Molecular biology is only the complex beginning of Darwinism's explanatory deficits?

 The Extracellular Space: Where the Rest of Life Takes Place

Howard Glicksman

When it comes to the discussion of how life came into being, whether by intelligent design or by the unguided processes proposed by evolutionary biology, I have a pet peeve.

It’s that almost all of the discussion from both camps revolves around just molecular and cellular biology — DNA, RNA, genes and their regulatory networks (GRNs), proteins and their various shapes, sizes, and functions, the cell membrane and cytoskeleton, and all the other fascinating intricacies of the cell. 

Don’t Get Me Wrong

When it comes to the dialogue about the causal hurdles that life must overcome, every component mentioned above is important. And to my mind, they all favor ID.  

After all, as chemist James Tour wrote in his chapter in The Mystery of Life’s Origin: The Continuing Controversy, when considering what is known about the laws of chemistry, “we’re still clueless about the origin of life.” Biologist Douglas Axe, in his book Undeniable: How Biology Confirms Our Intuition That Life Is Designed, tells us that “of the possible genes encoding protein chains 153 amino acids in length, only about one in a hundred trillion trillion trillion trillion trillion trillion is expected to encode a chain that folds well enough to perform a biological function.”

Zooming Out

But what about multicellular organisms, like us? Isn’t there more to think about and explain than just molecular and cellular biology? Here’s how Steve Laufmann and I posed the problem in our book Your Designed Body.

Zooming out from a single cell, the human body as a whole is made up of around thirty trillion cells. It needs to solve all the same kinds of problems that a cell does, plus quite a few more. And it needs new ways to solve old problems, ways completely different from how the same problems were solved at the cellular level. 

For example, a single-celled organism is like a microscopic island of life. The cell gets what it needs and gets rid of what it doesn’t need from its surrounding environment. In contrast, a large multi-cellular organism (like you) is more like a continent with a deep and dark interior. Most of the cells reside deep in the interior with no direct access to the body’s surrounding environment. For a multi-cellular organism, then, harvesting the raw materials its cells need and getting rid of toxic byproducts becomes a major logistical problem. 

Several hundred such problems must be solved for a complex body to be alive. And many of the solutions to these basic problems generate new problems that must also be solved, or that constrain other solutions in critical ways. The result is that for a complex body to be alive, thousands of deeply interconnected problems must be solved, and many of them solved at all times, or life will fail. 

The bottom line is that, as hard as it is for a cell to maintain life, it’s much harder for an organism with a complex body plan like yours.

Besides knowing what’s going on inside our cells (within the intracellular space), don’t we also need to consider what’s going on outside our cells (but within our body) — in the extracellular space? Where one-third of our body’s total water resides? Where the various biomolecules that provide the framework for structure and support to all the different tissues in our body are located? Where the precise chemistry allowing for tissue survival and proper nerve and muscle function must be present? And much, much more.

My Experience as a Physician

As a hospice physician, I can tell you that all this is a matter of “life and death.” It’s something that evolutionary biologists rarely mention. This may be, at best, because they’ve never considered or understood it, or at worst, because they can’t explain it and it undermines their theory. 

Let me give you a practical example from what I see and do every day. That way, you can understand why adding what goes on inside the extracellular space as a causal hurdle for multicelluar life is important. Meet my patient Joe.

Joe had had several heart attacks and now his heart wasn’t pumping as well as it should. In fact, it was doing so at one-quarter its normal strength — meaning he had heart failure. Since his heart wasn’t pumping efficiently, it caused a reduction in the force of arterial blood flow which turned on certain hormone systems in his body. These systems were designed (yes — designed) to try to correct such a situation. Unfortunately, this caused Joe’s body to start holding on to excessive amounts of water. 

Joe’s body’s inability to control how much water was in his extracellular space put him at risk of death. Fluid was taking up more and more space in his lungs, making it harder and harder to breathe. Since he kept going in and out of the hospital and his physicians could not solve his recurrent fluid overload problem, he was put on hospice. By the time I first saw him, Joe could barely move or even talk without becoming short of breath. Fortunately for Joe, I knew exactly what medication adjustments were needed to safely remove his excessive fluid. Within a few months, we were able to discharge him alive from our service.    

The above case (and I’ve had dozens of them) clearly shows that what’s going on in the extracellular space matters. It matters so much that to not even talk about it, in the context of biological origins, is frankly unscientific.   

It also shows that my pet peeve about the absence of this discussion in the origins debate is my own fault. So, please watch this space for articles in the future on the extracellular space and ID. 

This Titan is guilty of war crimes?

 

Our self-styled betters in their own words.

 Whatever you think about think about JEHOVAH'S Witnesses We (unlike our self-styled betters) can guarantee you that it will never be our politicians, magistrates,police trampling your rights,

Ps. We know that the religious left also have their version of the police state .

Lizard brain for the win?

 

Pope francis the universalist?

 

Franciscan media

...Fazio asked Pope Francis how he imagines God. “Like a generous father,” the pope responded, citing the prodigal son parable (Lk 15:11–32). Pope Francis said that he believes “in a God who is not scandalized by our sins because he is a father and accompanies us.” The pope asked: “Does God accompany sinners or immediately condemn them to hell? No, he chooses to accompany us. . . . So it’s hard to even imagine hell, a father who condemns someone for all eternity.” The pope said he hopes that hell is empty. 

In fact, we cannot believe in hell in the same way that we believe in the God described in the Bible. The former is a possibility while the latter is a fact... 

Alfred Russel Wallace for the win?

 Alfred Wallace’s Views Hold Up Well Today — Unlike Those of His Friendly Rival Charles Darwin

Evolution News

On a classic episode of ID the Future, science historian Michael Flannery concludes his conversation with host Michael Keas about his book Intelligent Evolution: How Alfred Russel Wallace’s World of Life Challenged Darwin. Wallace was co-founder with Charles Darwin of the theory of evolution by random variation and natural selection. Unlike Darwin, however, he saw teleology or purpose as essential to life’s history, and a teleological view as essential to the life sciences. According to Flannery, Wallace’s views on the nature of the cell, the special attributes of humans, the irreducible nature of life, and the fine-tuning of the universe hold up well today. They are also remarkable in foreshadowing modern intelligent design theory. Wallace and Darwin disagreed on much of this, yet they maintained a mutual respect. In this, Flannery says, the two are a great model for scientists who disagree today.

Find the podcast and listen to it here. 

The crocodilian explosion?

 Fossil Friday: The Sudden Appearance of Crocs in the Triassic Fossil Record

Gunter Bechly

This Fossil Friday we will look at a clade of reptiles that is called Pseudosuchia, which includes living crocodiles and their fossil relatives such as the featured Postosuchus from the Late Triassic of Texas. Like so many other groups, pseudosuchians appeared very abruptly in the Early Triassic period after the ‘Great Dying’ of the end-Permian mass extinction event about 250 million years ago.

