Thursday, 29 August 2024
More on why there is no place like home.
Beauty and Our Privileged Planet
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
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.
Tuesday, 27 August 2024
A complex beginning?
The Elegant Spindle Assembly Checkpoint
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.
Sunday, 25 August 2024
Yet more re:Darwinian occultism
Will Evolution’s New Synthesis Be Hard or Soft Magic?
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.
Friday, 23 August 2024
The struggle to replant Darwinism's tree of life is real?
Fossil Friday: The Mystery of the Frankenstein Dinosaur
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
Thursday, 22 August 2024
Monday, 19 August 2024
Sunday, 18 August 2024
A gift from the heavens?
The Story of Metals Points to Nature’s Foresight, Planning, Preparation
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.
Saturday, 17 August 2024
The engineered hard power of soft roots vs. Darwin.
How Roots Become Jackhammers
Many of us have wondered how seedlings get into the smallest cracks in driveways and sidewalks, finding openings and then penetrating hard layers to reach sunlight. In time, the seemingly flimsy shoots can cause the asphalt or concrete to buckle! Homeowners know that without stopping this natural process in time, a driveway can become a field of weeds. It’s amazing to think that such delicate stems, without muscles, can penetrate hard surfaces that greatly exceed their own strength.
A similar thing happens down at the tips of roots. A growing root tip may encounter a layer of hardpan that blocks its progress. It can either bend sideways or remain in place and call in its team of jackhammers. How it does that was the subject of a paper in Current Biology by 11 researchers, mostly from China, who want to know how to increase rice crops on which many people around the world depend for food. Rice farmers can try to plow the soil to loosen it up, which is very work intensive on terraced hillsides. An alternative would be to genetically modify the plant’s own built-in jackhammers to increase their ability to penetrate whatever soil they encounter
High School Lab Work with University Finesse
Those of us who experimented with bean sprouts in high school, watching how they grow in response to light and gravity, can relate to parts of this paper. The researchers grew rice seedlings in agar dishes and photographed their progress. Like us, they also experimented with auxin, a common plant growth hormone. What we never did in high school, though, was to genetically modify hormones with green fluorescent protein or determine the specific genes involved in root growth. Only grad level research gets that heavy into experimentation. The team also determined specific proteins involved in the “jackhammer” process and grew mutant strains lacking them to compare with the wild type (WT) seedlings. Their results were simple yet profound.
For controls, they filled agar dishes with soft (1 percent) agar and hard (3 percent) agar halfway down, simulating a hardpan layer that a root tip would encounter as it grows. One intuitive finding was that a root tip approaching the hard layer has a better chance of penetrating it if it approaches it at a right angle (90°). Gravitropism generally takes care of that. A protein named “auxin influx carrier AUXIN RESISTANT 1” (OsAUX1) was implicated in keeping the root tip pointed down. They found this out by creating a mutant form osaux1-3 lacking its function.
How can OsAUX1 facilitate root penetration into harder layers? OsAUX1-mediated shootward auxin transport is required for root gravitropism and root hair elongation in response to environmental stimuli. Consistently, osaux1-3 exhibits a reduced gravitropic response, as evidenced by a bending angle of approximately 30°, in contrast to the approximately 90° exhibited by the WT (Figures S1A and S1B). The osaux1-3 mutant also displays shorter root hairs (but with a normal number of root hair) in the split system compared with the WT (Figures S1C–S1H), indicating that the elongation of root hair in response to encountering a harder layer is dependent on OsAUX1.
Root Hairs as Anchor Bolts
Here the experiments get interesting. OsAUX1 plays two roles: keeping the root tip oriented downward and signaling for more root hairs to grow. The root hairs grow out horizontally from the root farther above the tip. Images of root tips with green fluorescent protein (GFP) show flows of auxin rising from the tip, where OsAUX1 triggers root hairs to produce more auxin. As a result, the root hairs grow longer, where they can anchor the main root in position. If you think of a jackhammer not being firmly held by an operator, it would bounce on the concrete instead of penetrating it. It needs to be anchored. Similarly, root hairs growing outward into the surrounding soil anchor the main root in position.
Root hairs are reported to aid seedling establishment through providing anchorage for emerging roots to penetrate the soil surface. Quantification of the maximum reaction force (anchorage) provided by root hairs is frequently based on the force required to extract a root. In uniform systems, the force needed to pull out a WT root was significantly greater than that required for root hair mutants across different densities of agar layers (Figure S5). Our findings support that increased root hair lengths enhance the anchorage of growing root tips to penetrate harder layers.
