AK. Mitosis-specific MPM-2 phosphorylation of DNA topoisomerase IIalpha is regulated directly by protein phosphatase 2A. Biochem J. 2007 Apr 15;403(2):235-42. doi: 10.1042/BJ20061460. PMID: 17212588; PMCID: PMC1874246.

Deming PB, Cistulli CA, Zhao H, Graves PR, Piwnica-Worms H, Paules RS, Downes CS, Kaufmann WK. The human decatenation checkpoint. Proc Natl Acad Sci U S A. 2001 Oct 9;98(21):12044-9. doi: 10.1073/pnas.221430898. Epub 2001 Oct 2. PMID: 11593014; PMCID: PMC59764.

Brown EJ, Baltimore D. ATR disruption leads to chromosomal fragmentation and early embryonic lethality. Genes Dev. 2000 Feb 15;14(4):397-402. PMID: 10691732; PMCID: PMC316378.

Brown EJ, Baltimore D. Essential and dispensable roles of ATR in cell cycle arrest and genome maintenance. Genes Dev. 2003 Mar 1;17(5):615-28. doi: 10.1101/gad.1067403. PMID: 12629044; PMCID: PMC196009.

Liu Q, Guntuku S, Cui XS, Matsuoka S, Cortez D, Tamai K, Luo G, Carattini-Rivera S, DeMayo F, Bradley A, Donehower LA, Elledge SJ. Chk1 is an essential kinase that is regulated by Atr and required for the G(2)/M DNA damage checkpoint. Genes Dev. 2000 Jun 15;14(12):1448-59. PMID: 10859164; PMCID: PMC316686.

More memories of an iconoclast.

 Humor, Humility, and a Treasured Friend and Colleague: Sternberg Remembers Jonathan Wells

Andrew McDiarmid

On a new episode of ID the Future, I continue a series of interviews celebrating the life and legacy of Dr. Jonathan Wells, our close colleague and friend who passed away in 2024 at the age of 82 years old. Dr. Wells was one of the first Fellows of Discovery Institute’s Center for Science and Culture and made significant contributions to science and to arguments for intelligent design. Today, evolutionary biologist Dr. Richard Sternberg shares personal anecdotes and insights into Dr. Wells’s character, his contributions to biology and epigenetics, and the profound impact he had on those around him.

One of the character traits Sternberg most admired in Wells was his humility, which formed a backdrop for their many conversations. Wells would occasionally bring up lessons he had learned about hubris from Faust, the famous tragic play by German polymath Johann Wolfgang von Goethe. “The more you know, the more you realize that you know too little and there’s always some other horizon,” says Sternberg, encapsulating his friend’s view. Wells’s commitment to intellectual honesty served him well in his career as a biologist and in the debate over evolution.

Dr. Sternberg also highlights Dr. Wells’s deep concern for the truth. “He saw how ideology could be used to not only bend the truth, but also to just subvert it,” explains Sternberg. Wells committed himself early in his career to following the evidence wherever it led, a decision that led to a brave and relentless search for scientific truth. And the perfect compliment to that bravery and humility? Wells’s sense of humor. Sternberg gives examples. The episode concludes with reflections on Dr. Wells’s lasting influence on the future of intelligent design. Download the podcast or listen to it here.

More on our privileged homeworld.

 The Growing Evidence of Earth’s Privilege

Andrew McDiarmid

On a classic episode of ID the Future, astrobiologist Guillermo Gonzalez, co-author of The Privileged Planet, begins a two-part conversation with host Casey Luskin by providing a rapid survey of some of the growing evidence that Earth is finely tuned in numerous ways to allow for life. He draws a helpful distinction between local fine-tuning and universal fine-tuning. And he tells us about the many extra-solar planets astronomers have discovered in recent years and how all that new data continues to undermine the misguided assumption (encouraged by the misnamed “Copernican principle”) that Earth is just a humdrum planet. Far from it, Gonzalez argues.

