Tuesday 29 November 2022
On OOL science's chirality issues
Same-Handed Molecules Are an “Overarching Design Principle” in Life, Say Researchers
David Coppedge
Homochirality, the same-handedness of building blocks of DNA and proteins, poses a severe challenge for those who deny the intelligent design of life. Design advocates have explained the problem: James Tour, Casey Luskin, Rob Stadler, and many others (see a description of the problem here). The odds of random, blind forces selecting every amino acid in a protein to be left-handed, and every sugar in a DNA chain to be right-handed, are vanishingly small.
Materialists also recognize this hurdle in their origin-of-life theories, because homochirality would have had to become established before natural selection could be called upon for assistance. But what happens when heterochiral molecules do make it into our cells? Bad things happen.
Heterochirality Syndrome
Normally, cells do a good job of keeping our molecules 100 percent homochiral. Stray wrong-handed molecules are either destroyed or turned into the correct hand before a protein or nucleic acid goes into service. A research team in France wondered what would happen if they forced certain genes to go rogue, or heterochiral. (Good thing they tried this on fruit flies and not humans.) They published the dire results in Nature Communications (open access). The Abstract of the paper by Banreti et al., “Biological effects of the loss of homochirality in a multicellular organism,” hints at troubles to come:
Homochirality is a fundamental feature of all known forms of life, maintaining biomolecules (amino-acids, proteins, sugars, nucleic acids) in one specific chiral form. While this condition is central to biology, the mechanisms by which the adverse accumulation of non-l-α-amino-acids in proteins lead to pathophysiological consequences remain poorly understood. To address how heterochirality build-up impacts organism’s health, we use chiral-selective in vivo assays to detect protein-bound non-l-α-amino acids (focusing on aspartate) and assess their functional significance in Drosophila. We find that altering the in vivo chiral balance creates a ‘heterochirality syndrome’ with impaired caspase activity, increased tumour formation, and premature death. Our work shows that preservation of homochirality is a key component of protein function that is essential to maintain homeostasis across the cell, tissue and organ level.
The authors call homochirality “an overarching design principle in all living organisms.” They do not delve into the origin of homochirality, and say essentially nothing about evolution (except for noting that a certain amino acid in a specific position of a gene is “evolutionarily conserved,” meaning it has not evolved).
Surprisingly, the health effects of heterochirality have not been studied in detail before, they say.
Furthermore, a direct link between the partial loss of homochirality and protein dysfunction has not been shown, and hence the underlying molecular and cellular mechanisms connecting heterochirality to pathophysiological sequelae remains unknown.
The bulk of the paper documents what happened to hapless flies forced to endure “heterochirality syndrome.” For example, one intervention involved knocking out the Pimt gene. This gene is an enzyme essential for repair of heterochiral proteins. It recognizes wrong-handed aspartame residues after translation and converts them into the correct left-handed form. Here’s what happened to the poor fly:
Importantly, Pimt knock-out flies showed premature death, dying 14 days earlier than control flies (Fig. 5a). Premature death was due solely to the lack of Pimt activity, as the phenotype could be fully rescued by a Pimt wild type (Pimtwt), but not a Pimt catalytic dead (PimtS60Q) knock-in construct (Fig. 5a), in which the evolutionarily conserved serine60 residue (Supplementary Fig. 5) was replaced by glutamine. Furthermore, we found that loss of Pimt activity led to the formation of protein aggregates and large melanotic tumours inside the body (Fig. 5b, c).
The loss of the heterochirality repair enzyme also gives mice a miserable, short life. And when the enzyme fails in humans, brain damage and lung cancer can result.
Importantly, Pimt knock-out mice showed significant growth retardation succumbing to fatal seizures at an average of 42 days after birth, and increased proliferation and granule cell number in the dentate gyrus. Pimtexpression and enzyme activity were significantly decreased in human astrocytic tumours and promoted epithelial mesenchymal transition in lung adenocarcinoma cell lines, indicating that impaired Pimt activity has several pathophysiological consequences.