Just a few weeks ago a new fossil poposauroid pseudosuchian was described from the Middle Triassic Favret Formation in Nevada (Smith et al. 2024). The new genus received the almost unpronounceable name Benggwigwishingasuchus. The find was very surprising, because only marine organisms (e.g., ichthyosaurs and ammonites) were previously known from these sediments, which have been produced in an open sea environment. A co-author of the study remarked that their first reaction was “What the hell is this?” (Baisas 2024). They certainly did not expect to find a terrestrial animal in these layers, but the well-preserved leg bones left no doubt that this reptile lacked any secondary aquatic adaptations and had a primarily terrestrial mode of life (Klein 2024). Because the preservation of the skeleton suggests a minimal post-mortem transport, the researchers suppose that it lived along the shores of the ancient Panthalassan Ocean. The authors concluded that the new discovery “implies a greater undiscovered diversity of poposauroids during the Early Triassic, and supports that the group, and pseudosuchians more broadly, diversified rapidly following the End-Permian mass extinction” (Smith et al. 2024). They also emphasize that more generally “recent studies have inferred a rapid diversification of archosaurs and their stem lineages, which established major clades by the end of the Early Triassic” (Smith et al. 2024).

A Kind of “Explosion”

In other words, all the subgroups of archosaurs appeared abruptly in a kind of “explosion,” similar to the sudden appearance of 15 different families of marine reptiles in the Early Triassic (Bechly 2023a), or the sudden appearance of different groups of gliding and flying reptiles during the Middle Triassic (Bechly 2023b). Also, dinosaurs appeared so suddenly in the Late Triassic that one expert commented that “it’s amazing how clear cut the change from ‘no dinosaurs’ to ‘all dinosaurs’ was” (University of Bristol 2018). And famous paleontologist Peter Ward (2006: 160) explained that “the diversity of Triassic animal plans is analogous to the diversity of marine body plans that resulted from the Cambrian Explosion.” The Triassic period proves to be a real carpet bombing of bursts of biological creativity (Bechly 2024), which does not resonate well with a Darwinian paradigm at all.

References

Baisas L 2024. Say hello to the surprising crocodile relative Benggwigwishingasuchus eremicarminis. Popular Science July 11, 2024. https://www.popsci.com/science/triassic-crocodile/

Bechly G 2023a. Fossil Friday: The Triassic Explosion of Marine Reptiles. Evolution News March 31, 2023. https://evolutionnews.org/2023/03/fossil-friday-the-triassic-explosion-of-marine-reptiles/

Bechly G 2023b. Fossil Friday: The Explosive Origin of Flying Reptiles in the Mid Triassic. Evolution News May 19, 2023. https://evolutionnews.org/2023/05/fossil-friday-the-explosive-origin-of-flying-reptiles-in-the-mid-triassic/

Bechly G 2024. Fossil Friday: Discontinuities in the Fossil Record — A Problem for Neo-Darwinism. Evolution News May 10, 2024. https://evolutionnews.org/2024/05/fossil-friday-discontinuities-in-the-fossil-record-a-problem-for-neo-darwinism/

Klein N 2024. Diverse growth rates in Triassic archosaurs—insights from a small terrestrial Middle Triassic pseudosuchian. The Science of Nature 111:38, 1–5. DOI: https://doi.org/10.1007/s00114-024-01918-4

Smith ND, Klein N, Sander PM & Schmitz L 2024. A new pseudosuchian from the Favret Formation of Nevada reveals that archosauriforms occupied coastal regions globally during the Middle Triassic. Biology Letters 20(7):20240136, 1–8. DOI: https://doi.org/10.1098/rsbl.2024.0136

University of Bristol 2018. Dinosaurs ended – and originated – with a bang! University of Bristol press release April 16, 2018. http://www.bristol.ac.uk/news/2018/april/dinosaurs-ended-and-originated-with-a-bang-.html

Ward PD 2006. Out of Thin Air. Joseph Henry Press, Washington DC, 296 pp. https://books.google.at/books?id=baJVAgAAQBAJ

Origin of Life science is not a thing?

 

More on why there is no place like home.

 Beauty and Our Privileged Planet

Guillermo Gonzalez

This past July 13 several Discovery Institute fellows (Jay Richards, Melissa Cain Travis, and I) participated in the “Encountering Beauty in the Sciences” conference at the Museum of the Bible. I spoke on the topic “Beauty and Scientific Knowledge,” which was a first for me.

My basic thesis is that there is a connection between beauty in nature and the acquisition of important knowledge about nature. I made a cumulative case argument based on multiple relatable examples. As a corollary, I also argued that Earth’s residents enjoy more beautiful phenomena that lead to scientific advancement than would hypothetical extraterrestrial beings in other places in the cosmos, if there are any.

I was inspired to make this argument from the evidence for design I collected in the pages of The Privileged Planet, whose new and expanded 20th anniversary edition is out today. As Jay Richards and I argue in our book, nature seems designed in such a way that the most habitable places are the best places to do science. In addition, Earth is particularly gifted with life and the tools to do science. I am now convinced that beauty is in the mix as well. 

The Starry Heavens

The beauty of the starry heavens attracts us. We can say the same about rainbows, total solar eclipses, certain minerals, comets, aurorae, meteors, and electrical storms. These phenomena are not only beautiful; they have also revealed important scientific truths about nature. I would rank their importance to science roughly in the order I just listed them.

That these aspects of nature are beautiful is hardly controversial. People spend big bucks to go see a total solar eclipse, or spend vacation time camping away from cities, at least in part, to enjoy the views of the dark night skies. They will vacation in Fairbanks, Alaska, to see the aurorae. People will even pause their busy lives, if only briefly, to gaze at a rainbow.

It’s obvious how dark nights have given us important knowledge about the nature of reality. And, we cover the scientific value of total solar eclipses in Chapter 1 of The Privileged Planet. But, rainbows?

A Clue Across the Sky

I like to think of rainbows as a clue writ large across the sky. They are not only beautiful, but they seem completely out of place and out of the ordinary. When I see one, I feel like exclaiming, “Who ordered that?!” or “How does that form?” Rainbows invite us to ask questions.

Over the centuries scholars proposed theories to explain rainbows. The first breakthrough came in the early 14th century when the Dominican theologian and physicist Theodoric of Freiberg proposed an essentially correct explanation. He arrived at his theory through the application of geometry and experimentation with glass spheres filled with water, simulating what happens within raindrops when sunlight passes through them. Theodoric and others after him not only advanced our understanding of the rainbow phenomenon, but they also advanced the entire field of optics.

The next breakthrough came when Isaac Newton began experimenting with glass prisms in the 17th century to make artificial rainbows. These were the first rudimentary “rainbow makers” or spectroscopes. Later, chemists heated elements in a flame and discovered that each has a unique spectrum. The spectroscope revealed the “fingerprints” of the elements. At the same time, astronomers captured the spectra of distant stars with spectroscopes attached to telescopes. They talked with the chemists and soon astronomers learned how to determine the chemical composition of stars and nebulae. 

Spectra of the Galaxies

Cosmology was born just over a century ago when astronomers began getting spectra of galaxies. They discovered that nearly all the galaxies they observed had red-shifted spectra. That discovery led to the realization that the universe had a beginning. The spectroscope, even today, is the most important tool of the astronomer. It is no exaggeration to say that rainbows provided clues that unlocked the most profound truths about the nature of nature.

What’s more, rainbows are connected to our existence. You need an atmosphere. You need a water cycle. A dune world won’t do. A completely cloud covered sky won’t do. Of all the places in the Solar System, Earth’s surface is the best one for seeing rainbows.

I’ll leave the other examples I listed as an exercise for the reader.