The conversation highlights Gonzalez’s essay in the open-access anthology Science and Faith in Dialogue. The book presents a cogent, compelling case for concordance between science and theism. In addition to chapters from Dr. Gonzalez and Dr. Luskin, the book also contains entries from other scientists and scholars in the intelligent design research community, including philosopher of science Stephen Meyer, Brazilian chemist Marcos Eberlin, historian of science Michael Keas, and physicist Brian Miller. The book is available as a free PDF download.

Download the podcast or listen to it here. This is Part 1 of a two-part conversation. 

Total structural collapse.

 Non-Adaptive Order: An Existential Challenge to Darwinian Evolution

Michael Denton February 15, 2016 12:07 AM 

Editor's note: In his new book Evolution: Still a Theory in Crisis, Michael Denton not only updates the argument from his groundbreaking Evolution: A Theory in Crisis (1985) but also presents a powerful new critique of Darwinian evolution. This article is one in a series in which Dr. Denton summarizes some of the most important points of the new book. For the full story,get your copy of Evolution: Still a Theory in Crisis. For a limited time, you'll enjoy a 30 percent discount at  CreateSpace by using the discount code QBDHMYJH.

At London's famous Natural History Museum in South Kensington, a statue of Richard Owen had been prominently placed for many decades at the head of the main staircase. But in a curiously symbolic event on May 23, 2008, the statue was moved to one of the adjacent balconies to make room for a statue of Charles Darwin, which now sits in pride of place.


The reason for this gesture? The Natural History Museum is a grand temple to Darwinian evolution, and Owen was a staunch defender of the alternative structuralist conception of nature -- a conception that, if true, would relegate Darwinian selectionism to a very trivial role in the evolution of life.Owen founded the museum and served as its first curator and director. He made huge contributions to comparative anatomy and paleontology in the 19th century, including coining the term "dinosaur" and defining the term "homology." Owen believed that there was a substantial degree of order inherent in living systems, manifest in what he termed "primal patterns," the grand taxa-defining homologs or ground plans that underlie the adaptive diversity of life.

Because of his vigorous opposition to the functional conception of nature, Owen was vilified by Huxley and other supporters of Darwin. After the publication of the Origin, Owen's contribution to biology was increasingly downplayed by the Darwin camp, and his rejection of the conception that all biological order was to "serve some utilitarian end" was dismissed as archaic and treated as based on failed metaphysical assumptions. Little wonder they moved his statue!

While many of the taxa-defining homologs -- including, among others, the feather, the poison claw of the centipede, the retractable claw of cats, the mammalian diaphragm, and mammary glands -- are clearly adaptive, a great many others, such as the odd number of segments in centipedes, the concentric whorls of the flower, the insect body plan, and the pentadactyl limb, convey the powerful impression of being basically non-adaptive Bauplans. The fact that many exhibit curious geometric and numeric features reinforces the impression that they are indeed abstract non-adaptive patterns, quite beyond the explanatory reach of any adaptationist or selectionist narrative.

In all those cases Darwinian explanations are simply ruled out of court. The difficulty of accounting for arbitrary geometric and numerical patterns in terms of bit-by-bit selection was one of the basic thrusts of William Bateson's vigorous attack on Darwinian orthodoxy, where he argued that such stories descend into "endless absurdity."1

If indeed a significant proportion of the taxa-defining primal patterns serve no specific adaptive function and never did, as common sense dictates and as Owen thought to be true of the Bauplan of the tetrapod limb, then I think a fair assessment has to bethatDarwinism(more specifically, cumulative selection) cannot supply an explanation for the origin of a significant fraction of the defining homologs of the Types and hence for the natural system itself.

References:

(1) Bateson, Materials for the Study of Variation, 410.

On the validity of the God hypothesis.

 

More tales of iconoclast and zombie hunter Jonathan Wells.

 

If you are loosing on every sale no amount of market share will help you.

 

 Natural Selection Subtracts, It Doesn’t Add — And That Matters

In  my previous post (“A New Look at Natural Selection”), I said that “natural selection” was Charles Darwin’s crowning intellectual achievement, for it created what appeared to be a naturalistic and mechanistic explanation for how organisms evolved. I also noted that evolution itself was already considered to have been well demonstrated in the fossil record by Lamarck and others some fifty years before Darwin. 