The team excised the working part of Pimt using CRISPR-Cas9. Their observations of the aftereffects demonstrated that Pimt is “ubiquitously expressed in tissues throughout the fly life cycle” and in probably most other life forms. This fact adds to the materialist’s challenge, because even if simple cells found a way to start homochiral, they would quickly succumb to what we could dub the “right hook punch” from a wrong-handed amino acid.
What Causes the Trouble?
The team found that wrong-handed amino acids change the 3-D conformation of proteins. One right-handed aspartate (D-aspartic acid, as opposed to the correct L- form), induces structural changes to the caspase cleavage site where the correction must occur. So altered, the enzyme cannot “fit” the repair site. Caspases are involved in cutting out defective parts of proteins. They also participate in programmed cell death, or apoptosis.
Our results show that caspases malfunction when the consensus cleavage site of target proteins suffer a stereoinversion, which could potentially affect many important cellular processes.
In summary, heterochirality syndrome reduces lifespan, increases susceptibility to tumors, inhibits apoptosis, and more. People suffering from even one enzyme with a wrong-handed amino acid “are expected to have massive physiological consequences on cell and tissue homoeostasis,” and the defect “might be implicated in many human diseases.” Due to cascading effects from a heterochiral building block, it’s all downhill when random chance lands a right hook.
Overall, our results show that accumulation of non-l-α-AAs in proteins, promotes a progressive heterochirality syndrome, through a cascading effect across biological scales spanning from loss of molecular homochirality to increased resistance to caspase activity in cells, increased tumour susceptibility in organs and, consequently, premature death of the chiral-deficient animal (Fig. 6h). We further suggest that heterochirality spreading in living organisms represents a novel causal factor that may be associated with a broad range of defective cellular processes, diseases and ageing.
What Are the Implications?
Without foresight to solve heterochiral incidents, a primordial cell would quickly perish even if, against all odds, it began homochiral. These authors have shown one of the enzymes that prevents heterochirality syndrome by recognizing and fixing a single D-amino acid to its L- form. This is fascinating to ponder, since even intelligent chemists have difficulty separating the isoforms of chiral molecules (example 1, example 2).
Biochemists realize that homochirality is functionally beneficial and would tend to be preserved by natural selection. A paper in the journal Chem explained why but failed to address the origin of homochirality. Occasionally a materialist will attempt to speculate about how a protocell “emerged” from a pool of heterochiral building blocks and evolved toward homochirality via “chance aided by luck,” but those attempts usually end like this example from 2010:
Whether or not we will ever know how this property developed in the living systems represented on Earth today, studies of how single chirality might have emerged will aid us in understanding the much larger question of how life might have, and might again, emerge as a complex system.
Statements like this beg the question of emergence. Must it be materialistic? If understanding is the goal, Ockham’s razor would favor the simplest cause that is capable of separating thermodynamically equivalent objects that differ only in geometry. That cause is intelligence. Even a child could easily separate left- and right-handed toy soldiers of equal mass.
It’s been over 170 years since Louis Pasteur recognized chirality as a fundamental feature of biology (see here). Were it not for the philosophical preferences of some, the strength of intelligence over randomness in achieving perfect homochirality and maintaining it with molecular machines would universally be recognized as the most obvious choice to account for this “overarching design principle in all living organisms.”
On God and grades.
Not a family matter: The effects of religiosity on academic outcomes based on evidence from siblings
Ilana M.HorwitzaBenjamin W.DomingueaKathleen MullanHarrisb
Abstract
Religiosity has been positively linked with multiple measures of academic success, but it is unclear whether the “effect” of religiosity on academic outcomes is causal or spurious. One source of heterogeneity that may contribute to a child's level of religiosity and his/her academic success is family background. This paper is the first to use sibling differences to estimate the associations between religiosity on short and long-term academic success. Our analysis yields two main results. First, more religious adolescents earned higher GPAs in high school, even after including family fixed effects. Second, because they earned higher GPAs in high school, more religious adolescents completed more years of education 14 years after their religiosity was measured. Our findings suggest that adolescents' religious commitments influence their schooling in both the short and long term and should be more actively included and theorized as important drivers of educational and economic stratification.