Root hairs are extremely thin and tiny, but enough of them spread out in all directions are sufficient to hold the main root in position for its task of penetrating the hard layer. As we learned in high school, root hairs are important for increasing the sampling area of soil for nutrient exploration. Another vital task they perform was mentioned in the paper: acquiring phosphate. As I wrote here, phosphorus is often a limiting factor for biological productivity.
The elongation of root hair results in an increased surface area of root-soil contact, generating the required anchorage force to support root penetration into compacted layers. Our previous research has also unveiled the pivotal role of OsAUX1 in facilitating root hair elongation under low phosphate conditions. This process is crucial for transporting auxin back to the differentiation zone, where root hair elongation takes place. This finding underscores the possibility that longer root hair in compacted soil may have contributed to enhanced phosphate uptake.
Accessory Proteins Essential Too
Engineering foresight took care of another problem. If the root tip grew at a constant rate when encountering the hard layer, it would likely buckle or bend. And so, as if knowing this possibility in advance, an impedance switch was built into the system. The impedance of hardpan triggers another protein, OsYUC8, to go into action switching on auxin synthesis at the root tip. OsAUX1 is then carried by transporters up to the root hairs where they also start producing more auxin, growing longer for better anchoring and nutrient exploration.
How does contact with hardpan switch this activity on? The slowdown of the root tip apparently is triggered by our friend PIEZO1 (discussed here), the touch-sensitive protein.
The mechanistic basis of OsYUC8 upregulation after encountering mechanical impedance remains unclear (Figure 2). Mechanical stimulation induces higher expression of the mechano-inducible calcium channel PIEZO1(PZO1) in columella and lateral root cap cells in Arabidopsis. Furthermore, pzo1 seedlings exhibited reduced calcium transients and failed to penetrate hard agar, indicating the involvement of PZO1 in the root’s short-term response to mechanical detection of compacted soil layers. This calcium-signaling pathway may act upstream of auxin (and OsYUC8) in the root barrier-touching response.
As usual, additional players take part in this process, increasing the complexity of the system. There are 13 other OsYUC proteins, as well as other genes, promoters, hormones, and tissues discussed in the paper. This brief overview, however, gives a taste of what’s needed for a rice root to grow in hard soil. The plant has to switch on numerous signals, transporters and promoters to slow the root down, build up the anchors in the soil, and with added auxin growth hormone, begin a controlled penetration by the tip through the hardpan. All this for a single root facing a challenge. When it succeeds, the root can explore deeper for the nutrients it needs and be more likely to survive dryness at the surface.
Not Just Rice
The authors realize that similar processes are built into other plants. Their opening sentence says, “Compacted soil layers adversely affect rooting depth and access to deeper nutrient and water resources, thereby impacting climate resilience of crop production and global food security.” Pretty important. Knowing now what they have learned — without relying on evolutionary theory even once — they can offer hope to a needy world. Their ending sentence says, “Our results provide new insights into a key root trait for breeders to select to enable crops to be more resilient to soil stresses by exploiting variation in root hair length.”
“For breeders to select” — that’s intelligent design.
Friday, 16 August 2024
More on why neanderthal Man is disinherited no more.
Fossil Friday: Human Nature of Neanderthals Supported Again
In a recent Fossil Friday article (Bechly 2024) I discussed the many lines of evidence that have accumulated in the past decade in favor of a fully human nature of Neanderthal men. As I documented with many references to the most up-to-date peer-reviewed research, we know that Neanderthals used fire, buried their dead, created stone circles and bone tools, made jewelry from eagle talons and used feathers as body decoration, made cave art with paintings and engravings, played music with bone flutes, used ochre as pigment and sophisticated fiber technology, produced flour from processed plants, dived for seafood, cooked food and self-medicated with herbal painkillers and antibiotics, and even produced glue from birch bark with a complex chemical procedure.
Hints of Compassion
Now, we can add compassion to this growing list of very human behaviors. A new study by Conde-Valverde et al. (2024) described fragments of hominin fossils from the Cova Negra cave in Spain, which have been dated by electron spin resonance (ESR)/U-series to an age of 273-146 thousand years ago. The age and the morphology clearly suggest an attribution to Neanderthals. But the truly remarkable finding was that the remains of a six-year-old child showed the typical congenital pathologies of the inner ear associated with debilitating Down syndrome. The authors suggest that this disabled child “would have required care for at least 6 years, likely necessitating other group members to assist the mother in childcare.” The press release emphasized that this “Fossil of Neanderthal child with Down’s syndrome hints at early humans’ compassion” (Reuters 2024).