In the 20th century, natural selection has been almost uniformly adopted by biologists as the explanatory agency for evolution. What appeals to naturalists is that it provides an explanation for the appearance of design in organisms, without an actual designer. Moreover, Darwin had invoked the presence of heritable changes between generations that provided the variety among organisms upon which natural selection could operate. Half a century later, genetics came into focus, seeming to provide the biochemical foundation for Darwin’s intuition as to the cause of heritable variance among species.

Real but Not as Envisioned

Natural selection, we saw, is indeed quite real, but by no means in the way that Darwin envisioned. There can be no doubt that the natural environment establishes severe constraints and requirements upon organisms. In the wild, all organisms must live within their niche. There are no wild polar bears in Arizona, and no iguanas in Alaska. To be sure, the single most incredible fact of the biosphere is the fastidiously precise formation of creatures whose physiology so exquisitely fits their environment. The wonder of this goes far beyond the fact that cetaceans do not breathe through their mouths. Their very existence depends on echolocation, but the funny thing is, it is difficult to hear underwater. Difficult, that is, unless you have a middle ear unique to cetaceans among mammals, making their underwater existence and communication possible. And it’s not just that penguins, who are birds, have bones of greater density than elephants, quite unlike their hollow-boned flying ancestors. They need those iron-dense bones in order to be able to dive for fish, because the rest of their body is composed of fat and feathers, both lighter than water, yet necessary for insulation. 

I have further pointed out that the natural environment, which does passively exert selection on living creatures in all of the varying environments, was consciously designed, making the reality of the ecological niche possible.

In Keeping with the Times

History teaches that ideas and inventions comport with the times. Petroleum until 1900 was only used for kerosene, while gasoline was discarded. Now it is the reverse. We do not see any steam engine locomotives in operation anymore. We are actually on the precipice of eliminating internal combustion even for cars. In the same way, ideas from 150 years ago may have been suitable for their time, but very few scientific ideas last forever. When Darwin thought of natural selection, it seemed to make sense in an incredibly oversimplified version of how life actually operates. We are at least fifty years beyond that now. The examples I gave above about exquisite adaptability to unique environments for whales and penguins are utterly trivial compared to the intracellular and inter-organ physiology and biochemistry of every living thing. There really is no reasonable way to believe that all of those trillions and trillions of modifications occurred randomly and without a designer.

It has been said many times before but it is certainly worth repeating: Natural selection creates nothing. It only subtracts. The big question is, how does the uniqueness of form and function among organisms actually originate? That will be the subject of upcoming posts.

Natural selection designs intelligence?

 Did Sexual Selection Make Male Mosquitofish Really Smart?

Evolution News

Australian National University tells us that the matchstick-size mosquitofish is much smarter than we think:

According to the ANU scientists, male mosquitofish possess impressive problem-solving skills and can successfully navigate mazes and other tests. Males that perform better have a higher chance of mating.

Lead author Dr Ivan Vinogradov said male mosquitofish likely evolved better cognitive abilities over time because of the advantage it gave them in finding females and producing offspring — a phenomenon known as “sexual selection.”

“Evolution of intelligence in animals has long been thought to have been driven by natural selection. Animals that were better at problem solving were more adept at gathering food, finding shelter, and avoiding predators and hence lived longer,” Dr Vinogradov said.

“They then passed on these genes to their offspring, helping future generations become smarter over time.

“But there is another explanation for the evolution of intelligence: braininess is an attractive quality to the opposite sex. A better brain might help an animal find more mates, have more sex, and eventually have more babies. 

“’Smarts’ count: Evolution of intelligence,” February 25, 2025

Presumably, Vinogradov’s thesis assumes that the female fish are clever too; otherwise, they wouldn’t recognize or appreciate cleverness in the males.

After performing more than 2,000 paternity tests, the scientists found that smarter males who successfully navigated the underwater tests mated with more females and produced more offspring than less-intelligent fish that failed the tests. 

“Evolution of intelligence” Here’s the paper.