Introduction
Religion permeates every aspect of American society. Religious commitments shape where Americans live, how they vote, who their friends are, and even how happy they are. Religion is a particularly salient feature for millions of American teenagers: one in two see faith as central to their daily life, and one in three say they pray daily (Smith and Denton, 2005).1 When it comes to academic performance, religiously engaged adolescents appear to have better academic outcomes than those who are not religiously active. They earn higher GPAs (Glanville et al., 2008; Good and Willoughby, 2011; McKune and Hoffmann, 2009; Milot and Ludden, 2009; Regnerus and Elder, 2003; Tirre, 2017; Toldson and Anderson, 2010), aspire to go farther in school2 (Al-fadhli and Kersen, 2010; Muller and Ellison, 2001; Regnerus, 2000), and actually stay in school longer (Brown and Gary, 1991; Kim, 2015; Lee et al., 2007; Lee and Pearce, 2019; Lehrer, 2010, 2004; Loury, 2004; Mohanty, 2016). The theoretical reason for this positive association is that increased religiosity tends to deter young people from risky behaviors, promotes social capital and network closure, and motivates youth to act in ways that adhere to the moral grounding of their religious teachings (Smith, 2003).
While the evidence suggests that more religiously engaged students have better academic outcomes, questions remain as to how to interpret this evidence. The existing evidence has been derived from observational approaches that inherently limit the scope of inference; as a consequence, there is uncertainty about whether the “effect” of religiosity on academic outcomes is causal or spurious (Bagiella et al., 2005; Cochran et al., 1994; Freeman, 1986; Regnerus and Smith, 2005). We are particularly concerned about the role of family background—a key source of heterogeneity that influences children's level of religiosity as well as their academic success (Eirich, 2012; Ludwig and Mayer, 2006). While previous studies have attempted to eliminate family-level confounders by including a set of observed family-level controls (e.g., parental education, family income, and family structure), these controls do not effectively address family-level heterogeneity, especially when these factors are unobserved (Kim, 2018). Thus, previous studies may be overstating the actual effect of religiosity, which could be null or even negative. Approaches that allow for more stringent analyses of such observed associations are useful in such settings. Here, conduct within-family analysis by analyzing sibling pairs to better understand the association of religiosity, high school GPA, college aspirations, and educational attainment. Data on sibling pairs allow us to separate the contribution of religiosity from families by examining whether sibling differences in religiosity translate into sibling differences in academic achievement (since family differences are muted between siblings).
The Lord JEHOVAH explanation/heuristic?
Coast to Coast — Stephen Meyer Takes the God Hypothesis to a Huge and Unusual Audience
David Klinghoffer
I suppose Stephen Meyer could do the safe thing and talk only to audiences that largely already accept his picture of reality. That would be safe. But would it be fun? Find out the meaning of “fun” when Dr. Meyer talks with host George Noory tonight on the phenomenally popular overnight radio show Coast to Coast AM, with 2.75 million weekly listeners. You can locate a station near you by consulting this link.
As a rule, the show covers a fascinating a mix of topics, with an emphasis on the strange and supernatural, and is never dull. For example, after the Return of the God Hypothesis author is on for two hours, from 10-12 pm Pacific / 1-3 am Eastern, the next guest is a gentleman who says he communicates with the dead. That’s right, first it’s Steve Meyer, talking about the Webb Space Telescope and the Big Bang, then a necromancer. It’s quite the pairing. Well, there are more things in Heaven and Earth than are dreamt of in any materialist’s philosophy! I intend to stay up and listen.
Also, look here for Meyer’s recent article for the Daily Wire, “Here’s Why James Webb Telescope Discoveries Are Causing Scientists To Rethink Galaxy Formation (But Not The Big Bang).”
On Darwinism's failure as a predictive model.
By Cornelius Hunter.