The most pregnant pause of all?

Wrap Your Mind Around the Synapse — Just Try

David Coppedge 

After poring through scientific papers and articles, the complexity of synaptic transmission baffles me. For a neural signal to make it through the steps of packaging neurotransmitters, sending them across a gap, and then triggering a response inside the next neuron, seems needlessly complicated. Dozens of proteins and factors are involved at every synaptic crossing.

Why would evolution, or intelligent design, end up with such a method? It looks like a kludge. The power lines that engineers build do not operate that way. They keep continuous contact for the nonstop flow of electrons. It wouldn’t make sense at each power pole to convert the electricity to chemical energy and back again. Why does the body do it? 

But one has to admit that it works very well, and extremely rapidly. Within milliseconds, a signal from your foot makes it to the brain and back again. On its way, that signal repeatedly undergoes the energy conversion at each synapse. Signals from the feet continuously traverse nearly two meters of nerve fibers packed with molecular machines and ion pumps, crossing synapses at each junction. It’s uncanny, but that’s what biophysicists and biochemists have found. Professors at UC Santa Barbara estimate that some neural signals can travel over 100 miles per hour!

As an avid hiker and backpacker, I have often crossed streams, walking across narrow logs over rushing water. I have leaped from rock to rock to get over a boulder pile, at each moment needing to decide where to place my feet, adjusting quickly if I feel the rock moving. The flow of information from eyes to brain to feet and back again, giving rapid and continuous feedback on my path, is something I am tremendously grateful for. Those synapses have given me invigorating experiences and have saved me from nasty falls uncountable times. The rapid, risky movements of gymnasts and parkour players and squirrels far exceed my exploits, but any of us who have walked irregular paths, up and down stairs, or quickly dodged a moving object have reason to be interested in how the body accomplishes rapid signaling through neurons. Now, cryo-electron microscopy has allowed scientists to peer deeper into the mysteries of the synapse.

Advancing Knowledge

The basic function of the synapse has been understood for many years. Neurotransmitter molecules, usually glutamate (the anion of the amino acid glutamic acid), are packaged into synaptic vesicles (SVs) with COPI proteins like birds in a cage. This process is elaborate in itself, as my article on coatomers described last year. Triggered by calcium ion bursts, the SVs bind to the membrane facing the cleft and release their neurotransmitters into the gap. The molecules bind to receptors on the receiving side, triggering another chain of ion channels that continue the signal down the neuron. The signal propagates all the way to the next synapse.

This much was known, but there were many questions. Biochemists have been limited in their ability to envision the details in the 20-nanometer synaptic cleft and adjacent neural receptors. In PNAS, Richard G. Held and colleagues from Stanford described how they observed synaptic vesicles at the nanoscopic scale by applying cryo-electron tomography after “slicing” synapses from the hippocampus with focused ion-beam milling. This gave them an unprecedented view of the positions of numerous proteins during movement of neurotransmitters across the synapse. Sure enough, the SVs look like little balls with protein tethers attached to guide them.       

Zooming In

Jeremy S. Dittman of Cornell commented on the paper in PNAS. He summarized what happens in preparation for traversing the synapse:

Many of the big questions currently being explored by synaptic biologists are centered on the mechanistic details of the exocytic process and how the two sides of the synapse coordinate signal transmission with reception,briefly summarized as follows: On the presynaptic side, small neurotransmitter-filled synaptic vesicles (SVs) traffic to the cleft-facing electron-dense region of the plasma membrane termed an “active zone” (AZ) where they become tightly attached to the membrane by a core set of proteins (a process termed vesicle docking and priming). Upon arrival of an action potential and subsequent opening of presynaptic voltage-gated Ca2+channels (VGCCs), elevated Ca2+ triggers some of these prepared SVs to fuse with the plasma membrane within a fraction of a millisecond, rapidly transmitting a chemical signal across the cleft

This all happens in a fraction of a millisecond. Let that sink in. 

A local reserve of SVs replenishes the “release-ready” vesicles on a subsecond time scale to sustain ongoing synaptic activity. Just after fusion, the bolus of neurotransmitter rapidly dissipates within the cleft via diffusion, binding to transporters, and in some synapses, by enzymatic degradation.

The neurotransmitters only have a brief window of time to bind to one of the receptors on the receiving neuron, usually AMPA receptors. The signals are received by a protein-dense region called the post-synaptic density (PSD). 

Held et al. wanted to know if the neurotransmitters follow a direct path from AZ to receptor, in what has been dubbed a “nanocolumn” (NC). The surprising answer was: some do, but others do not. A membrane-proximal synaptic vesicle (MPSV) usually travels straight to an AMPA receptor but might travel obliquely to a different one, or to a different receptor like NMDA. This mechanism possibly allows additional information to be conveyed to the receiving neuron. 

Whether AMPA receptors were corralled within PSD nanoclusters or randomly distributed across the postsynaptic membrane, the average response to the fusion of a MPSV (mean number of open AMPA receptors) was similar. By contrast, variability between each distinct MPSV simulation was increased when AMPA receptors were clustered instead of uniformly distributed. One implication of this simulation is that, assuming AMPA receptors adopt a clustered arrangement within the PSD, then some SVs have a larger postsynaptic impact than others. Given previous observations that NCs at these synapses may be altered by synaptic plasticity, perhaps the lack of correlation between MPSVs and PSD nanoclusters observed in this study provides a substrate for boosting synaptic strength via tightening the alignment between MPSVs and PSD receptor clusters. Combined with previous proposals for enhanced AMPA receptor clustering in response to plasticity induction, these effects could harness the variability observed on the simulations of Held et al to produce a large enhancement in synaptic strength.

For those interested in getting into the weeds, the paper and commentary give the names of numerous proteins involved in this rapid transfer of information across the synapse. The authors conclude with a statement of fine tuning:

Together, our data support a model in which synaptic strength is tuned at the level of single vesicles by the spatial relationship between scaffolding nanoclusters and single synaptic vesicle fusion sites.

As impressed as Dittman was by the work, he realizes it leaves many questions:

How are the AZ protein complexes arranged to couple Ca2+ elevation to exocytosis on such a rapid time scale? And related to this, are there special sites in the AZ where SVs dock, prime, and fuse or can SVs fuse anywhere on the AZ membrane? Are SV fusion sites precisely aligned with postsynaptic receptor clusters to ensure maximal receptor activation? Are there different types of synaptic transmission events that convey distinct information between the synaptic partners?

That last question opens the possibility of reasons for the kludge of synaptic transmission: “distinct information” can be transmitted depending on the neurotransmitter, its path, its timing, and its receptor. Indeed, a team of researchers in China and Singapore has been inspired to mimic the synapse in smart wearable materials to allow for more efficient and variable information flow via multiplexing — i.e., conveying multiple types of information over the same communication channel. Why? Because “Information in biological entities is conveyed by solvated ion carriers in water environments, allowing integration, parallelism, and optimal power consumption to control motion,” they said in their paper that was published in PNAS.

Pruning and Self-Tuning

Functioning neural circuits rely on the precise wiring of neurons to their appropriate synaptic partners. Initially, these connections are imprecise, with neurons making contacts with multiple different potential partners. These connections become more precise through a process called synaptic pruning, which eliminates unnecessary synapses.