It’s worth considering that the fish who can solve mazes may also be better able to stay out of the way of predators than the ones who couldn’t. The females, after all, can only mate with survivors…

Still a Mystery…

It’s still not clear just how the fish significantly increases its intelligence, relative to other fish. Natural selection and sexual selection only show why it may be an advantage; they don’t account for how, exactly, it is done.

But then, we are still trying to figure out how the solitary, exothermic, invertebrate octopus got to be so smart too. Lots of room for new research!

Drink deep from or taste not of this cup.

 

A little science tends to lead us away from design but a lot of science tends to lead us right back?

 As Science Observes, Talk of Evolution Fades

David Coppedge

Here is something that emerges from stories that have appeared recently in journals and at science sites, including news that updates some of my previous articles. We find that the more detail that scientists observe, the less talk there is about evolution. Why would that be? Another point worthy of note: the more sophistication that is found in biological engineering, the more scientists want to imitate it. 

Jumping Robot Success

One of the most fascinating animal stories I have reported was about springtails (here). These miniature gymnasts, ranging from 2 to 6 mm long, perform Olympic-grade leaps, accelerating up to 80g, rotating at a phenomenal rate of 290 revolutions per second. Harvard reported success at mimicking the springtail with small robots that can jump 1.4 m, 23 times their length, using a rapidly unfolding furcula resembling the device the springtail uses to launch. 

Robert J. Wood’s lab had earlier reported mimicking the mantis shrimp’s club, a device that I described here. Both the springtail and mantis shrimp use “latch-mediated spring actuation, in which potential energy is stored in an elastic element … that can be deployed in milliseconds like a catapult.” Does he believe it evolved? Hard to say. The news release only says that the inspiring springtail is ubiquitous “both spatially and temporally across evolutionary scales.” That could be interpreted as stasis

Our Bubble-Wrap Noses

Feel your nose. New Scientist announced a new fact about that monument on our facial map: “Your ears and nose are made from tissue that looks like bubble wrap.” It’s a different form of cartilage from that found in other parts of the body. Maksim Plikus at UC Irvine found this by accident when studying mouse ears, lending support to Young’s Law of Science: “All great scientific discoveries are made by mistake.”

Our bubble wrap cartilage, which the UCI team calls lipocartilage due to its fat content, does not pop when squeezed, nor does it make good shipping material, but the UCI team believes that “harnessing it could make facial surgery, like nose reshaping, easier.” One item of ethical concern appeared in the article: “The team also found lipocartilage in human ear and nose samples collected from medically aborted fetuses.”

Magnetic Navigators

A sea turtle hatchling disappears into the waves. How does it know where to go? And how does it know the way back years or decades later? These questions were explored ten years ago in Illustra Media’s film Living Waters: Intelligent Design in the Oceans of the Earth. It suggested that the turtles follow magnetic waypoints in an inherited map. Now, scientists at the University of North Carolina at Chapel Hill have filled “an important gap in our knowledge” by confirming that the turtles can memorize magnetic signatures. “Through controlled experiments, the research team demonstrated that loggerhead turtles can indeed learn and remember the magnetic fields of areas where they receive food.” Incidentally, it was good to hear from Deakin University that the endangered turtles are making a comeback thanks to conservation efforts.

UNC’s discovery adds understanding about animal migration in general. “More broadly, these findings could apply to a wide range of migratory animals that rely on magnetic cues for navigation,” they said. Indeed, earlier news from the University of Oldenburg found that desert ants memorize their nest location when out on learning walks by paying attention to the polarity of the earth’s magnetic field. Changing the inclination of artificial magnetic fields had no effect, they found, but changing the azimuth made the ants aim in the wrong direction. All is not lost, however; a recent paper in Current Biology reports that desert ants use a “variety of navigational tools” in their learning walks, including path integration: “Once the learning walks are completed the ants can reach the nest from any direction.” For more on the remarkable abilities of animals to navigate by the earth’s magnetic field, see Eric Cassell’s excellent book Animal Algorithms published by Discovery Institute Press.