It was known already that Neanderthals cared for sick and injured individuals (Hublin 2009, Noble 2010, Spikins et al. 2010, 2018, Tilley 2015, 2022, Thorpe 2016, Spikins 2022), but such behavior can also be found in some of the more intelligent and social animal species like the great apes, elephants, and whales. However, extended caregiving for a strongly disabled child is a highly non-Darwinian behavior that indeeds suggests compassion on a level only found in humans, because it is not driven by mere survival of the fittest and differential reproductive success. Elephants abandon or even kill disabled infants (Rodrigo 2011). Monkeys and apes usually neglect or reject disabled infants (Hogenboom 2015), or at best bother to care for a few weeks (Jackson 2023, Valença & Falótico 2023). There exists just a single report of maternal care for a 23-months-old disabled chimp infant with symptoms similar to Down syndrome (AFP 2015, Matsumoto et al. 2016). The compassionate caregiving of Neanderthals is clearly not intermediate between such animal behaviour and human behavior, but rather as Noble (2010) put it: Modern research “rejects the popular portrayal of Neanderthals as simple, unfeeling brutes and suggests that our closest ancient relatives may well have demonstrated a level of compassion that would put many modern humans to shame, caring for the infirm and the vulnerable for years at a time in organised groups.”
Strongly Corroboration
As I discussed in my previous article (Bechly 2024), the strong evidence for significant and common genetic admixture with modern humans, also suggests that Neanderthals and modern humans belonged to the same species. This was recently strongly corroborated by a new genetic study published in the journal Science (Li et al. 2024; also see Choi 2024b and Starr 2024), which found clear evidence for a “recurrent gene flow between Neanderthals and modern humans over the past 200,000 years”, suggesting a decreasing Neanderthal population that “was ultimately being absorbed into the modern human gene pool” as already suggested by a previous study (Stringer & Crété 2022). This definitely goes far beyond just some rare instances of admixture. Instead, it confirms a shared gene pool of different subpopulations within the same biospecies. Neanderthals were not a separate species of primitive hominins that went extinct, but were one of us and are still with us in our genes. They only vanished as a distinct group just like many other ancient subpopulations of humans, such as the Jomon people in Japan.
A Somewhat Different Result
Strangely, another new genetic study by Iasi et al. (2024), which is still in preprint stage and not yet peer-reviewed, comes to a somewhat different result and “suggests that humans interbred with Neanderthals 47,000 years ago for a period lasting 6,800 years” (Choi 2024a), but that “interbreeding that occurred at other times, such as the earlier events that impacted the Neanderthal genome, likely did not leave a detectable trace in our genome” (Choi 2024b). Looks like there is still much room for disagreement and different interpretation of the data, leading to quite different speculative scenarios.
Anyway, neither compassionate human behavior nor a shared gene pool would by itself refute a Darwinian evolution of modern humans, but such evidence certainly better resonates with the views of Darwin critics, who have always championed the view that there is only one humankind and that it is unique and distinct from the animal kingdom. Neanderthals and other ancient representatives of our genus Homo are not “stepping stones” on the way from bacteria to Beethoven, but just examples of human diversity in space and time.
References
AFP 2015. Japan researchers find chimps caring for disabled infant. Phys.org November 11, 2015. https://phys.org/news/2015-11-japan-chimps-disabled-infant.html
Bechly G 2024. Fossil Friday: New Evidence for the Human Nature of Neanderthals. Evolution News February 2, 2024. https://evolutionnews.org/2024/02/fossil-friday-new-evidence-for-the-human-nature-of-neanderthals/
Choi C 2024a. Neanderthals and humans interbred 47,000 years ago for nearly 7,000 years, research suggests. LiveScience June 7, 2024. https://www.livescience.com/archaeology/neanderthals-and-humans-interbred-47000-years-ago-for-nearly-7000-years-research-suggests