To me, it’s not enough to quote Hebb’s Law that “New branches tend to be added at the loci where spontaneous activity of individual branches is more correlated with retinal waves, whereas asynchronous activity is associated with branch elimination.” Something else is controlling the synchronization of activity, else the pruning would leave only the strongest branch. A rose gardener knows when the pruning has been optimized for flowering. Something is telling a nerve network when optimality has been reached.

Another paper in PNAS offered additional reasons for synapses instead of direct junctions. Xiong et al. wrote about self-tuning of presynaptic neurons, even in lowly roundworms:

Faced with a myriad of internal and external challenges, neurons display remarkable adaptability, adjusting dynamically to maintain synaptic stability and ensure the fidelity of neural circuit function. This homeostatic adaptability is essential not only for neural circuit integrity but also has implications for various psychiatric and neurological pathologies. At the presynaptic terminal, the influx of calcium through specific ion channels is necessary for the exocytosis of neurotransmitter-filled synaptic vesicles. Our studies in the nematode Caenorhabditis elegans reveal a sophisticated mechanism where the abundance of presynaptic calcium channels is negatively regulated by the efficiency of synaptic vesicle exocytosis. This self-regulating mechanism ensures that presynaptic neurotransmitter release is autonomously adjusted, thereby maintaining synaptic function and safeguarding the robustness of neural communication.

Now I’m starting to get it. The reason for the kludgy synapse design is greater flexibility, information flow, and adaptability. And if the transmission still occurs within milliseconds, who is going to complain about the result? I can still jump onto that rock without falling. Life is good.

Only a designed universe can be known?

 

Settled science vs. Scientific advancement?

 

A complex beginning?

 The Elegant Spindle Assembly Checkpoint

Jonathan McLatchie

In a recent article, I discussed the astounding role of motor proteins in eukaryotic cell division. But this is just one of many incredible engineered features associated with mitosis. In this and a subsequent article, I will provide an overview of the elegant molecular mechanisms that underlie the spindle assembly checkpoint and discuss the implications of its dysfunction.

Without this exquisitely engineered system, the cell risks distributing an uneven number of chromosomes to the daughter cells, potentially resulting in cancer or (in the case of meiosis), trisomy conditions such as Down Syndrome (which is characterized by an extra copy of chromosome 21).

Mitotic division (“M phase”) is the culmination of the eukaryotic cell cycle for somatic cells. Mitotic cell division is divided into six phases, illustrated in the figure above. The first is prophase, which is characterized by chromosome condensation (the reorganization of the sister chromatids into compact rod-like structures). Following condensation, assembly of the mitotic spindle apparatus occurs outside the nucleus between the two centrosomes which have duplicated and moved apart to the poles of the cell. 

The second stage of mitosis is prometaphase, which is marked by the disintegration of the nuclear envelope. This is followed by metaphase, where sister chromatids are attached to opposite spindle poles by microtubules bound to protein complexes called kinetochores. In animal cells, 10-40 microtubule-binding sites are associated with any one kinetochore. In yeast, each kinetochore contains only one attachment site. At this point, the chromosomes are seen to be aligned at the cell’s equator (the metaphase plate). The sister chromatids are themselves held together by the protein cohesin.

At anaphase, the sister chromatids separate to form two daughter chromosomes that are pulled towards opposite poles of the spindle. Microtubules bound to kinetochores, as well as the centrosome, are reeled in towards the cell’s periphery by specialized dynein motor proteins that “walk” towards the minus end of the microtubule but are held stationary by cargo-binding domains that are anchored to the cell cortex.

The next phase in the cycle is telophase, the stage at which the daughter chromosomes de-condense at the spindle poles and a new nuclear envelope is assembled. A contractile ring is then formed, marking the final stage of the process — cytokinesis. The contractile ring is comprised of actin and myosin filaments. The cell thus differentiates to form two new daughter cells, each with a nucleus containing a complete and identical set of chromosomes.

The consequences of improper attachment can be catastrophic, with segregation of two chromosome copies to a single daughter cell. The spindle assembly checkpoint pathway is responsible for inhibiting progression of mitosis from metaphase to anaphase until each of the sister chromatids has become correctly bi-oriented and securely associated with the mitotic spindle.

Controlling Metaphase-to-Anaphase Progression

Progression from metaphase to anaphase is mediated by the anaphase promoting complex or cyclosome (APC/C), an E3 ubiquitin ligase. When bound to a protein, Cdc20, the APC functions to ubiquitinate securin (a protein that prevents the cleavage of cohesin by the enzyme separase), as well as the S and M cyclins, thereby targeting them for destruction.1,2,3 The APC/C is phosphorylated by cyclin dependent kinases (Cdks), thus rendering it able to bind to Cdc20 and form the APC/CCdc20 complex. The APC/CCdc20 complex is autoinhibitory, since destruction of Cdks results in a decreased rate of APC/C phosphorylation and, as a consequence, binding of Cdc20.

Microtubule attachment to kinetochores during prometaphase is governed by a “search and capture” mechanism.4,5,6 The property of dynamic instability facilitates the process by which microtubules “search” for kinetochore attachment sites. When a microtubule encounters a kinetochore, the kinetochore is “captured” by means of side-on attachment. The sister chromatids are subsequently positioned at one of the poles of the cell, where more microtubules become attached. After the kinetochore becomes associated with a microtubule from the other pole, the chromosomes move to the equator. Though this process has been viewed for decades as being stochastic, recent work has suggested that it may in fact be more deterministic than previously recognized (see this article for a good discussion).7

This checkpoint pathway relies on a specialized mechanism for monitoring the security of kinetochore-microtubule attachment.8,9 In the case of improper attachment, the kinetochore sends out a signal — the wait anaphase signal — that inhibits activation of APC/CCdc20, thereby arresting metaphase-to-anaphase progression.

Monitoring Spindle-Kinetochore Attachment

The precise mechanism by which the spindle checkpoint system detects improper chromatid biorientation has not been fully elucidated. Two main hypotheses have been proposed, each with its own supporting data.10 One proposal suggests that the system monitors the level of tension at the kinetochore.11,12,13 Another hypothesis is that the system detects attachment of the ends of the microtubules to the kinetochore.14 The spindle assembly checkpoint pathway most likely uses a combination of those two mechanisms.

The importance of tension sensing in the spindle assembly checkpoint was first examined in insect spermatocytes, using a micromanipulation needle to apply tension to an improperly associated chromosome. Tension resulted in the commencement of anaphase in 56 minutes, whereas it was delayed by 5 to 6 hours in the absence of tension.15

Aurora kinase B plays a crucial role in tension sensing, and its inhibition results in an accumulation of improperly attached kinetochores.16,17,18,19,20 Aurora kinase B is believed to induce the inhibitory signal that destabilizes kinetochore-microtubule attachments by phosphorylating components of the kinetochore’s microtubule attachment site, including the mammalian histone-H3 variant centromere protein A (CENP-A) at serine 7.21,22 Aurora kinase B is itself recruited to the centromere by phosphorylation of CENP-A at the same residue by Aurora kinase A.23 When the function of Aurora kinase B is inhibited, one also observes a decrease in concentration of checkpoint components BubR1, Mad2 and CENP-E, and also an inability of BubR1 to rebind to the kinetochore following a decrease in tension at the centromere.24 Aurora kinase B is inactivated only after correct biorientation has occurred.