Zooming in on the Flagellar Stator

Calling the iconic bacterial flagella “amazing natural machines!”, news from the Nagoya Institute of Technology announced new details in the stator at unprecedented resolution. Using CryoEM (see my article here about super-resolution microscopy), Japanese scientists peered into sodium ion channels that are arranged in a ring around the stator. They determined that these channels contain “key molecular cavities for sodium ions” that “act as size-based filters that allow the intake of sodium ions — but not other ions — into the identified cavities.” This is remarkable given that some flagellar motors operate on protons, which are smaller.

As hydrated sodium ions flow through the cavities, an accompanying video explains, they generate conformational changes, “transferring the mechanical energy to the rotor to make the motor spin.” The team identified numerous specific amino acid residues in the channel involved in size filtering. Even so, “the mechanism of how the ion flux drives the rotation is still unknown,” their paper in PNAS says. As scientists around the world continue collecting detailed clues about this molecular outboard motor, it’s exciting to see them approach the secret of torque generation. And so far, as this evolution-free paper illustrates, the irreducible complexity has been growing ever since Michael Behe brought this iconic motor to our attention in 1996.

Machine Recycling

Some eukaryotes alternate between amoeboid and flagellated forms. Swiss scientists publishing in EMBO Reportsexamined one shape-shifter: “The early branching eukaryote Naegleria gruberi can transform transiently from an amoeboid life form lacking centrioles and flagella to a flagellate life form where these elements are present, followed by reversion to the amoeboid state.” When it comes time to recycle the eukaryotic flagellum (different in design from bacterial flagellum), the axonemes “fold onto the cell surface and fuse within milliseconds with the plasma membrane” (emphasis added). That’s radically fast recycling! Then, a molecular machine called spastin cuts up the axonemes into similarly sized chunks and sends them to the lysosome, where the molecules are disassembled for reuse. 

The researchers also found that the centrioles, parts of the basal bodies of the flagella on the inside, get recycled by lysosomes or proteasomes too. Some centrioles, though, are shed to the outside of the cell. “Remarkably, we discovered that externalized centrioles can be taken up by another cell,” they noted. What they found is probably not unique. “Collectively, these findings reveal fundamental mechanisms governing the elimination of essential cellular constituents in Naegleria that may operate broadly in eukaryotic systems.” Evolution made only a cameo appearance in the paper but was not essential to the science.

Cable Bacteria Update

Finally, new research on cable bacteria (see here) was published in PNAS in January. A study from the Naval Research Laboratory “presents the direct measurement of proton transport along filamentous Desulfobulbaceae, or cable bacteria. So it’s not just electrons that can travel on these miniature wires, but protons, too. And they go long distances. (Well, that is, if you consider 100 micrometers a long distance.) Why is this significant? “The observation of protonic conductivity in cable bacteria,” they say, “presents possibilities for investigating the importance of long-distance proton transport in microbial ecosystems and to potentially build biotic or biomimetic scaffolds to interface with materials via proton-mediated gateways or channels.” Proton transfer, they believe, may play essential roles in the ecology at the micro level. And as they point out, the imitation of nature in biomimetics remains a hot pursuit. Has Darwinism helped? “However, despite these hypotheses, the evolutionary benefit of this phenomenon, its role in environmental settings, and its role in microbial interaction remain unknown.” Let engineers figure it out.

On the evolution of the design debate.

 Michael Kent: “12 Discoveries That Have Changed the Debate about Design”

Granville Sewell

Michael Kent is a Fellow with the Center for Science and Culture and a recently retired bio-scientist from Sandia National Laboratories in Albuquerque. He has been interested in intelligent design for many years. Since 2005 he has organized quarterly meetings on intelligent design in or near the University of New Mexico campus. Over this twenty-year period, he has developed slide presentations on “12 recent discoveries that have changed the debate about design in the universe,” and now he is turning those presentations into videos. 

The 12 discoveries are: 

The universe (space-time, matter, energy) had a beginning.

The laws of physics, the fundamental constants, and the initial conditions of the universe are fine-tuned to allow for the possibility of life.

Protein sequence space is far too large to be searched and highly functional sequences (i.e., enzymes) are incredibly rare (~ 1 in 1077).

The number of genes in the simplest free-living organism is about 450.