In addition to the DNA code, there are other fundamental molecular processes that appear to be common to all life. One intriguing example is DNA replication which copies both strands of the DNA molecule, but in different directions. Evolution predicts these fundamental processes to be common to all life. Indeed this was commonly said to be an important successful prediction for the theory. As Niles Eldredge explained, the “underlying chemical uniformity of life” was a severe test that evolution passed with flying colors. (Eldredge, 41) Likewise Christian de Duve declared that evolution is in part confirmed by the fact that all extant living organisms function according to the same principles. (de Duve, 1) And Michael Ruse concluded that the essential macromolecules of life help to make evolution beyond reasonable doubt. (Ruse, 4)
But this conclusion that the fundamental molecular processes within the cell are common to all species was superficial. In later years, as the details were investigated, important differences between species emerged. For example, key DNA replication proteins surprisingly “show very little or no sequence similarity between bacteria and archaea/eukaryotes.” (Leipe) Also different DNA replication processes have been discovered. These results were not what were expecte
In particular, and counter-intuitively, given the central role of DNA in all cells and the mechanistic uniformity of replication, the core enzymes of the replication systems of bacteria and archaea (as well as eukaryotes) are unrelated or extremely distantly related. Viruses and plasmids, in addition, possess at least two unique DNA replication systems, namely, the protein-primed and rolling circle modalities of replication. This unexpected diversity makes the origin and evolution of DNA replication systems a particularly challenging and intriguing problem in evolutionary biology. (Kooni
Some evolutionists are reconsidering the assumption that all life on Earth shares the same basic molecular architecture and biochemistry, and instead examining the possibility of independent evolution, and multiple origins of fundamentally different life forms. (Cleland, Leipe).
References
Cleland, Carol. 2007. “Epistemological issues in the study of microbial life: alternative terran biospheres?.” Studies in History and Philosophy of Science Part C: Studies in History and Philosophy of Biological and Biomedical Sciences 38:847-861.
de Duve, Christian. 1995. Vital Dust. New York: BasicBooks.
Eldredge, Niles. 1982. The Monkey Business. New York: Washington Square Press.
Koonin, E. 2006. “Temporal order of evolution of DNA replication systems inferred by comparison of cellular and viral DNA polymerases.” Biology Direct 18:1-39.
Leipe, D., L. Aravind, E. Koonin. 1999. “Did DNA replication evolve twice independently?.” Nucleic Acids Research 27:3389-3401.
Ruse, Michael. 1986. Taking Darwin Seriously. New York: Basil Blackwell.
In search of an RNA world?
When Popular Mechanics is Dissing Your Evolution Theory You Know You Have Problems
Cornelius Hunter
Don’t Two Wrongs Make a Right?
We’ve long since lost track of how many times the RNA World hypotheses—which states that life originated from an RNA enzyme-genome combination rather than from DNA—failed only to be once again resurrected, but we do know this crazy idea will, for a long time to come, continue to be cited as “good solid” evidence for evolution. This despite new research which gives yet another reason for its failure.
There are big problems with the idea that life arose from a random assembly of DNA. Aside from the little problem of generating astronomical amounts of crucial information from, err, random mutations, the resulting DNA doesn’t do anything by itself. That is because proteins are needed to extract said information and do something with it.
So, evolutionists came up with the clever idea of using RNA instead of DNA, since RNA can both store genetic information and also do something with it. Of course, this idea still has that little problem of generating the information in the first place. Oh, also, there is precisely zero evidence of any “RNA World” organisms.
Now or ever.
There is no organism that does this. There is no organism that does anything like this. There is no controlled, laboratory, version of such a thing. There isn’t even a computer simulation of it, at least in any kind of detail.
Not only does this call the entire idea into question, it also raises another little problem that if there was this so-called RNA World, then it must have gone away at some point, and neatly transitioned into a DNA world, without leaving a trace. But aside from vague speculation, there is no compelling notion of how this would occur.
This is but a brief introduction to the problems one finds with the RNA World, that have led to its repeated downfall, before its repeated resurrections.
Now, this new research points out the rather inconvenient fact that RNA is too sticky:
But while RNA strands may be good at templating complementary strands, they are not so good at separating from these strands. Modern organisms make enzymes that can force twinned strands of RNA—or DNA—to go their separate ways, thus enabling replication, but it is unclear how this could have been done in a world where enzymes didn’t yet exist.
Amazingly enough, this story was picked up by, of all mags, Popular Mechanics.