The role of microtubule attachment is demonstrated by the activity of checkpoint proteins at the kinetochore. For instance, Mad2 is present on unattached kinetochores during prometaphase, but is removed from the kinetochores as they become associated with the spindle.25 Moreover, when mammalian cells are treated with low concentrations of taxol and other microtubule-targeting drugs (thereby removing tension but retaining microtubule-kinetochore attachment), the onset of anaphase is significantly delayed.26,27

A Factory Assembly Line

Eukaryotic cell division is, in many respects, like a factory assembly line, complete with quality-control check points and robotic machines. The sheer number of things that need to go just right for successful division to take place without major complication renders it implausible that such an elegant process could have been produced by a gradual, unguided process. 

By what mechanism is the wait anaphase signal generated? Moreover, how is the spindle assembly checkpoint turned off when proper kinetochore-microtubule attachment has been established? My next article will be taken up with these questions.

Notes

Zachariae, W., Nasmyth, K. (1999) Whose end is destruction: cell division and the anaphase-promoting complex. Genes and Development 13, 2039-2058.

Barford, D. (2011) Structural insights into anaphase-promoting complex function and mechanism. Philosophical Transactions of the Royal Society B. 366, 3605–3624.

Schrock MS, Stromberg BR, Scarberry L, Summers MK. APC/C ubiquitin ligase: Functions and mechanisms in tumorigenesis. Semin Cancer Biol. 2020 Dec;67(Pt 2):80-91.

Kirschner, M., Mitchison, T. (1986) Beyond self-assembly: From microtubules to morphogenesis. Cell 3(9), 329-342.

Biggins S., Murray A.W. (2001) The budding yeast protein kinase Ipl1/ Aurora allows the absence of tension to activate the spindle checkpoint. Genes and Development 15: 3118–3129.

Hauf, S., Watanabe, Y. (2004) Kinetochore orientation in mitosis and meiosis. Cell 119, 317-327.

Soares-de-Oliveira J, Maiato H. Mitosis: Kinetochores determined against random search-and-capture. Curr Biol. 2022 Mar 14;32(5):R231-R234.

Lara-Gonzalez, P., Westhorpe, F.G., Taylor, S.S. (2012) The Spindle Assembly Checkpoint. Current Biology 22, 966-980.

McAinsh AD, Kops GJPL. Principles and dynamics of spindle assembly checkpoint signalling. Nat Rev Mol Cell Biol. 2023 Aug;24(8):543-559.

Pinsky, B.A., Biggins, S. (2005) The spindle checkpoint: tension versus attachment. Trends in Cell Biology 15(9), 486-493.Li, X., Nicklas, B. (1995) Mitotic forces control a cell-cycle checkpoint. Nature 373, 630-632.

Nicklas, R.B., Ward, S.C., Gorbsky, G.J. (1995) Kinetochore Chemistry Is Sensitive to Tension and May Link Mitotic Forces to a Cell Cycle Checkpoint. The Journal of Cell Biology. 130(4), 929-939.

Larson JD, Asbury CL. Relax, Kinetochores Are Exquisitely Sensitive to Tension. Dev Cell. 2019 Apr 8;49(1):5-7.

Waters, J.C., Chen, R., Murray, A.W., Salmon, E.D. (1998) Localization of Mad2 to Kinetochores Depends on Microtubule Attachment, Not Tension. The Journal of Cell Biology 141, 1181-1191.

Li, X., Nicklas, B. (1995) Mitotic forces control a cell-cycle checkpoint. Nature 373, 630-632.

Adams, R.R., Maiato, H., Earnshaw, W.C., Carmena, M. (2001) Essential roles of Drosophila inner centromere protein (INCENP) and Aurora-B in histone H3 phosphorylation, metaphase chromosome alignment, kinetochore disjunction, and chromosome segregation. Journal of Cell Biology 153, 865-880.

Biggins S., Murray A.W. (2001) The budding yeast protein kinase Ipl1/ Aurora allows the absence of tension to activate the spindle checkpoint. Genes and Development 15: 3118–3129.

Kallio, M.J., McCleland, M.L., Stukenberg, P.T., Gorbsky, G.J. (2002) Inhibition of aurora B kinase blocks chromosome segregation, overrides the spindle checkpoint, and perturbs microtubule dynamics in mitosis. Current Biology 12, 900-905.

Tanaka T.U, Rachidi N., Janke C., Pereira G., Galova M., Schiebel E., Stark M.J., Nasmyth K. (2002) Evidence that the Ipl1-Sli15 (Aurora kinase-INCENP) complex promotes chromosome bi-orientation by altering kinetochore-spindle pole connections. Cell 108: 317–329.

Hauf, S., Cole, R.W., LaTerra, S., Zimmer, C., Schnapp, G., Walter, R., Heckel, A., van Meel, J., Rieder, C.L., Peters, J.M. (2003) The small molecule Hesperadin reveals a role for Aurora B in correcting kinetochore-microtubule attachment and in maintaining the spindle assembly checkpoint. Journal of Cell Biology 161, 281-294.Zeitlin, S.G., Shelby, R.D., Sullivan, K.F. (2001) CENP-A is phosphorylated by Aurora B kinase and plays an unexpected role in completion of cytokinesis. Journal of Cell Biology 155, 1147-1157.

Liu, D., Lampson, M. (2009) Regulation of kinetochore–microtubule attachments by Aurora B kinase. Biochemical Society Transactions 37(5), 976-980.

Kunitoku, N., Sasayama, T., Marumoto, T., Zhang, D., Honda, S., Kobayashi, O., Hatakeyama, K., Ushio, Y., Saya, H., Hirota, T. (2003) CENP-A phosphorylation by Aurora-A in prophase is required for enrichment of Aurora-B at inner centromeres and for kinetochore function. Developmental Cell 5, 853-864.

Ditchfield, C., Johnson, V.L., Tighe, A., Ellston, R., Haworth, C., Johnson, T., Mortlock, A., Keen, N., Taylor, S.S. (2003) Aurora B couples chromosome alignment with anaphase by targeting BubR1, Mad2, and Cenp-E to kinetochores. Journal of Cell Biology161(2):267-80.

Waters, J.C., Chen, R., Murray, A.W., Salmon, E.D. (1998) Localization of Mad2 to Kinetochores Depends on Microtubule Attachment, Not Tension. The Journal of Cell Biology 141, 1181-1191.

Waters, J.C., Chen, R., Murray, A.W., Salmon, E.D. (1998) Localization of Mad2 to Kinetochores Depends on Microtubule Attachment, Not Tension. The Journal of Cell Biology 141, 1181-1191.

Hoffman, D.B., Pearson, C.G., Yen, T.J., Howell, B.J., Salmon, E.D. (2001) Microtubule-dependent changes in assembly of microtubule motor proteins and mitotic spindle checkpoint proteins at PtK1 kinetochores. Molecular Biology of the Cell 12(7), 1995-2009.

A house ever more divided?

 

The religiopolitical left and the religiopolitical right are two sides of the same coin?

 

The dragon is a bad neighbor? Pros and cons.

 

Yet more re:Darwinian occultism

 Will Evolution’s New Synthesis Be Hard or Soft Magic? 