Life is based on a digital information processing system.

Molecular machines and sophisticated software algorithms are essential to all life-forms.

Random mutation + natural selection has severe limitations as a creative mechanism that are now well understood.

So many highly improbable factors make Earth habitable that it is VERY unlikely that another truly “Earth-like” planet exists in our galaxy.

The “junk DNA” paradigm has been shown to be false. Most, if not all, non-coding DNA has function.

The Cambrian (and other) explosions in the fossil record are not consistent with the Darwinian model of gradual evolution.

Extensive post-translational processing (editing) of genes occurs in eukaryotes: the spliceosome and the splicing code.

Genes extensively overlap in the same or opposite directions within a stretch of DNA (overlapping codes).

The first six plus an introductory video are now viewable here. Though these seven may still undergo further editing, the videos are very much worth watching already. The last six in the list will be converted into videos later but slide presentations for all 12 are viewable here.

Science acknowledges the thumb print of JEHOVAH?

 

Darwin Skeptic vs. Design Skeptic II

 

On recognizing JEHOVAH’S Signature.

 Richard Dawkins, the Koala, and the Giraffe

Wolf Ekkard Lonnig

Editor’s note: We are pleased to offer this Abstract from Part I of a new paper by Wolf-Ekkehard Lönnig, “Richard Dawkins, the Koala, and the Giraffe: How Evolutionists Overlook Signatures of Design, Part I.”

Abstract: Key Points of the Contents

Referring to science broadcaster Robyn Williams (Australia), Richard Dawkins believes that the koala’s pouch opens downwards due to its ancestry from a wombat-like animal instead of upwards as in the kangaroo — “a legacy in history.” A similar legacy, he assumes, also accounts for the recurrent laryngeal nerve in the giraffe.  

The Australian Koala Foundation contradicts him on this: The pouch “faces straight outwards rather than backwards” (emphasis added). The IFAW (Australia) agrees that, as compared with kangaroos, koalas “have a more centrally located opening.” And that is for good reasons: “The pouch protects young koalas, called joeys, from injury while the mother climbs among trees.” 

Now, Darwin correctly observed that “false facts are highly injurious to the progress of science, for they often long endure.” I consider the statement about the backwards opening pouch of the koalas to be “a false fact” to bolster neo-Darwinism — a false fact still widely repeated in many public statements. Check Google on the pouch of the koala. 

A series of links to videos and pictures shows the enormous differences between koala (Phascolarctos cinereus) and wombat (Vombatus ursinus) babies emerging from their pouches. This is likewise for good reasons: koalas are fully arboreal whereas wombats live on the ground and especially underground. 

As for the recurrent laryngeal nerve of the giraffe, see here.   

I remind the reader of a massive contradiction within the theory of evolution itself: “The genetic message, the program of the present-day organism…resembles a text without an author, that a proof-reader has been correcting for more than two billion years, continually improving, refining and completing it, gradually eliminating all imperfections” (Nobel laureate Francois Jacob). I give similar assertions by other authors in the text. And now, as a result of limitless, omniscient, and omnipotent natural selection over millions of years, “gradually eliminating all imperfections,” how are we to account for the koala’s imperfection, a pouch that “opens downwards, instead of upwards as in a kangaroo,” or an entirely superfluous long detour of the recurrent laryngeal nerve in the giraffe?

I cite thirty special adaptations in the arboreal/tree-living koala. Most of them are problematic from the perspective of gradual evolution, but, according to Dawkins, “evolution not only is a gradual process as a matter of fact; it has to be gradual if it is to do any explanatory work.” I subsume the overall system of synorganizations (the term used by evolutionist A. Remane), or “co-adaptations,” under the subheading “Signatures of Design in the Koala.”

Applying neo-Darwinism to the koala’s “two thumb adaptation” is shows — when starting with a hand/front paw like that of the wombat — the following result: After discussing several presuppositions and implications of gradualism, thousands of steps in millions of years would be necessary for the specific adaptation of the koala’s hand alone. And, just to emphasize the point: according to population genetics, here also “each new successful evolutionary step would imply the substitution of an entire Phascoarctos-like population.” 