Choi C 2024b. Neanderthals didn’t truly go extinct, but were rather absorbed into the modern human population, DNA study suggests. LiveScience July 11, 2024. https://www.livescience.com/health/genetics/neanderthals-didnt-truly-go-extinct-but-were-rather-absorbed-into-the-modern-human-population-dna-study-suggests
Conde-Valverde M, Quirós-Sánchez A, Diez-Valero J, Mata-Castro N, García-Fernández A, Quam R, Carretero JM, García-González R, Rodríguez L, Sánchez-Andrés Á, Arsuaga JL, Martínez I & Villaverde V 2024. The child who lived: Down syndrome among Neanderthals? Science Advances 10(26):eadn9310, 1–10. DOI: https://doi.org/10.1126/sciadv.adn9310
Iasi LNM, Chintalapati M, Skov L, Bossoms Meta A, Hajdinjak M, Peter BM & Moorjani P 2024. Neandertal ancestry through time: Insights from genomes of ancient and present-day humans. bioRxiv May 13, 2024. DOI: https://doi.org/10.1101/2024.05.13.593955
Hogenboom M 2015. The wild chimpanzee who cared for her child with disability. Projeto GAP November 17, 2015. https://www.projetogap.org/en/news/the-wild-chimpanzee-who-cared-for-her-child-with-disability/
Hublin J 2009. The prehistory of compassion. PNAS 106(16), 6429–6430. DOI: https://doi.org/10.1073/pnas.0902614106
Jackson J 2023. Compassionate disabled infant care from a wild capuchin monkey mother. Phys.org March 7, 2023. https://phys.org/news/2023-03-compassionate-disabled-infant-wild-capuchin.html
Li L, Comi TJ, Bierman RF & Akey JM 2024. Recurrent gene flow between Neanderthals and modern humans over the past 200,000 years. Science 385(6705), 1–10. DOI: https://doi.org/10.1126/science.adi1768
Matsumoto T, Itoh N, Inoue S & Nakamura M 2016. An observation of a severely disabled infant chimpanzee in the wild and her interactions with her mother. Primates 57, 3–7. DOI: https://doi.org/10.1007/s10329-015-0499-6
Noble C 2010. My bright idea: Neanderthals could show compassion. The Guardian October 10, 2010. https://www.theguardian.com/technology/2010/oct/10/bright-idea-neanderthals-evolution
Reuters 2024. Fossil of Neanderthal child with Down’s syndrome hints at early humans’ compassion. The Guardian June 26, 2024. https://www.theguardian.com/science/article/2024/jun/26/fossil-of-neanderthal-child-with-downs-syndrome-hints-at-early-humans-compassion
Rodrigo M 2011. Handicapped baby jumbo left bleeding and abandoned in paddy field. Sunday Times May 1, 2011. https://www.sundaytimes.lk/110501/News/nws_28.html
Spikins P 2022. Material evidence: Caring for adult vulnerabilities. pp. 71–127 in: Hidden Depths: The Origins of Human Connection. White Rose University Press, New York (NY). DOI: https://doi.org/10.22599/HiddenDepths.c
Spikins P, Rutherford H & Needham A 2010. The Prehistory of Compassion. Blurb, 106 pp. https://www.blurb.com/b/1628917-the-prehistory-of-compassion
Spikins P, Needham A, Tilley L & Hitchens G 2018. Calculated or caring? Neanderthal healthcare in social context. World Archaeology 50, 384–403. DOI: https://doi.org/10.1080/00438243.2018.1433060
Starr M 2024. Humans And Neanderthals Had a Longer, More Intertwined Relationship Than We Thought. ScienceAlert July 12, 2024. https://www.sciencealert.com/humans-and-neanderthals-had-a-longer-more-intertwined-relationship-than-we-thought
Stringer C & Crété L 2022. Mapping Interactions of H. neanderthalensis and Homo sapiens from the Fossil and Genetic Records. PaleoAnthropology 2, 401–412. DOI: https://doi.org/10.48738/2022.iss2.130
Thorpe N 2016. The Palaeolithic Compassion debate – Alternative Projections of Modern-Day Disability into the Distant Past. Chapter 6, pp. 93–110 in: Powell L, Southwell-Wright W & Gowland R (eds). Care in the Past: Archaeological and Interdisciplinary Perspectives. Oxbow Books, Oxford (UK), 208 pp. https://www.jstor.org/stable/j.ctt1kw290q.11
Tilley L 2015. Setting the Scene for a Bioarchaeology of Care. pp. 13–64 in: Theory and Practice in the Bioarchaeology of Care. Springer, Cham, xvii+319 pp. DOI: https://doi.org/10.1007/978-3-319-18860-7_2
Tilley L 2022. Disability and Care in the Bioarchaeological Record. Meeting the Challenges of Being Human. pp. 457–481 in: Grauer AL (ed.). The Routledge Handbook of Paleopathology. Routledge, London (UK), 692 pp. https://www.taylorfrancis.com/chapters/edit/10.4324/9781003130994-28/disability-care-bioarchaeological-record-lorna-tilley
Valença T & Falótico T 2023. Life and death of a disabled wild capuchin monkey infant. Primates 64, 207–213. DOI: https://doi.org/10.1007/s10329-023-01052-1
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