Daniel Witt

The popular fantasy novelist Brandon Sanderson likes to divide magic into two categories: “soft magic” and “hard magic.”

In a hard magic system, the rules of the magic are made explicit to the reader: If you do x, y happens. If Harry Potter points his magic wand at someone and says, “Stupify!” then that person will be knocked unconscious. 

In a “soft” magic system, by contrast, everything is left vague. If Gandalf raises his staff and hollers, then…something will happen. Possibly. 

Sanderson points out that soft magic is best used for creating a sense of awe and wonder, while hard magic is best used for moving the plot forward and solving problems. Hard magic is not ideal for stirring up those magical feelings, because there is less mystery involved. Soft magic is not good for moving the plot, because if the reader doesn’t understand how the magic works, using it to solve the characters’ problems will feel like cheating.

This leads to Sanderson’s First Rule of Magic: An author’s ability to solve conflict with magic is DIRECTLY PROPORTIONAL to how well the reader understands said magic.

For example, this is why J. R. R. Tolkien had to keep Gandalf well out of the way for the most crucial parts of his plots. If Tolkien had made Gandalf simply magic the ring into the fires of Mount Doom and save the day, the readers would have lost interest.

Some scientists could stand to apply Sanderson’s First Rule.  

These days, quite a few biologists are saying that the neo-Darwinian synthesis has failed as an explanation for life. The magic just isn’t working anymore. There’s a lot of talk about a new synthesis to replace it. Ideas like emergence, self-organization, self-construction, panpsychism, teleonomy, and more are being put forward.

The question is: Will this new synthesis be soft magic, or hard?

Darwin’s Hard Magic

Darwin’s theory, for all its flaws, was “hard magic.” It had clearly defined rules: Self-reproducing organisms experience tiny, random variations. The beneficial ones accumulate over (practically limitless) time. This causes the organisms to slowly diversify into countless species, with each one suited to its environment. 

It was clear what this could explain, and what it couldn’t. For example, it could explain the gradual diversification of the species, but not the origin of life, or any sudden changes in the fossil record. 

Because the rules were clear, the explanation was satisfying to many people. The only problem was that it didn’t take into account some things Darwin didn’t know:

First, it turned out that the universe is probably not eternal. Darwin didn’t know that.

Second, DNA and the genetic basis of “random variation” were discovered, and it became possible to compare the amount of time needed to have a reasonably high chance of getting a given variation with the time actually available to get it. 

Third, better microscopes revealed the mind-boggling sophistication of life at the molecular level. 

Fourth, tying all these together, the molecular biologist Michael Behe noticed that many molecular structures are characterized by a high level of interdependency among parts, meaning that tiny changes on the path to creating one of these structures would not yield any survival advantage (and therefore not be selected for) until the whole structure was complete. He ran the math on the number of mutations you would need to get a typical complex feature functioning (and therefore visible to natural selection), and found that quite literally all the time in the world is not enough. 

Darwin’s theory was well-formulated and explicit. He just didn’t understand what we do now.

The Hard Magic of ID

I would say that evolution’s oldest rival, intelligent design, is also in a sense “hard magic.” 

That may be a surprising assertion. If the designer is God, per Stephen Meyer’s Return of the God Hypothesis, God is certainly a Gandalf-like figure who can do whatever he wants. (Correction: Gandalf is a God-like figure.) In fact, that is one of the main criticisms of ID: that because God is inherently unpredictable, you can’t legitimately do science on him. 

This is correct, actually. There can never be a formal science of God, or even a science that says definitively when some effect was caused by God and when it wasn’t. God — by definition — can do whatever he wants. Unlike natural phenomena, he has no limits, and therefore cannot be studied as a natural phenomenon. 

But intelligent design is the study of design, not of God. 

It’s possible to infer that something was designed, and this inference can be made mathematically rigorous, given enough data. This is not even controversial; the design inference is applied to non-deific minds in many uncontroversial fields, such as forensics, despite the facts that human minds are not much better understood by science than God’s mind is.

That’s because, while minds are not well understood, one of the only things we do understand about them is that they can design things that would not have otherwise arisen by chance and contingency, and that they do this to achieve goals. Based on this (universal) observation, intelligent design posits that if something has a specified, identifiable function, then the likelihood it was designed by a mind is the inverse of the likelihood that it arose by chance and contingency. 

But that doesn’t mean that ID theory can say who the designer was. Forensics can’t tell you whether a person or a supernatural genie of infinite power murdered someone. (You can find DNA, but the genie could have faked it.) But it can tell you that they didn’t die by chance. Whether a murderer or a devious genie is more likely is a question for philosophy. Likewise, mathematical analysis of proteins can’t tell you whether those proteins were designed by God, or a genie, or Jack the Ripper. But it most certainly can tell you that the proteins didn’t emerge by chance. 

Gandalfing the Ring into Mount Doom

So much for Darwinism and ID. What about the new contenders to replace/modify neo-Darwinism?   

Well, they’re certainly good at creating magical feelings.

Take the self-construction theorist Stuart Kauffman, waxing poetic on the theory. He says:

I invite you to do something. Go into a forest, by yourself — with some animals and some plants and some bacteria and stuff — and look around and say, “All that’s happened is that for the past 3.5 billion years the sun’s been shining, there’s been a few other sources of free energy, and all this stuff came to exist with nobody in charge.” That’s true. How much do you want for God? It’s so awesome, mysterious, grand. That’s God enough for me. 

It is indeed a very cool feeling. For me, it’s similar to the feeling I get watching Mickey Mouse struggle with the animated brooms in Fantasia. Very magical. 

It cannot, however, “move the plot.” 

How, exactly, do these theories make the emergence of life more likely than by chance? And by how much more likely? What are the odds of any specific feature emerging through teleonomy, synergism, self-organization, self-construction, autopoiesis, or emergence? How would one go about calculating these odds?

Hard to say.

It seems that kind of math Behe applied to neo-Darwinism simply can’t be applied to the new theories, because there is nothing solid to run the numbers on. To the extent that hard details are actually given, you usually find that the scientist is either (1) sneaking in an unexplained mind (for example, positing unaccounted-for intelligence in bacteria), or (2) merely describing the developing sophistication of life without actually accounting for it. 

Of course, it’s only fair to expect that an idea will start out vague. Even Darwin’s theory didn’t become really “hard” until it was integrated with Mendelian genetics after his death. I hope that these new hypotheses will be filled out with concrete details soon. Then they can become actual competitors with neo-Darwinism and ID. 

But until that happens, they will continue to leave their intended audience unsatisfied. Even in a fantasy novel, you need to do better than that. 

Hype vs. Reality re:the last cavalry charge.

 

An interlude XX

 

On persian military history.

 

Darwinism's metaphysics: a brief history

 

The struggle to replant Darwinism's tree of life is real?

 Fossil Friday: The Mystery of the Frankenstein Dinosaur

Gunter Bechly

This Fossil Friday we will look at a paleontological enigma that reveals a lot about the weaknesses of reconstructions of evolutionary trees and the phylogenetic classification of organisms, based on such shaky tree reconstructions. Paleobiologists use a methodology called cladistic analysis to reconstruct the assumed evolutionary relationships of fossil organisms. Of course, this cladistic methodology makes certain unproven assumptions such as the principle of parsimony and bifurcating (dichotomous) branching, even though nature is under no obligation to favor the most parsimonious trees or to avoid polytomous branchings or even network-like relationships (e.g., due to hybridization). But anyway, here is in simple words how cladistic tree reconstruction works in principle.