In summary: According to evolutionary biologist Danielle Clode in her book about the koala (2023), “Koalas are singular creatures: idiosyncratic and inimitable. They are sometimes described as being ‘like bears,’ ‘like wombats,’ ‘like sloths,’ or ‘like pandas.’ They share some parallels, some traits with these creatures, but they are not in any way ‘like’ them. Koalas are simply unlike anything else we know of” 

Photo: the koala’s hand in action grasping a twig, by W.-E. L.

Now, if one is free to break away from the prohibitions of materialistic philosophy, one could, for example, accept the following reasoning. According to Austrian cell physiologist Siegfried Strugger, professor of botany at the University of Münster: “In comparison to the cell, all automation of human technology is only a primitive beginning of man in principle to arrive at a biotechnology.” Well, if the first steps on the path to the ingenious level of cybernetic complexities of the cell, i.e., the “primitive beginning” in Strugger’s formulation, demands conscious action, imagination, perception, intelligence, wisdom, mental concepts, spirit and mind — all being absolutely necessary for the basic start — how much more so does this have to apply to the origin of the thousand times more complex cybernetic systems of the many complex life forms themselves. And those include the specified and irreducibly complex structures inescapably necessary for the koala and countless other organisms 

(see more here).

Materialism of the gaps?

 

Recognizing JEHOVAH'S Signature?

 Intelligent Design in Action: DNA Cryptography

David coppedge

Twelve years ago, in a series on Intelligent Design in Action, I discussed the science of cryptology as an example. A review of terms is in order; what is the difference between cryptology and cryptography? Basically, it’s theory vs application.

Merriam-Webster defines cryptology as “the scientific study of cryptography and cryptanalysis.” Cryptography is the process of writing or reading secret messages in code. Cryptanalysis involves the theory of solving cryptographic systems. There’s a Journal of Cryptology. There are professors of cryptology. Cryptology involves theories, data, experimentation, and testing. It has all the accouterments of science — and is entirely based on intelligent design principles. Which makes sense. It takes a mind to encode a message, and mind to decode it. 

If cryptology is an example of ID in action, how much more when it involves biologically coded information? Such is a new application of cryptology discussed in The Scientist. Dr. Danielle Gerhard explained why “DNA Cryptography” represents a cutting-edge technique to reduce biosecurity risks. 

Over the last two decades, synthesizing DNA has become faster and easier, but researchers worry that this will make it easier for people to access potentially dangerous products. While many experts call for more federal guidance and regulation over the production of synthetic nucleic acid sequences, others have drawn focus to biosecurity concerns that are a little closer to home: in research labs. Jean Peccoud, a synthetic biologist at Colorado State University, and Casey-Tyler Berezin, a molecular biologist on Peccoud’s team, discussed the biggest biosecurity issue facing research, approaches for encrypting messages into DNA sequences, and the importance of sequencing technologies for mitigating biosecurity risks. 

Sequencing: that word rings a bell. Doug Axe in his book Undeniable, and Stephen Meyer in Signature in the Cell, explained that the carrier of information in biomolecules is not the building blocks but the sequence in which they are arranged. In The Design Inference 2.0, Dembski and Ewert expanded their earlier concept of complex specified information, showing that “short description length” is sufficient to identify design. A sequence of ones and zeroes that looks random might only be describable by repeating the whole sequence, unless a pattern like “the series of prime numbers” were found in it. That would shorten the description and identify the product of a mind.

How does this relate to the new science of DNA Crytography? Similar to a series of numbers, DNA consists of building blocks or “letters” whose sequence can—and does—convey information. As we know from genetics, DNA conveysfunctional information when it codes for proteins. It can also, as discussed here, convey non-biological information in human language. Craig Venter’s team, for instance, embedded their own watermark in DNA when completing their “synthetic cell” project. A highly versatile molecule, DNA has also been used to encode music, art, and even movies

Biosecurity with DNA

Dr. Gerhard writes that “Hidden Messages in DNA Could Reduce Biosecurity Risks.” The reason is that DNA is a good substrate for digital information. The subtitle says, “To improve traceability and enable authentication of synthetic nucleic acid sequences, researchers are embedding digital signatures into DNA.” Her article includes a transcript of a recording between Jean Peccoud, a synthetic biologist at Colorado State University, and Casey-Tyler Berezin, a molecular biologist on Peccoud’s team.