Yup. You know you have problems with Popular Mechanics is dissing your evolutionary theory.
And while one might have thought that this rather fundamental problem would have disqualified the RNA World hypothesis a long time ago—RNA’s “stickiness” was not just discovered yesterday—it turns out that fundamental problems such as this tend to be openly discussed only when a replacement theory is at the ready.
And sure enough, since DNA didn’t work, and perhaps now we can finally say that RNA also didn’t work, perhaps the trick is to combine them. Don’t two wrongs make a right? And so, it is, the new research indeed proposes that life got going by using fancy chimeric molecular strands that are part DNA and part RNA.
Well, evolution dodged another bullet. But we think we can at least say that Alexander Oparin’s 1924 prediction that origin of life research would be solved “very, very soon” hasn’t quite turned out right.Religion drives science, and it matters.
On being argumentative in lieu of making an argument.
Debunking “Professor Dave’s” Hit Piece Against Stephen Meyer
Günter Bechly
In a previous series at Evolution News (Bechly 2022a, 2022b, 2022c), I answered the diatribe by YouTuber “Professor Dave” directed against our Discovery Institute colleague, geologist Dr. Casey Luskin. The popular YouTuber, whose real name is Dave Farina, is neither a professor nor a PhD but just a failed ex-teacher who unsuccessfully tried twice to get a master’s degree in chemistry. These are simply facts about him. But his more than two million subscribers and others, who may come across his misleading content, deserve some fact-checking. Therefore, I exposed the non-professor’s propaganda and incompetence. In a second episode (Farina 2022) aimed at intelligent design proponents, Mr. Farina did it again, focusing on philosopher of science Dr. Stephen Meyer and in particular Meyer’s New York Times bestseller Darwin’s Doubt (Meyer 2013a). This YouTube video runs to about an hour and a quarter, so I will be answering him once again in a series, minute by minute. I have added timecodes in square brackets for easier reference.
So Let’s Begin
I have no problem at all with people who disagree strongly with intelligent design theory, nor with other worldviews including atheism, but one should at least assume that the other side is as honestly committed to a quest for truth as you yourself are. However, civilized discourse is not Farina’s cup of tea. In the first five minutes of his new video, he calls ID proponents “clowns,” “charlatans,” “frauds,” and “liars,” and calls ID arguments “pseudo-science,” “rubbish,” “horse manure,” and “dishonest tripe.” His personal agenda is revealed by the ridiculous statement [TC 3:00] that genocide, infanticide, eugenics, and other evils are “all the heinous acts that historically have been the exclusive domain of religion.” Has he never heard of Hitler, Stalin, Mao, or Pol Pot?
Apparently, Farina thinks the best way to deal with anybody he disagrees with is to bully and berate them with hate speech and gutter language. Here is an example of what I mean from one of his comments on YouTube (I’ve replaced certain letters with asterisks to make the profanity more tolerable to read):
Um, I’m pretty sure I would make Meyer cry. He’s a f****ing moron, as I demonstrated in this video you didn’t watch. Why are all you creationist tools such cowardly sh**bags?
When a commenter on his video against Stephen Meyer criticized his harsh language, Farina responded with even more over-the-top vituperation:
They are liars. I show how they are liars. That’s all it is. And for f****’s sake, I’m exposing the agenda of what is essentially a terrorist organization that wants to drag America back to an authoritarian theocracy and ruin millions of lives, and you have the balls to call me nasty and mean-spirited for speaking out against them? You’re f****ing stupid. I suggest you work on that. [“They” refers to Discovery Institute and ID proponents.]
What Is Wrong with This Guy?
This is not how a sane and reasonable adult writes. Since when are academic questions and intellectual debates settled by lobbing f-words? I can only pity the school kids who suffered under such an intolerant and rude person as a science teacher. Farina seems to have some significant anger management issues. He certainly is not the type of person any reasonable parents would like to have around their kids! This has nothing to do with intelligent design vs. materialism or religion vs. science. Farina’s immature pottymouth should disqualify him from any serious discourse about anything with anyone. He really needs a “time out.”