How It Is Done

The scientists compile a list of observable and relevant anatomical features of a fossil organism and possible fossil and living relatives. They construct a spread-sheet-like data matrix with different taxa as rows and different characters as columns. The fields of this data matrix allow for the coding of all character states for every taxon. These character states are usually coded as 0 for absent (or primitive / plesiomorphic state) and 1 for present (or derived / apomorphic state). Then a computer algorithm is used to find the most parsimonious branching pattern of a phylogenetic tree, which best explains the distribution of character states in the data matrix with the minimal number of necessary steps for evolutionary gains and losses. A so-called out-group taxon is included in the analysis, which is either a taxon that is presumed to be certainly more distantly related than all the other included taxa to each other, or is a hypothetical ancestor, which is coded with 0 for all character states. The tree is rooted in a way that this out-group represents the first branching of the tree. Only groups that include all branches of a node are recognized in the phylogenetic classification as monophyletic groups or clades, while grades of transitional series (paraphyletic groups) or polyphyletic groups that do not share a unique common ancestor are rejected as artificial groupings. This is why modern classifications no longer include taxa like invertebrates, or fish, or reptiles. The attribution of a fossil to a certain group must only be based on so-called shared derived characters (synapomorphies) but not on primitive similarities (symplesiomorphies) or convergent similarities (homoplasies).

So Far So Good

Now, given that we have a very extensive knowledge of most groups of dinosaurs, what would you expect if we find a new dinosaur that is almost completely and well preserved. Shouldn’t we be quite easily able to place it in the existing phylogenetic system based on the observed putative synapomorphies, thus the shared derived similarities with already known forms? Well, this works in happy Darwinian fantasy land of text books and the propaganda of popularizers of Darwinism like Richard Dawkins and Jerry Coyne, but the reality is up for a crude awakening. Often new discoveries show a confusing combination of characters that either overturn the previously preferred phylogenetic trees or require numerous ad hoc hypotheses to explain away the conflicting characters. Here is a very good example:

A few years ago, a new dinosaur genus and species, named Chilesaurus diegosuarezi, was described after a rather complete skeleton from the Late Jurassic of Chile (Novas et al. 2015). This dinosaur roamed Patagonia about 147-148 million years ago (Suárez et al. 2015). Actually, several isolated bones were already discovered and described previously, but erroneously considered to belong to different dinosaur taxa because they look so totally unrelated (Salgado et al. 2008, 2015). The original describers realized that the new dinosaur represents a quite enigmatic taxon with a bizarre combination of traits (Novas et al. 2015), and others called it “one of the most puzzling and intriguing dinosaurs ever discovered” (Barrett quoted in Rahim 2017). Initially, it was considered to be a derived theropod (Novas et al. 2015, Chimento et al. 2017, Lenin-Chávez et al. 2017, Cau 2018), thus a relative of the bipedal carnivorous dinosaurs, in spite of its spatulate dentition that clearly suggests a plant-eater (also see Lemonick 2015). It was even suggested that the forelimb structure foreshadows the acquisition of flight adaptations in avian theropods (Chimento et al. 2017). The very same year, a new study by Baron & Barrett (2017) suggested a very different affinity as basal ornithischian and a transitional ‘missing link’ between Ornithischia and Theropoda (University of Cambridge 2017). This was celebrated by media head lines around the globe as a final solution of the “mystery of the Frankenstein dinosaur” (Anonymous 2017, Geggel 2017, Gosh 2017, Rahim 2017).

One Year Later

However, just another year later a new study by Müller et al. (2018) disagreed and suggested that Chilesaurus was instead a basal representative of the sauropod lineage, but also cautioned that:

… these results demonstrate how search parameters, character scoring and taxon sampling could affect the phylogenetic position of C. diegosuarezi. Accordingly, our replication of Baron & Barrett’s [1] is compelling evidence that the phylogenetic status of C. diegosuarezi remains unstable and the mystery of this enigmatic dinosaur still remains unsolved.

Baron & Barrett (2018) defended their hypothesis, and subsequently, Müller & Dias-da-Silva (2019) changed their mind in a new study and now agreed that Chilesaurus is the basal-most member of Ornithischia, but again cautioned about unstable branches and “great uncertainty about the basic structure of the dinosaur family tree.”

A more recent study by Norman et al. (2022) recovered Chilesaurus as a highly derived ornithischian deeply nested in the family Heterodontosauridae. However, the authors also commented:

The ‘missing-link’ interpretation of its placement (Baron & Barrett, 2017) is incongruent chronologically (Late Jurassic) and evolutionarily, in the context of the acquisition of the fundamental ornithischian bauplan, but its curious opisthopubic pelvic anatomy may point toward either iterative (the repeated theropodan acquisition of opisthopuby) or atavistic anatomical phenomena. It is clear that the relationship of Chilesaurus in Dinosauria needs clarification. Most recently, Federico Agnolín (pers. comm., 25 April 2022) has reaffirmed the theropod affinities of Chilesaurus on the basis of the presence of pleurocoels, complex laminae on the cervical vertebrae, the shape of the ilium and carpal anatomy

Baron (2022) admitted that “despite these recent fluctuations, the original placement within Theropoda remains the most prevalent phylogenetic hypothesis” and that the results of his new “analysis do not by any means end the debate”, but claimed that it “produced results that again suggest that Chilesaurus could be an early diverging member of Ornithischia.” I suggest our confidence in this “could” should not be too high.

A Complete Revolution?

Of course, it is also interesting in this context that the working group of Matthew Baron and Paul Barrett published a sensational new Ornithoscelida-hypothesis of dinosaur relationships (Baron et al. 2017), which suggested a complete revolution of the traditional division of dinosaurs into those with lizard-like hips (Saurischia) and those with bird-like hips (Ornithischia). Needless to say, the new phylogeny is still highly controversial and was quickly met with some support (Cau 2018, Müller & Dias-da-Silva 2019) but also with strong skepticism and criticism by proponents of the classical hypothesis (Müller & Garcia 2020, Novas et al. 2021), which ruled dinosaur classification since 1888. Curiously, the feathered non-avian theropods and birds do not belong to the clade with bird-like hips in either hypothesis, which is quite telling in itself. Actually, the disagreement is even worse, as was convincingly shown by Norman et al. (2022: fig. 1), who documented that basically every possible topology of the relationships between the three major groups of dinosaurs has be advocated by some modern experts (see the image below).

The Collapsing Tree Challenge

This mess is yet another confirmation of my collapsing tree challenge to neo-Darwinists (Bechly 2024). Phylogenetics very much looks like a pseudoscience (such as astrology or homeopathy) with a very sophisticated methodology, which fails to produce any consistent results. Different studies based on different data do not converge on one true tree of life. When Darwin sketched his famous first tree of life in his notebook, he titled it “I think.” Maybe he would think again today. We definitely should!