Peccoud highlights a big risk that till recently was thought impractical: sending text messages across international borders that could be translated into DNA sequences for biological warfare. “How do we know that what we have in our labs is what we think it is?” Peccoud asks. Digital signatures — encoded strings difficult to crack — could provide needed assurance. Digital signatures have long been used in business and government to authenticate messages. If DNA is a form of text, it can be used in a similar way.

For example, every research sample, such as a tube with a DNA plasmid, has two facets: a computer record that contains information about the sequence or provides a plasmid map and then there’s the content of the tube. When the two don’t match, there are all sorts of potential problems that arise. This may not be a biosecurity problem in the regular sense because you’re not dealing with infectious agents, but people are spending millions of dollars on research that they cannot reproduce because they don’t know what they have in their flasks. It’s a security problem that comes from the fact that what you’re working with is not what you think it is.

This risk is not science fiction. “That’s something that is happening in every lab, every day, and we have very few tools to figure out what’s going on in our own lab,” he adds. Berezin shows why the time has come for DNA Cryptography.

I became interested in the topic when I joined Peccoud’s synthetic biology team. I realized that a lot of the methods that we’re using, such as polymerase chain reaction (PCR) and bacterial transformations, are methods I had used before but never wondered where the DNA sequences came from or how I would know if something had changed in the sequences. This is the status quo — we work with DNA and take for granted that it’s going to be what we think it is. Once you are aware of the biosecurity issues, it’s something you can’t turn your back on. Now, I see those issues everywhere.

DNA Cryptography mirrors existing methods to authenticate digital messages in communication channels. When sequences of code transfer across the internet, how does a receiver know that the message has not been corrupted by noise or malware? A system at the receiving end, such as a router, can recalculate the digital signature, often reduced to a string by a hashing algorithm, to find out. If not validated, the receiver can ask for a retransmission. This way, a human or software system at the end of the line can have confidence in the message.

Similarly, digital signatures in DNA can authenticate a product from a sender or warn the receiver if mutations in the DNA have corrupted it. DNA Cryptography reduces uncertainty.

DNA is going to mutate. That’s what it likes to do. It likes to replicate and sometimes that doesn’t go perfectly. So even if you might have something safe in a tube in your lab, after you propagate it 100 times or 1,000 times, you might not have what you think you do. Whether that’s dangerous or not really depends on the specific scenario, but that uncertainty of not knowing what you have, is very prevalent across academic research labs.It takes a lot of work on the part of the user to ensure that they’re tracking all the sequences that they have and that they are sequencing their plasmids as they go on. 

DNA barcoding is already widespread, Berezin adds. What’s new is creating ciphers in DNA that are secret and difficult to break. 

We’re interested in encoding encrypted messages that provide the user with information about the authenticityof the materials they’re working with. For this, our group has been developing a digital signature approach called DNA Identification Number (DIN), which is a more complex cryptography approach that makes it even more difficult for the receiver to open unless they know what they’re looking for.

The national security ramifications of DIN are obvious. Berezin goes on to explain how DINs are created and hashed into standard string lengths, and how techniques are being developed to assist those wishing to use it. From this article, we see several points relevant to ID:

Information is conveyed by the sequence, not the building blocks.

Information can be translated from one medium into another.

Mutations or noise degrade information, contrary to the expectations of Darwinism.

DNA is now a tool in steganography, another example of ID in action (here, here ).

Intelligent design is an integral part of many sciences. Now we see new applications with the building blocks of biomolecules. But what about all those sequences in DNA that were not manipulated by humans? I wonder if some of the non-coding DNA might turn out to include natural hidden messages. Will we find compression algorithms, digital signatures, or steganography in things labeled pseudogenes or junk DNA? Given our experience in artificial cryptography, intelligent design advocates have reason to investigate.