What is more, nobody who knows his stuff and is confident about his position talks or writes like Farina does. The only reason I bother to address his erroneous arguments is to equip viewers of his video with some accurate information about the scientific evidence. Therefore, I will have to heavily quote from the technical literature and provide references to mainstream peer-reviewed scientific sources. You’ll see that Farina is parroting familiar claims by ID critics like Charles Marshall (2013), Nick Matzke (2013), and Donald Prothero (2013) that have been addressed and refuted many times (e.g., Klinghoffer 2015 and CSC 2019).
Farina’s Ridiculous Parodies
[TC 5:06] Farina initially suggests that the two following arguments characterize the position of Stephen Meyer in Darwin’s Doubt:
“1) Some lies about the Cambrian explosion mean intelligent design is true.”
“2) I don’t understand genetics even a little bit so intelligent design must be true.”
Every reader should recognize these two points as ridiculous parodies. To justify his silly claims, Farina would have to establish that Meyer is not just wrong about the Cambrian Explosion and genetics, but that he is deliberately lying. He also would have to establish that Meyer suggests intelligent design is true only because of explanatory gaps in the Cambrian Explosion or genetics. Of course, Farina does nothing like that. He shows no evidence whatsoever that Meyer is lying, because of course Meyer is not doing so. He fails to show that Meyer’s claims about the Cambrian Explosion and about genetics are incorrect or that they do not represent good science. And of course, Farina himself is grossly misrepresenting the design argument, which as Meyer shows in meticulous detail is not an argument from ignorance but an inference to the best explanation based on what we do know about the causal structure of the universe.
[TC 6.55] Farina says that denying that the fossil record documents gradual change is a “huge lie.” He claims there are countless examples and lists the transitions of reptiles to mammals, fish to tetrapods, amphibians to reptiles to birds, land mammals to sea mammals (e.g., walking whales), and early hominids to humans. We will come back to these examples shortly.
A Claim of Science Denial
[TC 7:30] Farina also maintains that disputing transitional fossils is science denial. This claim has two major problems.
First, it uses an ambiguous term, “transitional fossil.” Evolutionary paleontologists and Darwin skeptics mean different things by this term. As I have written (Bechly 2021e: 346-7):
Evolutionists often say that there are many transitional fossils, while creationists often say that there are none. It seems that one side must be wrong, but actually both are right because they talk past each other and use the same term for two different things. When evolutionists talk about transitional fossils, then they usually only mean transitional in the anatomical sense. This refers to fossils that possess a mosaic pattern of characters, with some primitive characters of the assumed ancestors still retained, while some (but not all) derived characters of the assumed descendants are already developed so that the fossil is anatomically intermediate. Evolutionists do not necessarily imply with the term transitional fossil that these forms are direct ancestors, as they could well be side branches from the ancestral lineage. Therefore, transitional fossils are not necessarily in the correct temporal sequence, because such side branches could persist and even outlive more advanced forms.
When creationists and critics of Darwinism say that there is a lack of transitional fossils, they usually mean transitional in the sense of a gradual sequence of direct ancestor-descendent relationships, which implies not only a fine-graded directional anatomical transition but also a correct temporal order. While transitional fossils in the first sense are indeed very common and exist for most groups of organisms, transitional fossils in the second sense are extremely rare and mostly missing indeed
Second, it is a total red herring because, as I and others have emphasized ad nauseam in the past, intelligent design theory is agnostic concerning the question of material common descent. Farina over and over confuses intelligent design with Biblical creationism. Many prominent design proponents explicitly affirm common descent (e.g., Michael Behe, Michael Denton, Richard Sternberg, and myself) and therefore have no problems with transitional fossils and transitional series at all.
Farina gives his viewers the misleading impression that the fossil sequences he mentions establish a gradual and continuous development as predicted by Darwin. This is false.