References

Anonymous 2017. Monster mash: does the Frankenstein dinosaur solve the mystery of the Jurassic family tree? The Guardian August 16, 2017. https://www.theguardian.com/science/shortcuts/2017/aug/16/frankenstein-dinosaur-chilesaurus-diegosuarezi-mystery-jurassic-family-tree

Baron MG 2022. The effect of character and outgroup choice on the phylogenetic position of the Jurassic dinosaur Chilesaurus diegosaurezi. Palaeoworld 33(1), 142–151. DOI: https://doi.org/10.1016/j.palwor.2022.12.001

Baron MG & Barrett PM 2017. A dinosaur missing-link? Chilesaurus and the early evolution of ornithischian dinosaurs. Biology Letters 13(8):20170220, 1–5. DOI: https://doi.org/10.1098/rsbl.2017.0220

Baron MG, Norman DB & Barrett PM 2017. A new hypothesis of dinosaur relationships and early dinosaur evolution. Nature 543(7646), 501–506. DOI: https://doi.org/10.1038/nature21700

Baron MG & Barrett PM 2018. Support for the placement of Chilesaurus within Ornithischia: a reply to Müller et al. Biology Letters 14(3):20180002, 1–2. DOI: https://doi.org/10.1098/rsbl.2018.0002

Bechly 6 2024. Fossil Friday: Three Modern Scientific Challenges to the Causal Adequacy of Darwinian Explanations. Evolution News May 17, 2024. https://evolutionnews.org/2024/05/fossil-friday-three-modern-scientific-challenges-to-the-causal-adequacy-of-darwinian-explanations/

Cau A 2018. The assembly of the avian body plan: a 160-million-year long process. Bollettino della Società Paleontologica Italiana 57(1), 1–25. https://www.researchgate.net/publication/324941372 [DOI is broken]

Chimento NR, Agnolin FL, Novas FE et al. 2017. Forelimb Posture in Chilesaurus diegosuarezi (Dinosauria, Theropoda) and Its Behavioral and Phylogenetic Implications. Ameghiniana 54(5), 567–575. DOI: https://doi.org/10.5710/amgh.11.06.2017.3088

Geggel L 2017. This Enigmatic Dinosaur May Be the Missing Link in an Evolution Mystery. LiveScience August 16, 2017. https://www.livescience.com/60150-dinosaur-family-tree-missing-link.html

Ghosh P 2017. ‘Frankenstein dinosaur’ mystery solved. BBC August 16, 2017. https://www.bbc.com/news/science-environment-40890714

     Lemonick MD 2015. T. rex’s Oddball Vegetarian Cousin Discovered. National Geographic April 27, 2015. https://web.archive.org/web/20150429185152/http://news.nationalgeographic.com/2015/04/150427-theropod-dinosaur-vegetarian-rex-science/

Lenin-Chávez C, Ocampo-Cornejo P & Manzanero E 2017. Depicting Chilesaurus diegosuarezi (Dinosauria, Theropoda). Conference poster. https://www.researchgate.net/publication/376409197

Müller RT & Dias-da-Silva S 2019. Taxon sample and character coding deeply impact unstable branches in phylogenetic trees of dinosaurs. Historical Biology 31(8), 1089–1092. DOI: https://doi.org/10.1080/08912963.2017.1418341

Müller RT & Garcia MS 2020. A paraphyletic ‘Silesauridae’ as an alternative hypothesis for the initial radiation of ornithischian dinosaurs. Biology Letters 16(8):20200417, 1–5. DOI: https://doi.org/10.1098/rsbl.2020.0417

Müller RT, Augusto Pretto F, Kerber L, Silva-Neves E & Dias-da-Silva S 2018. Comment on ‘A dinosaur missing-link? Chilesaurus and the early evolution of ornithischian dinosaurs’. Biology Letters 14(3):20170581, 1–2. DOI: https://doi.org/10.1098/rsbl.2017.0581

Norman DB, Baron MG, Garcia MS & Müller RT 2022. Taxonomic, palaeobiological and evolutionary implications of a phylogenetic hypothesis for Ornithischia (Archosauria: Dinosauria). Zoological Journal of the Linnean Society 196(4), 1273–1309. DOI: https://doi.org/10.1093/zoolinnean/zlac062

Novas F, Salgado L, Suárez M et al. 2015. An enigmatic plant-eating theropod from the Late Jurassic period of Chile. Nature 522(7556), 331–334. DOI: https://doi.org/10.1038/nature14307

Novas FE, Agnolin FL, Ezcurra MD, Müller RT, Martinelli A & Langer M 2021. Review of the fossil record of early dinosaurs from South America, and its phylogenetic implications. Journal of South American Earth Sciences 10:103341. DOI: https://doi.org/10.1016/j.jsames.2021.103341

Rahim Z 2017. ‘Frankenstein dinosaur’ enigma solved. CNN August 16, 2017. https://edition.cnn.com/2017/08/16/health/frankenstein-dinosaur-chilesaurus/index.html

Salgado L, De La Cruz R, Suárez M, Gasparini Z & Fernández M 2008. First Late Jurassic dinosaur bones from Chile. Journal of Vertebrate Paleontology 28(2), 529–534. DOI: https://doi.org/10.1671/0272-4634(2008)28[529:FLJDBF]2.0.CO;2

       Salgado L, Novas FE, Suarez M, De La Cruz R, Isasi M, Rubilar-Rogers D & Vargas A 2015. Late Jurassic Sauropods in Chilean Patagonia. Ameghiniana 52(4), 418–429. DOI: https://doi.org/10.5710/amgh.07.05.2015.2883

Suárez M, De La Cruz R, Fanning M, Novas F & Salgado L 2015. Tithonian age of dinosaur fossils in central Patagonian, Chile: U–Pb SHRIMP geochronology. International Journal of Earth Sciences 105(8), 2273–2284. DOI: https://doi.org/10.1007/s00531-015-1287-7

University of Cambridge 2017. Study identifies dinosaur ‘missing link’. University of Cambridge press release August 16, 2017. https://www.cam.ac.uk/research/news/study-identifies-dinosaur-missing-link

More on ID as heuristic.

 

The rise of biology's heterodoxy re:Darwin

 

A gift from the heavens?

 The Story of Metals Points to Nature’s Foresight, Planning, Preparation

Andrew McDiarmid

A confluence of conditions conspired to bring metals to Earth and make them accessible to humans. But can a Darwinian process take the credit? On a new episode of ID the Future, I conclude a two-part conversation with Eric Hedin, professor emeritus of physics and astronomy at Ball State University.

In Part 2, Dr. Hedin begins by reviewing the cosmic origins of our heavy metal minerals, including iron, copper, bronze, gold, silver, platinum, and others. He also reminds us of the beneficial interaction between metals and microbes that makes advanced life on Earth possible. Hedin describes the conditions within ourselves and the conditions within our environment that were finely tuned to allow for our successful utilization of metals. He also speaks to what our use of metals reveals about the moral character of human nature.

Hedin explains why our dependence on metals continues to this day. The development of technologies associated with consumer electronics, renewable energy, and specialty steel have sparked demand for a range of specialty mineral commodities that just happen to be available for human extraction from the Earth’s crust. Hedin argues that the finely tuned confluence of conditions that brought us metals cannot be chalked up to a Darwinian process. Instead, the story of metals points to foresight, planning, and preparation, hallmarks of an intelligent design at work in the cosmos.

Find the podcast and listen to it here. 

Part 2 of a two-part conversation. Listen to Part 1 here.