Let’s Look at Each of His Examples
Reptile-mammal transition: Even though the so-called mammal-like reptiles indeed form a nice roughly transitional series (according to the evolutionist’s definition, given above), which is elegantly explained by common descent, they do not form an unbroken gradual series, even though this has been claimed in a few older studies (e.g., Hopson 1994 and Sidor & Hopson 1998). Rather they exhibit four distinct radiations (i.e., pelycosaurs, therapsids, cynodonts, and mammaliaforms), where each new construction appears abruptly in the fossil record (Carroll 1988: fig. 17-1). The first synapsids, previously called “pelycosaurs,” appear without precursors in the Upper Carboniferous about 307-310 mya, so that the lack of a gradual series of ancestral forms cannot be attributed to the famous “Romer’s Gap” in the fossil record after the end of the Devonian. As Kemp (2012) has emphasized, “Pelycosaur-grade synapsids originated as one of the amniote lineages that constituted part of the explosive radiation of tetrapods in the Carboniferous.” The same authors talk about the “explosive Middle Permian radiation of therapsids.” Kemp (2005: 84) mentions in his textbook on the evolution of mammals “the sudden appearance of the diverse therapsid fauna 270 Ma,” which has also been called the “therapsid event” (Lucas & Shen 2018: 13) or “Kazanian revolution” (Bakker 1980). Spindler (2014) says that the successful clade of therapsids occurs rather suddenly in the fossil record.” He refuted the alleged earlier therapsid Tetraceratops, and described a possible older bone fragment, but admits that its identification as a therapsid is weak because of limited anatomical information and conflicting characters.
Cynodonts appear suddenly in the latest Late Permian (Botha et al. 2007). The first mammaliaforms (i.e., Haramiyida) appear likewise suddenly about 247-245 mya in the Lower Triassic with an “explosive origin followed by a rapid early diversification” (Abdala et al. 2007). This was followed by a “Jurassic Big Bang” of mammaliaform evolution (Brusatte & Luo 2016). It was not Stephen Meyer who came up with terms like “therapsid event,” “Kazanian revolution,” or “Jurassic Big Bang,” but rather the experts in the mammalian fossil record, who would not have used such terms for a slow and gradual pattern of appearance.
Fish-tetrapod transition: This transition is far from being resolved in a gradual way, which is why a recent study concluded that “the fish-to-tetrapod transition is one of the fundamental problems in evolutionary biology” (Wood & Nakamura 2018). Is there a series of transitional fossils morphologically connecting lobe-finned fish and tetrapods? Yes, they are often called fishapods, and include famous taxa like Tiktaalik and Ichthyostega. Do tetrapods appear gradually from these fishapods? No, not by any stretch of the imagination! Actually, the oldest evidence for tetrapods (the Zachelmie tracks from Poland) predates the oldest fishapods by 10 million years (Ahlberg 2019). It even predates fish-like forms such as Eusthenopteron that rather resembled a salmon. Of course, this inconvenient truth can be explained away with ad hoc hypotheses like ghost lineages and an incomplete fossil record. What cannot be explained away is the simple fact of an extremely sudden appearance of tetrapods. But there is not just this temporal paradox of assumed descendants being older than their assumed ancestors. There are also large gaps in the morphological transition. This holds true especially for the transition from typical pectoral and pelvic lobe-fins to the typical tetrapod hand and foot skeleton with phalanges, for which the first evidence was just recently discovered in a well-preserved specimen of Elpistostege (Cloutier et al. 2020)
genetic changes, was achieved within the lifespan of a single species. This raises a severe waiting time problem (Evolution News 2016, also see further on) because a neo-Darwinian slow and gradual accumulation and selection of small changes over long periods of time cannot explain such fast transitions. It is not a question of implausibility, but a question of mathematical impossibility.
Early hominids to humans: It is a common misconception that the human fossil record shows a nice gradual transition from the ape-like early hominins (i.e., australopithecines) to our own genus Homo and modern humans. The truth is that there is a distinct gap between australopithecines and early Homo. The latter appears so abruptly that it has inspired a “Big Bang Theory of Human Evolution” (Swanbrow 2000). The renowned paleoanthropologist John Hawks has written (Hawks et al. 2000) that “In sum, the earliest H. sapiens remains differ significantly from australopithecines in both size and anatomical details. Insofar as we can tell, the changes were sudden and not gradual.” The authors explain it with an assumed population bottleneck two million years ago that led to a series of sudden, interrelated changes.